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PubMed1997

The nitric oxide donor nitroprusside intraperitoneally affects peritoneal permeability in CAPD.

Nitroprusside is a nitric oxide (NO) donor. To investigate effects of nitroprusside i.p. on peritoneal permeability and perfusion, standard peritoneal permeability analyses were performed. Ten stable CAPD patients were studied twice within one week with glucose based dialysate (1.36% Dianeal) with and without addition of nitroprusside 4.5 mg/liter. Mass transfer area coefficients (MTAC) of CO2 were calculated to estimate peritoneal blood flow. Nitrate, a stable metabolite of NO, and cGMP, a second messenger of NO synthesis, were measured in plasma and dialysate. The MTACs of low molecular weight solutes were greater with nitroprusside (NP) compared to the control dwell (C): creatinine median 14.1 (NP) versus 9.9 ml/min (C), urea 21.7 (NP) versus 18.5 ml/min (C) and urate 10.5 (NP) versus 8.6 ml/min (C) (P < 0.05 for all). This points to an increased effective peritoneal surface area with nitroprusside. Furthermore, the restriction coefficient for the low molecular weight solutes decreased from 1.28 (C) to 1.23 (NP) (P = 0.02), suggesting some effect also on the size selectivity to these solutes. The effect of nitroprusside on the clearances of serum proteins was more pronounced. The increase with nitroprusside was 34% for beta 2-microglobulin, 70% for albumin, 77% for IgG and 143% for alpha 2-macroglobulin. This reduction in size selectivity was reflected in a decrease in the restriction coefficient for macromolecules from 2.29 (C) to 1.86 (NP), P < 0.01. This implies an increase in the intrinsic permeability of the peritoneal membrane. Kinetic modeling, using computer simulations, was done to analyze these effects in terms of the pore theory, using a convection model and a diffusion model for the transport of macromolecules. Nitroprusside led to an increase of both the large pore radius and the small pore radius and of the unrestricted area over diffusion distance. These effects were more pronounced with the diffusion model. The MTAC CO2 was not different: NP 76.9 and C 84.1 ml/min. MTACs of nitrate were not greater than expected on the basis of the molecular weight during both dwells. The dialysate/plasma (D/P) ratio of cGMP was greater after addition of nitroprusside: 0.36, range 0.21 to 0.77 (C) and 0.74, 0.23 to 2.50 (NP), P = 0.02. With nitroprusside the D/P ratio of cGMP was greater than expected on the basis of its molecular weight (P < 0.001). This points to local generation of cGMP after the addition of nitroprusside, induced by NO. No differences were found in the dialysate concentrations of the prostaglandins (PG) PGE2 and 6-keto-PGF1 alpha and thromboxane B2 after addition of nitroprusside. The transcapillary ultrafiltration rate and the net ultrafiltration rate during four hours were not different with nitroprusside. In conclusion, nitroprusside i.p. increased the effective peritoneal surface area and the intrinsic permeability, but the peritoneal blood flow did not change. The greater than expected D/P ratios of cGMP point to local generation of cGMP with nitroprusside, induced by NO.

Adult↗
PubMed1995

Nitroprusside inhibition of platelet function is transient and reversible by catecholamine priming.

BACKGROUND: The time course and reversibility of sodium nitroprusside's in vivo inhibition of platelet function are unclear. METHODS: Platelet aggregation and P-selectin expression as measures of platelet dense and alpha-granule release, respectively, were examined before and after administration of sodium nitroprusside (18 mg) to human volunteers and in in vitro studies. Hypotension occurring with sodium nitroprusside administration was treated with intravenous crystalloid and/or phenylephrine. RESULTS: Compared with preinfusion studies, platelet aggregation to epinephrine was significantly inhibited immediately and 4 min after discontinuation of the sodium nitroprusside infusion but returned to baseline at 8 and 12 min after discontinuing sodium nitroprusside. However, both dense and alpha-granule release to adenosine diphosphate after in vivo sodium nitroprusside were never significantly inhibited even at the time when sodium nitroprusside infusion was maximal. In contrast to our in vivo findings, in vitro incubation of platelet-rich plasma with sodium nitroprusside resulted in significant inhibition of dense and alpha-granule release to adenosine diphosphate. These in vitro inhibitory effects of sodium nitroprusside were reversed by pretreatment with epinephrine but not phenylephrine. CONCLUSIONS: In normal volunteers, sodium nitroprusside inhibits platelet aggregation to epinephrine but not adenosine diphosphate; inhibition was reversed within 8-12 min after discontinuing sodium nitroprusside. Sodium nitroprusside in vitro inhibition of platelet function to adenosine diphosphate was reversed by epinephrine pretreatment. Because of the rapid reversibility of its antiplatelet effect, sodium nitroprusside may be clinically useful even when there is the potential for impaired coagulation.

Adenosine Diphosphate↗
PubMed1993

Diltiazem reduces the dose requirement for nitroprusside-induced hypotension.

The efficacy of diltiazem, a calcium channel blocker, for reducing the dose requirement for nitroprusside-induced hypotension was studied in 20 healthy patients during spine fusion for scoliosis. Anesthesia included methohexital (3 mg/kg followed by 3 mg.kg-1.h-1 intravenously), nitrous oxide, and alfentanil (40 micrograms/kg, followed by 0.7 microgram.kg-1.min-1 intravenously). Patients were assigned randomly to two groups, receiving either nitroprusside alone or nitroprusside and diltiazem (bolus of 80 micrograms/kg with two consecutive infusions of 4.5 micrograms.kg-1.min-1 during the first 30 min and then 1.3 micrograms.kg-1.min-1). Nitroprusside was used to maintain mean arterial pressure at 55-60 mm Hg in both groups. Hypotension was obtained in similar times, 4 min in the group receiving nitroprusside alone (range, 1-8 min) and 2 min in the group receiving nitroprusside and diltiazem (range, 1-8 min). Nitroprusside administration lasted 186 +/- 17 min (mean +/- SEM) in the group receiving nitroprusside alone and 214 +/- 26 min (mean +/- SEM) in the other group (NS). After hypotension, arterial blood pressure returned to its initial value in a time of 7 min in the group receiving nitroprusside alone (range, 5-9 min) and 9 min in the group receiving nitroprusside and diltiazem (range, 7-13 min) (NS). Cumulative doses of nitroprusside were larger in the group receiving nitroprusside alone (0.47 +/- 0.07 mg/kg; mean +/- SEM) than in the other group (0.24 +/- 0.05 mg/kg; mean +/- SEM) (P < 0.01). Significant increase in plasma thiocyanate concentration, cardiac index, and heart rate was observed only in the group receiving nitroprusside alone, but no intergroup differences were found.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Generation of reactive oxygen species by the redox cycling of nitroprusside.

The formation of oxygen species during the redox cycling of sodium nitroprusside by rat liver microsomes and by chemical reductants was evaluated. The reduction of sodium nitroprusside by ascorbate and glutathione results in formation of the nitroprusside nitroxide radical which, on freezing at 77 K, results exclusively in the tetracyano [Fe(CN4)NO]2- and pentacyano [Fe(CN5)NO]3- forms of nitroxide radicals, respectively. The role of reducing agents on the inter-conversion of these two forms of nitroxide radical is discussed. The NADH and NADPH dependent microsomal reduction of nitroprusside results in the production of nitroprusside nitroxide radical, which in the presence of oxygen undergoes redox cycling to generate superoxide radical, and eventually hydroxyl radical is formed by a Fenton-type of reaction. Studies on the effect of several biologically or toxicologically relevant iron chelators on NADPH-dependent microsomal reduction of nitroprusside and subsequent formation of hydroxyl radical indicate that certain iron chelators such as isocitrate act as hydroxyl radical scavengers (depending on its concentration), but other chelators such as EDTA and DPTA function as good catalysts for the generation of hydroxyl radicals. The NADH and nitroprusside dependent microsomal production of hydroxyl radical is better in the presence of ATP, or equal in the presence of acetate, or diminished in the presence of DTPA when compared to the NADPH- and nitroprusside-dependent microsomal production of hydroxyl radicals. The effect of these chelates on the redox cycling of iron and nitroprusside by microsomes is discussed. Rat liver sub-mitochondrial particles and human hepatoblastoma cells (HepG2 cell line) also generated superoxide and hydroxyl radicals during the redox cycling of nitroprusside. These results provide direct evidence for the production of reactive oxygen species during the redox cycling of nitroprusside, The use of nitroprusside as a nitric oxide donor in biological systems may be complicated by the necessity to consider the generation of reactive oxygen species due to redox cycling of this compound by cellular reductases and low-molecular weight reductants.

Animals↗
PubMed2001

Chronic infusion of dobutamine and nitroprusside in patients with end-stage heart failure awaiting heart transplantation: safety and clinical outcome.

BACKGROUND: in patients with severe heart failure additional therapeutic support with intravenous inotropic or vasodilator drugs is frequently employed in an attempt to obtain hemodynamic and clinical control. No data comparing the use and efficacy of chronic intravenous inotropic and vasodilator therapy in patients with advanced heart failure are available. AIMS: we evaluated, in a group of patients with advanced heart failure undergoing chronic infusion with dobutamine or nitroprusside, in addition to optimized oral therapy, (1) the safety of chronic infusion, (2) the efficacy of both drugs in managing unloading therapy and (3) clinical outcome of the two therapeutic strategies. METHODS: one hundred and thirteen patients receiving optimized oral therapy, in functional class III/IV with symptoms and signs of refractory heart failure and requiring additional pharmacological support with either intravenous dobutamine or nitroprusside were evaluated. Clinical and therapeutic management and clinical outcome of the two groups were considered. RESULTS: dobutamine was administered for 12 h/day for 20+/-23 days at a dosage of 7+/-3 microg/kg/min to 43 patients. The mean dose of nitroprusside was 0.76+/-0.99 microg/kg/min. The mean duration of use of this drug, administered as a 12-h/day infusion was 22+/-38 days. Nitroprusside infusion allowed greater doses of short-term ACE-inhibitors to be used compared to pre-infusion (ACE-inhibitor dose: 55+/-30 mg/day vs. 127+/-30 mg/day P<0.0001) and during dobutamine infusion (ACE-inhibitor dose: 85+/-47 mg/day vs. 127+/-30 mg/day P<0.002). Nitroprusside unlike dobutamine significantly improved the NYHA functional class. Of the 113 patients, 109 (97%) had a cardiac event during a mean follow-up of 337+/-264 days. Forty-four patients required hospitalization for worsening congestive heart failure, 45/113 (39%) patients died during the follow-up and 27/113 (24%) patients had a heart transplant in status one. Hospitalization, because of worsening heart failure was less frequent in the nitroprusside than in the dobutamine subgroup [29/51 (57%) vs. 19/22 (86%) P<0.02]. The overall mortality was 28% (20/70) in the nitroprusside group and 58% (25/43) in the dobutamine group (odds ratio 0.33 CI 0.16 to 0.73 P<0.006). In the group treated with nitroprusside, heart transplantation in status one was performed in 16/33 patients (48%), while in the dobutamine group this was done in 11/14 patients (78%) (odds ratio 0.25 CI 0.06-1.02 P<0.06). There was a significant reduction in the combined end-point of mortality/heart transplantation in status one in patients treated with nitroprusside compared to those treated with dobutamine (36/70 (51%) vs. 36/43 (84%) - (odds ratio 0.34 CI 0.14-0.80 P<0.01). The incidence of adverse events in the patients treated with nitroprusside was similar to that in those treated with dobutamine (20% vs. 17% P=ns). CONCLUSIONS: for patients awaiting heart transplantation chronic intermittent nitroprusside infusions are more effective and safer than dobutamine in relieving symptoms, facilitating unloading therapy management and improving survival. Whether chronic intermittent infusion of nitroprusside could represent a feasible medical strategy in out-patients with severe heart failure remains to be investigated.

Cardiac Output, Low↗
PubMed1998

Icodextrin with nitroprusside increases ultrafiltration and peritoneal transport during long CAPD dwells.

Addition of the nitric oxide (NO) donor nitroprusside to 1.36% glucose dialysate enlarges the effective peritoneal surface area during four-hour dwells. The theoretical positive effect on ultrafiltration is, however, counteracted by an increase in glucose absorption. The absorption of the glucose polymer icodextrin is much lower in comparison with glucose-based dialysis solutions, due to its high molecular weight. In the present study 7.5% icodextrin dialysis solution with and without the addition of 4.5 mg/liter nitroprusside was studied during eight-hour CAPD dwells. Two Standard Peritoneal permeability Analyses, adapted for eight-hour dwells, were performed in 10 stable CAPD patients. Nitrate and cGMP were measured as parameters of NO synthesis. The transcapillary ultrafiltration increased in a linear way with icodextrin (ICO) and was even higher after the addition of nitroprusside (NP): 666 (ICO) versus 834 (NP) ml/8 hr, P = 0.03. The effective lymphatic absorption rate was not different. The resulting net ultrafiltration increased with nitroprusside: 344 (ICO) versus 540 (NP) ml/8 hr, P < 0.01. The mass transfer area coefficient of urea increased 15% and that of creatinine 26% with nitroprusside, consistent with the expected enlargement of the vascular peritoneal surface area. The increase in protein clearances was more pronounced the larger the protein: beta 2-microglobulin 19%, albumin 47%, IgG 63% and alpha 2-macroglobulin 95%. Dialysate/plasma (D/P) ratios of nitrate were not higher than the expected values on the basis of its molecular weight (P < 0.001). They increased 19% with nitroprusside. Also, the D/P ratio cyclic guanosine monophosphate (cGMP) after four hours increased with nitroprusside (0.39, range 0.13 to 0.55 ICO, and 0.82, range 0.36 to 1.39 NP, P = 0.01). With nitroprusside the D/P ratio cGMP was higher than expected after four and eight hours (P < 0.001). This points to local generation of NO after addition of nitroprusside. The nitroprusside induced increase in the mass transfer area coefficients (MTAC) of creatinine and in the ultrafiltration caused an increase in the creatinine clearance from 4.2 ml/min to 5.0 ml/min during the eight-hour dwell. This means that nitroprusside adds 3 liters/week to the peritoneal clearance of creatinine. The adequacy of peritoneal dialysis can therefore be improved by the addition of nitroprusside to 7.5% icodextrin, used for the long exchange.

Adult↗
PubMed1995

Differential relaxant responses of guinea-pig lung strips and bronchial rings to sodium nitroprusside: a mechanism independent of cGMP formation.

The biochemical mechanism subserving smooth muscle relaxant effects of sodium nitroprusside was examined on U46619, 9,11-dideoxy-9 alpha,11 alpha-methanoepoxy PGF2 alpha, precontracted guinea-pig lung strips and hilar bronchial rings. Lung strips were resistant to the relaxant action of sodium nitroprusside or sodium nitrite (NaNO2), whereas they markedly relaxed to 8-bromo-cyclic GMP (8-Br-cGMP), a membrane permeable analogue of cGMP. Precontracted bronchial rings completely relaxed to sodium nitroprusside, NaNO2, or 8-Br-cGMP in a concentration-dependent manner. Sodium nitroprusside (10 microM) substantially raised tissue cGMP level in lung strips. Conversely, sodium nitroprusside had no detectable effect on cGMP levels in bronchial rings. In the presence of 10 microM dipyridamole, an agent which preferentially inhibits cGMP-specific phosphodiesterase, cGMP levels in lung strips treated with sodium nitroprusside was significantly enhanced, but sodium nitroprusside demonstrated no relaxant effect on the preparations. However, dipyridamole potentiated sodium nitroprusside-induced precontracted bronchial ring relaxation without affecting the bronchial tissue cGMP level. In the presence of 10 microM LY83583 (6-anilino-5,8-quinoline-dione), a specific cGMP concentration-lowering agent, sodium nitroprusside-mediated elevation of cGMP level in lung strips was significantly reduced with no effect on the functional response. LY83583 demonstrated no inhibitory effect on either relaxation or cGMP level in bronchial rings treated with sodium nitroprusside. Our results suggest that precontracted smooth muscle in lung strips and in hilar bronchi respond distinctly to sodium nitroprusside. Furthermore, sodium nitroprusside mediates bronchial smooth muscle relaxation by mechanisms unrelated to cGMP.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

Reductive metabolism of nitroprusside in rat hepatocytes and human erythrocytes.

The metabolism of nitroprusside by hepatocytes or subcellular fractions involves a one-electron reduction of nitroprusside to the corresponding metal-nitroxyl radical. Thiol compounds also reduced nitroprusside to the metal-nitroxyl radical apparently via a thiol adduct. The nitroprusside reduction by microsomes was shown to be due to cytochrome P450 reductase as an antibody to cytochrome P450 reductase inhibits the microsomal reduction of nitroprusside, and the inhibitors of cytochrome P450 such as carbon monoxide or metyrapone had no effect. The reduction of nitroprusside by mitochondria in the presence of NADH or NADPH also produced the metal-nitroxyl radical. In hepatocytes, both mitochondria and the cytochrome P450 reductase are involved in the reduction of nitroprusside. The reductive metabolism of nitroprusside was found to produce toxic by-products, namely, free cyanide anion and hydrogen peroxide. We have also detected thiyl radicals formed in the thiol compound reduction of NP. We propose that cyanide and hydrogen peroxide are important toxic species formed in the metabolism of nitroprusside. The rate of reductive metabolism of nitroprusside by rat hepatocytes was much higher than with human erythrocytes. Therefore the major site of nitroprusside metabolism in vivo may be liver and not blood as originally proposed.

Animals↗
PubMed1990

Sodium nitroprusside decreases spinal cord perfusion pressure during descending thoracic aortic cross-clamping in the dog.

Paraplegia is a devastating complication of surgery on the descending thoracic aorta. During surgical repair, the aorta is cross-clamped, and nitroprusside is often used to treat arterial hypertension that can occur above the cross-clamp. Twenty-one dogs were studied to determine the effects of nitroprusside on intraspinal pressures, mean aortic pressures below the cross-clamp, and spinal cord perfusion pressure. Perfusion pressure in spinal radicular arteries originating below the aortic cross-clamp was estimated as the distal aortic pressure minus intraspinal pressure. Nitroprusside was used to return the mean arterial pressure above the cross-clamp to values similar to the pre-cross-clamp levels in 7 dogs. Fourteen animals did not receive sodium nitroprusside. Aortic cross-clamping resulted in small but significant increases in intraspinal pressure (4.3 +/- 0.8 to 7.5 +/- 0.9 mm Hg in non-nitroprusside-treated dogs, and 3.4 +/- 1.0 to 5.6 +/- 1.5 mm Hg in the nitroprusside group before nitroprusside). Nitroprusside caused a further increase in intraspinal pressure (5.6 +/- 1.5 to 8.3 +/- 2.2 mm Hg) and a decrease in aortic pressure below the cross-clamp (26 +/- 5 to 18 +/- 4 mm Hg). The increase in intraspinal pressure and the decrease in aortic pressure below the cross-clamp after nitroprusside resulted in a decrease in spinal cord perfusion pressure from 19 +/- 5 mm Hg to 11 +/- 4 mm Hg. Because nitroprusside decreases spinal cord perfusion pressure and may increase the risk of spinal cord ischemia, the avoidance of large doses of nitroprusside to arbitrarily return mean arterial pressure above the cross-clamp to pre-cross-clamp levels is recommended.

Animals↗
PubMed1988

Systemic and coronary hemodynamic effects of prostacyclin and nitroprusside in conscious dogs.

In order to simulate physiologic conditions and eliminate the influence of anesthesia on the cardiovascular responses to prostacyclin (PGI2) and nitroprusside, hemodynamic parameters were monitored in conscious dogs prior to and during infusion of the two agents at equally hypotensive concentrations. Heart rate was significantly increased with nitroprusside (p less than or equal to 0.05) and decreased with PGI2 (p less than or equal to 0.01), while mean ascending aortic blood flow or cardiac output increased (p less than or equal to 0.05) in response to both PGI2 and nitroprusside, more with nitroprusside than with PGI2 (p less than or equal to 0.05). Stroke volume increased with PGI2 only (p less than or equal to 0.05 vs. control, p less than or equal to 0.05 vs. nitroprusside). Both systemic and coronary (circumflex) vascular resistances decreased more with nitroprusside than with PGI2 (p less than or equal to 0.05); however, characteristic impedance (index of aortic elasticity) decreased similarly with PGI2 and nitroprusside. Circumflex coronary blood flow increased (p less than or equal to 0.05) only with nitroprusside. These results indicate that in conscious dogs (a) nitroprusside causes a greater decrease in vascular (systemic and coronary) resistance compared to PGI2, but the effects of the two vasodilators on arterial distensibility are similar; (b) nitroprusside, but not PGI2, causes a marked increase in coronary blood flow; and (c) the major distinguishing hemodynamic response to these vasodilators relates to marked bradycardia with PGI2 and tachycardia with nitroprusside, which may account for the observed differences in aortic blood flow and stroke volume.

Animals↗
PubMed1985

Age-related changes in the sensitivity to verapamil and sodium nitroprusside of vascular smooth muscle of rabbit aorta.

Age-related changes in the sensitivity to verapamil and sodium nitroprusside were examined in isolated aortic strips of the rabbit. In the aortae of newborn rabbits within 10 days of birth, the resting tone of the muscle was strongly reduced by sodium nitroprusside but not by either Ca-deficient solution or by verapamil. High K-induced contraction and noradrenaline-induced contraction were both inhibited by verapamil or sodium nitroprusside. In the aortae of 24 day-old rabbits, resting tension was slightly reduced by sodium nitroprusside but not by verapamil. High K-induced contraction was less sensitive to sodium nitroprusside than to verapamil whereas noradrenaline-induced contraction was less sensitive to verapamil than to sodium nitroprusside. In the aortae isolated from 60 day-old or older rabbits, resting tension was not affected by either sodium nitroprusside or verapamil. High K-induced contraction was inhibited by verapamil whereas sodium nitroprusside showed only a weak inhibitory effect. Noradrenaline-induced contraction was inhibited by sodium nitroprusside although verapamil had only a slight inhibitory effect. In the aortae of 1 day-old and also in adult rabbits, noradrenaline induced an additional increase in muscle tension when applied during the sustained contraction induced by high K. It is suggested that, in the newborn rabbit aorta, the voltage-dependent Ca channel is sensitive to both verapamil and sodium nitroprusside and the sensitivity to sodium nitroprusside gradually decreases during maturation whereas the receptor-linked Ca channel is also sensitive to both of the inhibitors at birth but the sensitivity to verapamil gradually decreases with age.

Aging↗
PubMed2004

Coronary hyperemic dose responses of intracoronary sodium nitroprusside.

BACKGROUND: Sodium nitroprusside is one of several agents considered effective for treating the no-reflow phenomenon during acute coronary interventions. However, the coronary hyperemic dose responses and systemic hemodynamic effects of intracoronary nitroprusside have yet to be determined in humans. The purpose of this study was to compare the hyperemic and hemodynamic responses of intracoronary nitroprusside to intracoronary adenosine in patients during cardiac catheterization with angiographically normal anterior descending arteries. METHODS AND RESULTS: In 21 patients, coronary blood flow velocity (0.014-inch Doppler flow wire), heart rate, and blood pressure were measured in unobstructed left anterior descending coronary arteries at rest, after intracoronary adenosine (30- to 50-microg boluses), and after 3 serial doses (0.3-, 0.6-, and 0.9-microg/kg boluses) of intracoronary nitroprusside. Coronary reserve was calculated as hyperemia/basal coronary flow velocity. In an additional 9 patients with intermediate stenoses (53+/-7%), 14 fractional flow reserve (FFR) measurements (using 0.014-inch pressure wire) were performed with both intracoronary adenosine and nitroprusside (0.6 microg/kg). Intracoronary nitroprusside produced equivalent coronary hyperemia with a longer duration ( approximately 25%) compared with intracoronary adenosine. Intracoronary nitroprusside (0.9 microg/kg) decreased systolic blood pressure by <20%, with minimal change in heart rate, whereas intracoronary adenosine had no effect on these parameters. FFR measurements with intracoronary nitroprusside were identical to those obtained with intracoronary adenosine (r=0.97). CONCLUSIONS: Compared with adenosine, intracoronary nitroprusside produces an equivalent but more prolonged coronary hyperemic response in normal coronary arteries. Intracoronary nitroprusside, in doses commonly used for the treatment of the no-reflow phenomenon, can produce sustained coronary hyperemia without detrimental systemic hemodynamics. On the basis of FFR measurements compared with adenosine, sodium nitroprusside also appears to be a suitable hyperemic stimulus for coronary physiological measurements.

Adenosine↗
PubMed1999

Potential role of a membrane-bound NADH oxidoreductase in nitric oxide release and arterial relaxation to nitroprusside.

The site of metabolism in vascular smooth muscle responsible for the release of nitric oxide (NO) from nitroprusside is not well established. In this study we observed that a membrane-bound NADH oxidoreductase in the pulmonary artery activates nitroprusside to release NO, and we examined whether this process could potentially participate in relaxation to nitroprusside. Relaxation to nitroprusside in bovine calf pulmonary artery is inhibited by a scavenger of NO and by an antagonist of NO stimulation of guanylate cyclase. A flavoprotein probe that inhibits pulmonary artery NADH oxidoreductase (1 micromol/L diphenyliodonium) and electron acceptors for NADH oxidoreductase (0.3 mmol/L nitroblue tetrazolium and 0.1 mmol/L ferricyanide) inhibited pulmonary artery relaxation to nitroprusside, but not to nitroglycerin. Pulmonary arteries were observed to promote the release of NO from nitroprusside in vitro, and NO release was inhibited by the presence of nitroblue tetrazolium, ferricyanide, and diphenyliodonium. In homogenates of pulmonary arteries, NADH (0.1 mmol/L) increased the release of NO from nitroprusside by approximately 6-fold, whereas NADPH, mitochondrial substrates, and other redox cofactors had minimal effects on NO release, and the action of NADH on nitroprusside was inhibited by nitroblue tetrazolium, ferricyanide, and diphenyliodonium. A membrane fraction enriched in NADH oxidoreductase activity showed a NADH-dependent release of NO from nitroprusside; nitroprusside caused NADH consumption, and it also inhibited the NADH-dependent reduction of nitroblue tetrazolium. Thus, a membrane-bound NADH oxidoreductase appears to contribute to the release of NO from nitroprusside, but not nitroglycerin, in calf pulmonary artery.

Animals↗
PubMed1999

Vasodilatation by intraperitoneal addition of nitroprusside is not a model for high peritoneal transport.

It has been suggested that the peritoneal capillary is the major determinant for peritoneal fluid transport and that an increase in the number of peritoneal capillaries may be the reason for an increased peritoneal transport rate. In this study, we investigated the impact on peritoneal fluid and solute transport of vasodilatation (which may increase the number of perfused capillaries) by intraperitoneal addition of nitroprusside. A 4-hour dwell was performed in four groups of Sprague-Dawley rats (4-8 rats in each group) with 131I albumin as an intraperitoneal volume marker. Nitroprusside at concentrations of 0% (control), 0.0005%, 0.001%, and 0.002% was added to the 3.86% glucose solution before intraperitoneal infusion. Net ultrafiltration (NUF) was 13.2 +/- 0.6 mL, 14.5 +/- 0.7 mL, 13.4 +/- 0.9 mL, and 6.3 +/- 2.0 mL for the control group and the 0.0005%, 0.001%, and 0.002% nitroprusside groups, respectively. No significant differences in peritoneal fluid absorption rate (KE) were observed among the four groups. The intraperitoneal volume, transcapillary ultrafiltration rate (Qu), and peritoneal small-solute transport rate (glucose and urea) as assessed by diffusive mass transfer coefficient were significantly higher or tended to be higher in the 0.0005% nitroprusside group as compared to control. However, with further increase in the dose of nitroprusside, these parameters started to decrease as compared to the 0.0005% nitroprusside group, and NUF was significantly lower in the 0.002% nitroprusside group, conceivably suggesting a reduction in blood flow owing to the systemic effects of nitroprusside. Our study showed that: (1) a low dose of nitroprusside increased the peritoneal small-solute transport rate, but did not decrease peritoneal transcapillary ultrafiltration rate; (2) although a high dose of nitroprusside decreased peritoneal fluid removal, the decrease was not due to an increased small-solute transport rate, but more likely to a significant drop in peritoneal blood flow; (3) vasodilatation by nitroprusside did not change peritoneal fluid absorption rate. Overall, vasodilatation does not seem to produce a pattern of peritoneal fluid kinetics similar to that seen in high transporters, who have a higher peritoneal transport rate, lower transcapillary ultrafiltration rate, and higher peritoneal fluid absorption rate.

Animals↗
PubMed1994

Effect of sodium nitroprusside on sperm motility, viability, and lipid peroxidation.

OBJECTIVE: To analyze the effect of sodium nitroprusside, a nitric oxide releaser, on sperm motion and lipid peroxidation-induced membrane damage in cryopreserved human sperm. DESIGN: Post-thaw, cryopreserved, human sperm samples were washed and divided into three aliquots. Each aliquot was incubated with either 0, 50, or 100 nM sodium nitroprusside. INTERVENTIONS: Samples were analyzed for lipid peroxidation (measured by malonaldehyde-thiobarbituric acid reactivity) at 3 hours post-thaw. MAIN OUTCOME MEASURES: Percent viability and motion parameters were assessed at 0, 10, and 30 minutes and 2, 3, 5, and 6 hours post-thaw. RESULTS: All results represent a mean +/- SEM, n = 10. Lipid peroxidation in samples incubated with 50 nM sodium nitroprusside (15.1 +/- 2.1 nM malonaldehyde/10(8) sperm) or 100 nM sodium nitroprusside (13.2 +/- 2.1 nM malonaldehyde/10(8) sperm) was significantly lower than in controls (22.7 +/- 3.1 nM malonaldehyde/10(8) sperm). Percent viability was significantly reduced from 0 minutes (60.6% +/- 3.5%) to 6 hours post-thaw in controls (38.0% +/- 5.1%) but not in 50 nM (46.8% +/- 10.4%) or 100 nM (48.8% +/- 6.5%) sodium nitroprusside-treated samples. Compared with controls (18.3% +/- 3.4%), maintenance of percent motility at 3 hours post-thaw was significantly improved in 50 nM (24.5% +/- 2.9%) and in 100 nM (26.3% +/- 3.2%) sodium nitroprusside-treated samples. Straight line velocity maintenance was significantly improved in 50 nM (37.3 +/- 1.3) and in 100 nM (37.0 +/- 1) sodium nitroprusside-treated samples as compared with controls (30.5 +/- 1.7). Significant improvements in curvilinear velocity maintenance compared with controls (56.3 +/- 2.9) also were observed in 50 nM (65.9 +/- 2.1) and 100 nM (72.1 +/- 4.1) sodium nitroprusside-treated samples. Significant differences in the motion parameters of sodium nitroprusside-treated samples were maintained at 5 and 6 hours post-thaw in comparison to controls. CONCLUSION: These results suggest that sodium nitroprusside is beneficial to the maintenance of post-thaw sperm motion and viability for up to 6 hours and that reduction of lipid peroxidative damage to sperm membranes may be the mechanism for these benefits.

Cell Survival↗
PubMed1993

Spinal cord perfusion pressure in dogs after control of proximal aortic hypertension during thoracic aortic cross-clamping with esmolol or sodium nitroprusside.

BACKGROUND: Spinal cord perfusion pressure may be reduced when sodium nitroprusside is used to control proximal aortic hypertension during thoracic aortic clamping. The effect of esmolol infusion on spinal cord perfusion pressure during thoracic aortic clamping is unknown. This study compares spinal cord perfusion pressure following control of proximal hypertension with either sodium nitroprusside or esmolol during thoracic aortic clamping. METHODS: The thoracic aorta was cross-clamped for 30 min in 18 dogs anesthetized with halothane. A control group (n = 6) received no treatment of proximal hypertension during cross-clamping. In two other groups, proximal arterial pressure was controlled (100 mmHg) by infusion of either sodium nitroprusside (n = 6) or esmolol (n = 6). Brachial and femoral arterial pressures, spinal cord perfusion pressure, pulmonary artery occlusion, central venous pressures, and cardiac output were monitored. Neurologic assessment was performed 24 h following surgery. RESULTS: Femoral arterial pressure was lower with nitroprusside (14 +/- 3 mmHg) compared to esmolol (24 +/- 4 mmHg) after 15 min of aortic cross-clamping. Cerebrospinal fluid pressure increased during aortic cross-clamping in the sodium nitroprusside group (from 7 +/- 5 to 16 +/- 6 mmHg) but not in esmolol or control groups. Spinal cord perfusion pressure was lower with nitroprusside at 15 min of aortic cross-clamping (2 +/- 4 mmHg) compared to control (15 +/- 7 mmHg) and esmolol groups (17 +/- 11 mmHg). Esmolol infusion reduced cardiac output and increased ventricular filling pressures compared to control and nitroprusside groups. CONCLUSIONS: Esmolol was associated with greater spinal cord perfusion pressure, but adverse hemodynamic effects, when compared with nitroprusside during thoracic aortic cross-clamping. When only surviving dogs (4 control, 5 esmolol, 6 nitroprusside) are considered, the incidence of neurologic deficit was greater in nitroprusside-treated dogs than in either control or esmolol-treated dogs. No difference in outcome was present when all dogs are considered.

Adrenergic beta-Antagonists↗
PubMed1984

Comparative effects of verapamil and sodium nitroprusside on contraction and 45Ca uptake in the smooth muscle of rabbit aorta, rat aorta and guinea-pig taenia coli.

The effects of verapamil and sodium nitroprusside on muscle tension and 45Ca uptake activated in different ways were compared in rabbit aorta, rat aorta and guinea-pig taenia coli. In rabbit aorta, K-induced contraction was specifically inhibited by verapamil and noradrenaline-induced contraction by sodium nitroprusside. In rat aorta, both K-induced and noradrenaline-induced contractions were inhibited by verapamil or by sodium nitroprusside also. In taenia, both K- and histamine-induced sustained contractions were inhibited by verapamil but not by sodium nitroprusside. The effect of verapamil was competitively antagonized by external Ca, while that of sodium nitroprusside was not. High K, noradrenaline and histamine increased the rate of 45Ca uptake in aortae and taenia. In rabbit aorta the increment in response to high K was specifically inhibited by verapamil and the increment induced by noradrenaline was specifically inhibited by sodium nitroprusside. In rat aorta, increments induced by both high K and noradrenaline were inhibited by verapamil and by sodium nitroprusside. In taenia, the increments induced by high K and by histamine were inhibited by verapamil but not by sodium nitroprusside. These results suggest different characteristics of Ca entry systems in these smooth muscles. In rabbit aorta, there seem to be two Ca channels, one of which is activated by high K and inhibited by verapamil, while the other is activated by noradrenaline and inhibited by sodium nitroprusside. In rat aorta, both K- and noradrenaline-activated Ca pathways are sensitive to both verapamil and sodium nitroprusside whereas, in taenia, both K- and histamine-activated Ca pathways are sensitive only to verapamil.

Animals↗
PubMed1998

Prospective comparative study with intracavernous sodium nitroprusside and prostaglandin E1 in patients with erectile dysfunction.

PURPOSE: To compare the effectiveness of intracavernous administration of sodium nitroprusside and prostaglandin E1 to induce penile erection in men with erectile dysfunction. MATERIAL AND METHODS: 100 patients with erectile dysfunction entered the study prospectively. As part of the diagnostic workup, each patient received an intracavernous injection of 20 microg prostaglandin E1 and a second injection of 600 microg sodium nitroprusside 1-7 days later. A tourniquet was placed at the base of the penis before each injection. The data recorded included time required to initiate tumescence, local and systemic side effects, objective and subjective quality of erections, duration of tumescence and patient satisfaction by means of a personal questionnaire. RESULTS: Prostaglandin E1 induced better overall responses than sodium nitroprusside, the difference being almost significant (p = 0.055). The overall duration of erections was also significantly longer with prostaglandin E1 (mean 81.3 min) than with sodium nitroprusside (mean 65.4 min; p < 0.04). 67% of the patients considered the erections induced with prostaglandin E1 to be of better quality than those with sodium nitroprusside, and only 11% stated that sodium nitroprusside was superior. Side effects were minimal with both drugs, the most frequent side effect being systemic hypotension, which was induced by sodium nitroprusside in 7% of the patients. CONCLUSIONS: The moderate risk of systemic hypotension and the lower potency of sodium nitroprusside to induce erections compared to prostaglandin E1 rules out sodium nitroprusside as a routine alternative intracavernous drug in men with erectile dysfunction at the doses employed. Sodium nitroprusside, however, could be used in patients who have intolerance or penile pain with intracavernous prostaglandin E1.

Adult↗