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PubMed1984

Nifedipine versus nitroprusside for controlling hypertensive episodes during coronary artery bypass surgery.

Intraoperative hypertensive episodes are a common problem in patients undergoing coronary artery bypass grafting. Twenty patients who developed acute hypertension (mean arterial pressure increase to 110 mmHg) were studied. Ten patients received nifedipine (about 3 micrograms kg-1 min-1) and ten patients nitroprusside (about 0.75 micrograms/kg-1 min-1) to return arterial blood pressure to control levels. All patients were anaesthetized with flunitrazepam, fentanyl, pancuronium and N2O/O2. The study compares the effects of nifedipine and nitroprusside on systemic and pulmonary haemodynamics. Both nifedipine and nitroprusside decreased arterial pressure to baseline values within about 3 min by reducing the elevated systemic vascular resistance. Cardiac filling pressures and pulmonary artery pressure decreased significantly only with nitroprusside. Following nitroprusside cardiac output remained unchanged whereas nifedipine increased cardiac output and stroke volume when blood pressure was lowered by a comparable degree. The data suggest that nifedipine primarily affects resistance vessels in the systemic circulation without significantly changing venous tone as opposed to the effect of nitroprusside. Thus, nifedipine appears to be an appropriate vasodilator for controlling arterial hypertensive episodes in patients with coronary artery disease and normal left ventricular function.

Adult↗
PubMed1989

Differential stimulation of rat lung particulate guanylate cyclase activity by atrial natriuretic peptide and sodium nitroprusside.

The effects of alpha-rat atrial natriuretic peptide (alpha-rANP) and sodium nitroprusside on the activity of rat lung particulate guanylate cyclase were examined. The particulate guanylate cyclase in partially purified rat lung membranes was stimulated by both alpha-rANP and nitroprusside. The effects of alpha-rANP and nitroprusside were, however, not additive. Diamide and N-ethylmaleimide almost completely abolished the nitroprusside-mediated stimulation, while they had only moderate effects on the alpha-rANP-mediated stimulation of the enzyme activity. ATP potentiated the enzyme stimulation by alpha-rANP, whereas it had no effect on the nitroprusside-mediated stimulation. These findings suggest that the stimulation of lung particulate guanylate cyclase activity by alpha-rANP and nitroprusside is mediated by different mechanisms.

Animals↗
PubMed1987

In vitro cyanide release from sodium nitroprusside.

In vitro release of cyanide from sodium nitroprusside in 5% dextrose in water solution following exposure or non-exposure to fluorescent light (500 ft candles or 791 microwatt per square cm [muWcm-2]), was measured by a cyanide-specific ion electrode at 4, 8, 24, 48, and 72 h. The cyanide concentrations were significantly increased at 24 h in the light-exposed solution. In this group, 100% of the cyanide was released from sodium nitroprusside at 72 h exposure to light. However, cyanide concentrations showed no significant changes for 72 h in the light-protected solutions, which were either exposed to 500 foot candles fluorescent light or stored in a dark room. Less than 2.5% of the cyanide was released from sodium nitroprusside at 72 h in both of the light-protected groups. No significant differences in cyanide concentrations were observed at 8 h among the exposed or non-exposed solutions. After 24 h of exposure, the cyanide concentrations in the exposed group were significantly higher than those of the two light-protected solutions. However, there were no significant differences between the cyanide concentration in the light-protected solutions. These results substantiate the safety of sodium nitroprusside solution for 24 h if the sodium nitroprusside containing solutions are properly protected from light. An additional study performed showed that a significant amount of cyanide released from sodium nitroprusside was adsorbed to the surface of polyvinylchloride.

Cyanides↗
PubMed1988

Comparison of nitroprusside and hydralazine in isolated uterine arteries from pregnant and nonpregnant patients.

The purpose of the present study was to determine the relative potency of nitroprusside and hydralazine with respect to inhibition of norepinephrine-induced contraction of isolated, uterine arteries from pregnant and nonpregnant patients. The arteries, obtained after hysterectomy, were dissected free from surrounding tissue, and arterial rings were prepared and mounted in tissue chambers filled with Kreb's-bicarbonate solution. Isometric tension was recorded. At concentrations of 10(-9) M to 10(-5) M, both nitroprusside and hydralazine produced concentration-dependent inhibition of the contractile response to norepinephrine. Nitroprusside and hydralazine were more potent in relaxing arteries contracted by a lower concentration (3 X 10(-6) M) of norepinephrine than by a higher concentration (10(-5) M) of norepinephrine. Regardless of the concentration of norepinephrine, nitroprusside was considerably more potent than hydralazine. The concentrations of nitroprusside that produced 50% inhibition (IC50) of the contractile response to norepinephrine (3 X 10(-6) M) in uterine arteries from pregnant and nonpregnant patients were 3.2 +/- 0.5 X 10(-9) M (n = 5) and 1.2 +/- 0.1 X 10(-9) M (n = 6), respectively. The IC50 values for hydralazine acting against norepinephrine (3 X 10(-6) M) in the uterine arteries from pregnant and nonpregnant patients were 5.1 +/- 0.5 X 10(-7) M (n = 5) and 4.0 +/- 0.5 X 10(-7) M (n = 6), respectively. Nitroprusside (10(-6) M), compared to hydralazine (10(-5) M), produced the greater maximal inhibition of norepinephrine-induced contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteries↗
PubMed1997

Halothane-induced dilatation of intraparenchymal arterioles in rat brain slices: a comparison to sodium nitroprusside.

BACKGROUND: Halothane is a potent dilator of cerebral arteries. The predominant site of cerebrovascular resistance is thought to be intracerebral arterioles, and the effects of halothane on these vessels were not previously examined. This study compared the effects of halothane with those of the vasodilator and nitric oxide donor, sodium nitroprusside, on intraparenchymal microvessel responsiveness in a brain slice preparation. METHODS: Anesthetized Sprague-Dawley rats underwent thoracotomy and intracardiac perfusion and then were decapitated. Hippocampal brain slices were prepared and placed in a perfusion/recording chamber and superfused with artificial cerebrospinal fluid. An arteriole was located within the brain parenchyma and its diameter was monitored with videomicroscopy before, during, and after various concentrations of halothane or sodium nitroprusside were equilibrated in the perfusate. All vessels were preconstricted with prostaglandin F2 alpha before halothane or sodium nitroprusside treatment. An observer blinded to treatment analyzed vessel diameter changes with a computerized videomicrometer. RESULTS: Baseline microvessel diameter was 18 +/- 2 microns in the halothane group (n = 14) and 15 +/- 1 microns in the sodium nitroprusside group (n = 15). Prostaglandin F2 alpha (0.5 micron) preconstricted vessels by approximately 15% from resting diameter in both groups. Halothane significantly and dose dependently dilated intracerebral microvessels by 54% +/- 6%, 74% +/- 8%, 108% +/- 13%, and 132% +/- 7% (normalized to the preconstricted diameter) at 0.5%, 1.0%, and 2.5% halothane, respectively. This dilatation corresponds to a decrease in a calculated index of cerebrovascular resistance index of up to 117% +/- 2% at 2.5% halothane. Sodium nitroprusside, in concentrations ranging from 10(-8) to 10(-3)M, also dose dependently dilated these intraparenchymal vessels by 129% +/- 7% at the highest concentration. These alterations in microvessel diameter corresponded to a decrease in the cerebrovascular resistance index of up to 116 +/- 4% for the largest dose. CONCLUSIONS: Halothane produces dose-dependent vasodilatation of intraparenchymal cerebral microvessels, thus predicting marked decreases in cerebrovascular resistance in this in vitro brain slice preparation. The effects of halothane on these cerebral microvessels are similar to those of the potent vasodilator sodium nitroprusside. These findings suggest that direct effects of halathane on cerebral microvessels diameter contribute substantially to alterations in cerebrovascular resistance and flow produced by this agent.

Anesthetics, Inhalation↗
PubMed2000

Role of K+ channels in augmented relaxations to sodium nitroprusside induced by mexiletine in rat aortas.

BACKGROUND: A class Ib antiarrhythmic drug, mexiletine, augments relaxations produced by adenosine triphosphate (ATP) sensitive K+ channel openers in isolated rat aortas, suggesting that it produces changes in the vasodilation mediated by ATP-sensitive K+ channels. Nitric oxide can induce its vasodilator effect via K+ channels, including ATP-sensitive K+ channels, in smooth muscle cells. Effects of mexiletine on arterial relaxations to nitric oxide donors, have not been studied. Therefore, the current study in isolated rat aortas was designed to (1) evaluate whether mexiletine augments relaxation in response to nitric oxide donors, including sodium nitroprusside, and (2) determine the role of K+ channels in mediating effects of mexiletine on such nitric oxide-mediated relaxation. METHODS: Rings of rat aortas without endothelia were suspended for isometric force recording. Concentration-response curves of sodium nitroprusside (10(-10) to 10(-5) M) and 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene (NOC-7; 10(-9) to 10(-5) M) were obtained in the absence and in the presence of mexiletine, in combination with a soluble guanylate cyclase inhibitor, 1H-[1,2,4]oxadiazolo [4,3,-a]quinoxaline-1-one (ODQ), or inhibitors for ATP-sensitive K+ channels (glibenclamide), inward rectifier K+ channels (BaCl2), delayed rectifier K+ channels (4-aminopyridine), large conductance Ca2+-dependent K+ channels (iberiotoxin), or small conductance Ca2+-dependent K+ channels (apamin). RESULTS: Mexiletine (10(-5) or 3 x 10(-5) M) augmented relaxations to sodium nitroprusside and NOC-7. In arteries treated with glibenclamide (10(-5) M), mexiletine (3 x 10(-5) M) did not affect relaxations to nitric oxide donors, whereas mexiletine augmented relaxations to sodium nitroprusside despite the presence of BaCl2 (10(-5) M), 4-aminopyridine (10(-3) M), iberiotoxin (5 x 10(-8) M) and apamin (5 x 10(-8) M). Relaxations to sodium nitroprusside were abolished by ODQ (5 x 10(-6) M), whereas these relaxations were augmented by mexiletine (3 x 10(-5) M) in arteries treated with ODQ (5 x 10(-6) M). CONCLUSIONS: These results suggest that ATP-sensitive K+ channels in vascular smooth muscle, contribute to the augmented vasodilator effect of a nitric oxide donor, sodium nitroprusside induced by mexiletine, and that the vasodilator effect is produced, at least in part, via the guanylate cyclase-independent mechanism.

Animals↗
PubMed1992

Prostacyclin (not nitroprusside) preserves venous admixture in the injured canine lung.

OBJECTIVE: To compare the effects of a prostaglandin vasodilator (prostaglandin I2 [PGI2]) with that of sodium nitroprusside in the isolated lung during 3% and 35% oxygen ventilation. BACKGROUND AND METHODS: Pulmonary vascular resistance was divided into arterial, middle, and venous segmental resistances. Left lower lobes were injured in a patchy (atelectasis) or diffuse (oleic acid-induced edema) manner. RESULTS: Nitroprusside diminished, but PGI2 ablated, the usual increase in middle segment resistance observed during 3% oxygen ventilation in atelectatic lobes. In the oleic acid-treated lobes, both nitroprusside and PGI2 ablated the increase in middle segment resistance during 3% oxygen ventilation. During nitroprusside administration, as pulmonary vascular resistance decreased, venous admixture proportionately increased, but this correlation was lost during PGI2 administration. CONCLUSIONS: We hypothesize that exogenous PGI2 dilates the vessels most constricted by hypoxia but to a lesser degree than does nitroprusside. Therefore, increases in venous admixture may be reduced during PGI2 administration, compared with nitroprusside administration.

Animals↗
PubMed1994

Variability of response to atrial natriuretic peptide and sodium nitroprusside in cultured vascular smooth muscle cells from three blood vessels.

OBJECTIVES: Vascular beds vary in their responses to atrial natriuretic peptide and sodium nitroprusside. Both of these agents dilate blood vessels by increasing intracellular guanosine 3',5'-cyclic monophosphate (cyclic-GMP) but activate different enzymes in the vascular smooth muscle cell. We aimed to determine if the response of intracellular cyclic-GMP to atrial natriuretic peptide and sodium nitroprusside varies in smooth muscle cells cultured from different vascular beds. DESIGN: Prospective, repeated measures analysis of concentration-response curves. SETTING: Anesthesia research laboratory of an academic medical center. SUBJECTS: Guinea pigs: Cultured guinea pig smooth muscle cells were obtained from three different blood vessels. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Intracellular cyclic-GMP was measured by radioimmunoassay and concentration-response curves of cyclic-GMP to atrial natriuretic peptide and sodium nitroprusside were determined. Cells from the thoracic aorta were the most responsive to atrial natriuretic peptide. Atrial natriuretic peptide (1 microM) increased cyclic-GMP concentrations to 72 +/- 5 pmol/mg (20-fold increase) with a 50% effective concentration of 3 nM. The concentration-response curve in epicardial coronary smooth muscle cells was to the right with an 50% effective concentration for atrial natriuretic peptide of 20 nM and a maximum response of a ten-fold increase in cyclic-GMP. Coronary resistance vessel cells were unresponsive to atrial natriuretic peptide. In response to sodium nitroprusside, the concentration-response curve in coronary resistance vessel cells was significantly to the left of either thoracic aorta cells or the epicardial coronary cells. The 50% effective concentration for sodium nitroprusside in coronary resistance vessel smooth muscle cells was approximately 1 microM, while in both thoracic aortic cells and epicardial coronary cells, the 50% effective concentration was ten times higher. Coronary resistance cells were the most responsive with a 62-fold increase in cyclic-GMP in response to 1 mM of sodium nitroprusside. The maximum response in thoracic aorta cells and epicardial cells was 20- and 30-fold, respectively. CONCLUSIONS: Smooth muscle cells respond differently to vasodilators. The response of these cultured cells mimics the response of the intact vascular bed from which they were obtained. These findings suggest that phenotypic properties of smooth muscle cells within a blood vessel contribute to the responsiveness of the vessel.

Analysis of Variance↗
PubMedDate not supplied

Acute and chronic beta-receptor blockage with propranolol and the cardiovascular responses to intravenous sodium nitroprusside in the conscious rabbit.

Sodium nitroprusside infused intravenously into conscious rabbits lowered blood pressure and raised heart rate and plasma noradrenaline. Acute beta blockade with propranolol, 2 mg/kg/hr i.v. for 2 hr, increased resting plasma noradrenaline and did not change the hypotensive effects of nitroprusside or the rise in plasma noradrenaline but attenuated the increase in heart rate. Chronic treatment with propranolol, 2 mg/kg twice daily for 3 weeks, did not modify the cardiovascular or reflex effects of nitroprusside. However, bilateral sinoaortic denervation augmented the hypotensive effect of nitroprusside and abolished both the heart rate and plasma noradrenaline responses to the vasodilator. The fall in blood pressure after nitroprusside is therefore attenuated by baroreflex mechanisms, which did not appear to be mediated by beta adrenoceptors or by withdrawal of vagal tone but could involve alpha-receptor-mediated vasoconstriction. Propranolol does not lower noradrenaline or modify the increase in noradrenaline after sodium nitroprusside.

Animals↗
PubMed1981

Purification of a soluble, sodium-nitroprusside-stimulated guanylate cyclase from bovine lung.

A soluble, sodium-nitroprusside-stimulated guanylate cyclase as been purified from bovine lung by DEAE-cellulose chromatography, ammonium sulfate precipitation, chromatography on Blue Sepharose CL-6B and preparative gel electrophoresis. Apparent homogeneity was obtained after at least 7000-fold purification with a yield of 3%. A single stained band (Mr 72000) was observed after gel electrophoresis in the presence of sodium dodecyl sulfate. The purified enzyme migrated as one band also under non-denaturing conditions in acrylamide gels (5-12%). The mobility of this band corresponded to an Mr of 145000. The enzyme sedimented on sucrose gradients with an S20, w of 7.0 S. Gel filtration yielded a Stokes' radius of 4.6 nm. These data suggest that the enzyme has an Mr of approximately 150000 and consists of two, presumably identical, subunits of Mr 72000. Sodium nitroprusside stimulated the purified enzyme 15-fold and 140-fold to specific activities of 8.5 and 15.7 mumol of cGMP formed min-1 mg-1 in the presence of Mn2+ and Mg2+, respectively. Formation of cGMP was proportional to the incubation time and to the amount of enzyme added. The stimulatory effect of sodium nitroprusside was half-maximal at about 2 microM, was observed immediately after addition and could be reversed either by dilution or by removal of sodium nitroprusside on a Sephadex G-25 column. The purified enzyme in the absence of catalase was stimulated by sodium nitroprusside, N-methyl-N'-nitro-N-nitrosoguanidine and 3-morpholino-sydnonimine and in the presence of catalase by sodium nitrite and sodium azide. In the presence of Mn2+ and sodium nitroprusside, the purified enzyme catalyzed the formation of cAMP from ATP at a rate of 0.6 mumol min-1 mg-1.

Animals↗
PubMed1978

Effects of minoxidil and nitroprusside on reflex increases in myocardial contractility.

1 The effects of nitroprusside and minoxidil on increases in myocardial contractility resulting from carotid artery occlusion were investigated in anaesthetized dogs. The results were compared with those produced by intravenous influsion of noradrenaline. 2 Nitroprusside and minoxidil attenuated the pressor responses produced by carotid artery occlusion. 3 Nitroprusside, but not minoxidil, attenuated the maximal myocardial contractility resulting from carotid occlusion. 4 The pressor and contractility responses to noradrenaline infusion were unaffected by either agent. 5 Nitroprusside failed to alter the myocardial responses produced by dimethylphenylpiperazinium. 6 These results, in conjunction with those of other investigators who have demonstrated that nitroprusside does not affect the release of noradrenaline from adrenergic neurons, suggest that nitroprusside may inhibit sympathetic nervous system reflex activity via an afferent and/or central component.

Animals↗
PubMed1985

The effects of sodium nitroprusside and 8-bromo-cyclic GMP on electrical and mechanical activities of the rat tail artery.

The effects of sodium nitroprusside and 8-bromo-guanosine 3':5'-cyclic monophosphate (8-bromocyclic GMP) on the electrical and mechanical activities of the rat tail artery were compared. The inhibitory effects of sodium nitroprusside on the contractions induced by noradrenaline, phenylephrine, KC1 and clonidine were mimicked by 8-bromo-cyclic GMP. Sodium nitroprusside and 8-bromo-cyclic GMP increased the resting membrane potential only in preparations with low initial resting membrane potentials. In tissues previously contracted and depolarized with noradrenaline, KC1 and clonidine, both sodium nitroprusside and 8-bromo-cyclic GMP caused relaxation without significantly affecting the membrane potential. Both sodium nitroprusside and 8-bromo-cyclic GMP abolished neurally-mediated contractions without any significant effect on the electrical responses. These results suggest that the actions of sodium nitroprusside and 8-bromo-cyclic GMP are not related to membrane hyperpolarization or inhibition of membrane excitability.

Animals↗
PubMed1993

The effects of N omega-nitro-L-arginine methyl ester, sodium nitroprusside and noradrenaline on venous return in the anaesthetized cat.

1. The vascular actions of N omega-nitro-L-arginine methyl ester (L-NAME), sodium nitroprusside and noradrenaline were investigated in cats under chloralose anaesthesia with controlled vascular tone and ventilation. Cardiac output, heart rate, vascular pressures and mean circulatory filling pressure (MCFP) were measured. Total peripheral resistance (TPR) and resistance to venous return (Rvr) were calculated from steady-state readings. 2. L-NAME (37 mumol kg-1, i.v.) administered to ten cats receiving noradrenaline (6 nmol kg-1 min-1, i.v.) increased aortic pressure by 47.5 +/- 7.1 mmHg from 106 mmHg, and MCFP by 1.56 +/- 0.36 mmHg from 10.0 mmHg (means +/- s.e. means). Mean changes in portal venous pressure, RAP and heart rate were not significant. Cardiac output fell by 29.7 +/- 3.3% from 130 ml min-1 kg-1. TPR rose by 108 +/- 7.2% from 796 mmHg l-1 min kg and Rvr by 58.4 +/- 4.5% from 64 mmHg l-1 min kg. 3. Infusion of sodium nitroprusside into cats receiving noradrenaline evoked dose-related falls in aortic pressure, MCFP, TPR and Rvr. Changes in portal venous pressure, RAP and heart rate were not significant and cardiac output fell slightly. After L-NAME, sensitivity to nitroprusside was increased by 139 +/- 34% for MCFP, 176 +/- 19% for TPR and 351 +/- 39% for Rvr, and cardiac output rose slightly. The nitroprusside infusion required to restore TPR after L-NAME was estimated to be 5.8 x 10(+/- 0.41) nmol kg-1 min-1, which was approximately three times more than that required to restore MCFP. 4. Infusion of noradrenaline evoked dose-related increases in aortic and portal venous pressures, heart rate, cardiac output, MCFP, TPR and Rvr. After L-NAME and nitroprusside (4.4 nmol kg-1 min-1, i.v.),TPR and Rvr were not significantly different, but MCFP was reduced by 1.76 +/- 0.24 mmHg, and cardiac output by 22 +/- 1.9%. After subsequent expansion of the circulating blood volume (5-7.5 ml kg-1 dextran-saline), mean values for all parameters were restored to their previous levels. Sensitivity to noradrenaline was not significantly altered for heart rate, TPR and Rvr but was reduced by 31.8 +/- 12%for MCFP and by 66.5 +/- 18% for cardiac output.5. The depression of cardiac output by L-NAME is attributed to the increase in Rvr, partly compensated by the rise in MCFP. For a given rise in MCFP, the increase in R, was seven times greater after L-NAME than after noradrenaline, and the difference in the relative actions of the two drugs on resistance and capacitance vessels largely accounts for their contrasting effects on venous return. A procedure is suggested for replacement of vascular nitric oxide by nitroprusside infusion and blood volume expansion.

Anesthesia↗
PubMed1998

Sodium nitroprusside enhances contractions of the guinea-pig isolated vas deferens.

The effects of sodium nitroprusside on the electrical and mechanical properties of the smooth muscle of the guinea-pig vas deferens, and its responses to transmitter substances, have been investigated by use of the sucrose-gap technique. Isolated longitudinal segments of guinea-pig vas deferens contracted in response to electrical field stimulation (100 V, 0.04-0.1 ms, 1-5 Hz, 10 s train every 60 s) and application of ATP (1 mM) or noradrenaline (10 microM). Sodium nitroprusside (0.1 mM) did not affect resting tension but did enhance contractions evoked by electric-field stimulation but not by ATP or noradrenaline. The sodium nitroprusside-induced enhancement was unaffected by the nitric oxide synthase inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME) (0.1 mM). Conversely, electrically evoked contractions were unaffected by the nitric oxide precursor L-arginine (1 mM) or the nitric oxide donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) (0.1 mM). The amplitudes of electrically evoked excitatory junction potentials (EJPs) were not affected by application of sodium nitroprusside, although it caused a small depolarization of 0.7+/-0.3 mV. Similarly, the depolarization caused by exogenous application of ATP or noradrenaline was unaffected by the presence of sodium nitroprusside. L-NAME, L-arginine and SNAP did not affect EJP amplitude or baseline membrane potential. It is concluded that sodium nitroprusside enhances electrically evoked contractions of the guinea-pig vas deferens by reducing the threshold voltage for action potential firing in smooth-muscle cells.

Action Potentials↗
PubMed1980

Synergistic effects of a combined salbutamol-nitroprusside regimen in acute myocardial infarction and severe left ventricular failure.

The haemodynamic effects of a simultaneous infusion of salbutamol and nitroprusside were measured in 20 patients with acute myocardial infarction and severe left ventricular failure. Six patients also had clinical manifestations of cardiogenic shock. Ten patients received salbutamol first with the subsequent addition of nitroprusside; in the other 10 patients nitroprusside was infused first. Salbutamol was infused at a constant rate of 20 micrograms/min in all patients, while the dose of nitroprusside, which averaged 51.25 micrograms/min, was adjusted to reduce left ventricular filling pressure (measured as pulmonary artery end-diastolic pressure) to approximately 15 mm Hg with reference to sternal angle. Cardiac index increased in all patients from a mean of 1.8 to 2.6 l/min/m2 while pulmonary artery end-diastolic pressure fell significantly from 24 to 16 mm Hg. The adverse effects were small in most patients: heart rate did not increase significantly and systolic arterial pressure fell on average from 112 to 96 mm Hg. Ten of the 20 patients survived to leave hospital. Nitroprusside accounted for most of the fall in filling pressure irrespective of treatment sequence, whereas both drugs contributed to the augmented cardiac output. The haemodynamic benefits of this combined regimen were considerably greater than those achieved by either drug alone. Thus salbutamol and nitroprusside have synergistic effects which influence favourably the two principal manifestations of left ventricular dysfunction after extensive myocardial infarction.

Aged↗
PubMed1979

Myocardial relaxation. I. Effect of nitroprusside on the tension prolongation phenomenon.

The effects of nitroprusside and cyanide on myocardial relaxation were studied during hypoxia and reoxygenation of isolated rat papillary muscle, and during segmental ischemia and reperfusion in the intact dog heart. Nitroprusside did not affect isolated muscle performance before or during hypoxia. During reoxygenation of hypoxic muscles, the tension prolongation phenomenon (which characterizes abnormal or prolonged relaxation) was only slightly attenuated by the addition of nitroprusside to the muscle bath; in contrast, cyanide (at concentrations that did not prevent the return of tension) abolished tension prolongation during reoxygenation. During reperfusion of ischemic segments in intact hearts, the prolongation of segment tension was not affected by systemic administration of nitroprusside, but was abolished by intracoronary cyanide. Attenuation of the tension prolongation phenomenon by nitroprusside in the isolated muscle may be due to the liberation of cyanide. Inasmuch as nitroprusside did not affect the tension prolongation phenomenon in the intact heart, it is unlikely that the influence of this drug on left ventricular diastolic compliance is mediated through an alteration in the tension prolongation phenomenon.

Animals↗
PubMed1998

Similarities and differences between the effects of amino acids and nitroprusside on peritoneal permeability during CAPD.

OBJECTIVE: Intraperitoneal administration of amino acid based dialysis solutions affects the surface area available for diffusion, with almost no effect on the intrinsic permeability to macromolecules. Intraperitoneally administered nitroprusside affects the vascular surface area and the intrinsic permeability without effect on the peritoneal blood flow. In the present study, these differences were translated into different effects on the radii of the pores in the peritoneal membrane. METHODS: Effects of amino acid based dialysate and nitroprusside on peritoneal permeability characteristics were evaluated in standard peritoneal permeability analyses with L-arginine-containing amino acid dialysate (10 patients) or with 1.36% glucose dialysate with nitroprusside (10 patients). In each patient a control experiment with 1.36% glucose was performed. Kinetic modeling was done to analyze the effects in terms of the pore theory. RESULTS: Both interventions increased the mass transfer area coefficients of low molecular weight solutes. This is in accordance with an increase in the unrestricted area over diffusion distance found with modeling. With amino acids almost no effect was found on the protein clearances; the increase in the large-pore radius was only small. Nitroprusside induced a marked increase in protein clearances. This was in accordance with an evident increase in the average large-pore radius. CONCLUSIONS: Amino acids affect the radii of the small pores and the large pores to the same extent. Nitroprusside influences especially the large pores. Both amino acids and nitroprusside are vasoactive, although the effects on the peritoneal microcirculation are different.

Adult↗
PubMed1983

Effect of ouabain and alterations in potassium concentration on relaxation induced by sodium nitroprusside.

Relaxation of the rat thoracic aorta induced by sodium nitroprusside, 8-bromo-cyclic GMP and cyclic nucleotide phosphodiesterase inhibitor M & B 22,948 was inhibited by exposure to K+-free solution and ouabain in a concentration-dependent manner. Relaxation occurring with the change in potassium concentration in media from 1 to 2 to 10 mM was increased by sodium nitroprusside, 8-bromo-cyclic GMP and M & B 22,948. Thus, agents and procedures known to decrease and increase the activity of the Na+,K+-pump, and presumably alter the membrane potential, inhibited and enhanced relaxation, respectively. Exposure to 1 mM K+ solution increased the relaxation to low concentrations of sodium nitroprusside, but had no effect on relaxation induced by 8-bromo-cyclic GMP or M & B 22,948. Thus, another procedure which inhibits the Na+,K+-pump enhanced the effect of low concentrations of sodium nitroprusside on relaxation. Ouabain had no effect on sodium nitroprusside-induced accumulation of cyclic GMP. These results suggest that sodium nitroprusside may induce relaxation through cyclic GMP formation, effects on the Na+,K+-pump and/or hyperpolarization of the smooth muscle cell membrane.

Animals↗