Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Nitroprusside”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1978

Enhancement of tissue Po2 of strangulated bowel by topical application of sodium nitroprusside.

The Po2 was measured in the tissue of the ileal wall of dogs before, during, and up to one hour after reversible occlusion of segmental arteries. The occlusion was then released and the reoxygenation of the bowel wall was observed. Sodium nitroprusside (50 mg in 100 ml of solution) applied topically to the ischemic segment enhanced reoxygenation as compared to control animals. Nitroprusside absorbed into the portal system did not cause hypotension, as is usual with systemic administration, because nitroprusside is inactivated by passage through the liver. Topically applied sodium nitroprusside alleviates intestinal ischemia by direct local vasodilatation and relaxation of smooth muscle spasm in the ischemic bowel wall. The intraperitoneal use of sodium nitroprusside should be clinically evaluated in situations where visceral perfusion is impaired.

Administration, Topical↗
PubMed1998

Cutaneous vasodilation induced by local warming, sodium nitroprusside, and bretylium iontophoresis on the hand.

Local warming alone induces a cutaneous vasodilation considered as maximal. The argument that local warming generates a maximum flow is being tested by vasodilation with alternate approaches to see if a greater vasodilation is possible: blockade of the release of transmitters from the adrenergic nerve endings with bretylium tosylate or direct pharmacological action on vascular smooth muscle using sodium nitroprusside. Nine healthy subjects participated in two experiments in which SkBF was measured simultaneously by laser Doppler flowmetry on the dorsal aspects of both hands. In the first protocol the vasodilator effects of 20 min of local warming at 44 degreesC were measured on one hand and the effects of iontophoresis of sodium nitroprusside on the other. The second protocol was like the first except that iontophoresis of bretylium tosylate instead of sodium nitroprusside was performed. Local warming induced an increase of SkBF from 17.6 +/- 4.4 to 140.2 +/- 33.2 AU (P < 0.01) while it rose from 16.7 +/- 4.0 to 114.7 +/- 11.0 AU (P < 0.001) during sodium nitroprusside iontophoresis. During the second protocol local warming induced an increase of SkBF from 14.9 +/- 2.1 to 117.7 +/- 25.4 AU (P < 0.01) while it rose from 19.6 +/- 2.6 to 120.5 +/- 11.3 AU (P < 0.001) during bretylium iontophoresis. However, in both experiments, the increase of SkBF attained during iontophoresis did not differ significantly from the increase achieved by local warming. We conclude that the effects of iontophoresis of sodium nitroprusside or of bretylium produce a cutaneous vasodilation as high as a local warming on the dorsal aspect of the hand.

Adult↗
PubMed1981

Plasma catecholamines, plasma renin activity and haemodynamics during sodium nitroprusside-induced hypotension and additional beta-blockage with bunitrolol.

The effects of beta-blockade on certain physiological and haemodynamic responses to sodium nitroprusside-induced hypotension have been studied in 5 patients, aged 18--54 years, undergoing inner ear surgery. Samples of blood were collected under premedication, following induction of anaesthesia, during neuroleptanalgesia, during a sodium nitroprusside infusion adjusted to produce a 40% fall in blood pressure, during superimposed beta-blockage with bunitrolol and under stable haemodynamic conditions after discontinuation of sodium nitroprusside. The sodium nitroprusside-induced reduction in blood pressure led to a massive increase in plasma noradrenaline and adrenaline and in plasma renin activity. beta-blockade with bunitrolol did not affect the increased catecholamine concentrations, the increase in plasma renin activity was significantly reduced, the increase in heart rate was reversed, and total peripheral resistance and diastolic blood pressure were further reduced. These changes can be attributed to the intrinsic beta-synmpathomimetic activity of bunitrolol in addition to its beta-blocking effect. Since no adverse effect was observed in this study, combined therapy with sodium nitroprusside and beta-receptor blockade should be employed if the effects of increased sympathetic tone are considered to be undesirable.

Adolescent↗
PubMed1977

Cyanide toxicity following nitroprusside induced hypotension.

Several recently reported deaths following the use of sodium nitroprusside have been attributed to the accumulation of the nitroprusside metabolite, cyanide. In this study, brief nitroprusside infusions (mean = 36 minutes) were administered in currently recommended doses during intracranial surgery. The peak blood cyanide following the infusions was 65.2 +/- 17.5 microgram per cent (mean +/- SE) (n = 13). It occurred within 45 minutes after infusion. The highest cyanide level detected was 205 microgram per cent, which is within the range of reported lethal blood cyanide levels. Metabolic acidosis developed in the four patients with the highest blood cyanide levels (range 90-205 microgram per cent). This occurred between 45 and 180 minutes following the cyanide peak. Blood ATP levels were depressed in the same patients. These findings are indicative of disturbed aerobic metabolism. We conclude that there is evidence of cyanide toxicity when nitroprusside is infused into patients using currently recommended doses. We recommend that for short infusions the dose of sodium nitroprusside should not exceed 0.5 mg/kg.

Acidosis↗
PubMed2000

Responses of the skin microcirculation to acetylcholine and to sodium nitroprusside in chronic uremic patients.

The aim of the present study was to assess the endothelial function of the microcirculation in chronic renal failure. We investigated the responses of the cutaneous blood flow to locally delivered acetylcholine and sodium nitroprusside in uremic patients. The study included 60 chronic uremic patients: 40 patients with a creatinine clearance of 4-25 ml/min were on conservative treatment and 20 patients were on maintenance hemodialysis. The changes in skin blood flow following iontophoretic delivery of acetylcholine (an endothelium-dependent vasodilator) and sodium nitroprusside (an endothelium-independent vasodilator) were measured by laser Doppler flowmetry. Acetylcholine induced a progressive increase in blood flow in both groups, reaching approximately 100% of the maximal hyperemic response obtained by sodium nitroprusside delivery. The percent increase in blood flow from baseline was lower in hemodialysis patients than in patients on conservative treatment, after both acetylcholine (550 +/- 44 vs. 718 +/- 61%, P < 0.05) and sodium nitroprusside (553 +/- 46 vs. 735 +/- 69%, P < 0.05) delivery. In the hemodialysis group, the hyperemic responses to acetylcholine and sodium nitroprusside did not improve after the hemodialysis session. Hence, the hyperemic responses of the skin microcirculation are lower in hemodialysis patients than in patients on conservative treatment, and did not ameliorate after hemodialysis. It seems to be independent of endothelial dysfunction, and associated with the severity of uremia and with the maintenance hemodialysis treatment. This microcirculatory abnormality is in keeping with the arterial stiffness and vascular wall damages described in dialysis patients, which contribute to the cardiovascular morbidity of chronic uremia.

Acetylcholine↗
PubMed1987

Myocardial metabolism and coronary sinus blood flow during coronary artery surgery: effects of nitroprusside and nifedipine.

The effects of nitroprusside and nifedipine on hemodynamics, coronary dynamics, and global myocardial metabolism were compared in two groups of patients undergoing elective coronary artery surgery, who were anesthetized with fentanyl, 100 micrograms/kg. After induction of anesthesia, either nitroprusside or nifedipine was started as follows: group S (n = 11) received nitroprusside at an initial rate of 1.3 micrograms/kg/min; group N (n = 9) received nifedipine at an initial rate of 0.7 micrograms/kg/min. Infusion rates were adjusted to maintain systolic blood pressure (SBP) between 80% and 120% of preinfusion (control) values. Control measurements were obtained 10 minutes after intubation. Then vasodilator infusion was started. Additional measurements were obtained 10 minutes after the start of infusion (before surgery) and after sternotomy. The mean (+/- SD) total dose requirements were: nitroprusside, 1.6 +/- 0.3 micrograms/kg/min; and nifedipine 1.1 +/- 0.7 micrograms/kg/min. The mean (+/- SD) total infusion time was: nitroprusside, 32 +/- 5 minutes; and nifedipine, 37 +/- 7 minutes. After 10 minutes of infusion there were decreases in SBP (p less than 0.001) and diastolic blood pressure (DBP; p less than 0.01) in group S. In group N only SBP decreased (p less than 0.01). At this time there were no significant changes in coronary sinus blood flow (CSBF) or myocardial oxygen consumption (MVO2) in either group. After stenotomy DBP remained decreased (p less than 0.05) in group S.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1994

Divergent effects of intravenous dobutamine and nitroprusside on left atrial contribution to ventricular filling in dogs with chronic heart failure.

The left atrial (LA) contribution to left ventricular (LV) filling is often attenuated in patients with heart failure. It remains uncertain, however, whether therapy with positive inotropic agents or vasodilators improves or further impairs this maladaptation. In the present study, the effects of intravenous dobutamine and nitroprusside on the LA contribution to LV filling was examined in seven dogs with chronic heart failure produced by multiple sequential intracoronary microembolizations. Pulsed Doppler echocardiography was used to measure mitral inflow velocity before and after an intravenous infusion of dobutamine (4 micrograms/kg/min) and an intravenous infusion of nitroprusside (3 micrograms/kg/min). The percent LA contribution to LV filling was calculated as the ratio of the time-velocity integral of the LA component of mitral inflow velocity (Ai) to the time-velocity integral of total diastolic inflow velocity (Ti) times 100. Dobutamine increased LV filling pressure, LV end-diastolic wall stress, LV end-diastolic stiffness, and Ei, but had no effect on Ai or the percent LA contribution to filling (14% +/- 3% vs 12% +/- 2%) (p < 0.34). In contrast, nitroprusside decreased LV filling pressure, LV end-diastolic wall stress, and end-diastolic stiffness, and increased Ei, Ai, and the percent LA contribution to LV filling (12% +/- 2% vs 17% +/- 2%) (p < 0.01). The results indicate that dobutamine and nitroprusside have divergent effects on the LA contribution to LV filling. In dogs with chronic heart failure, dobutamine appears to impair LA contribution to the LV filling by augmenting LA workload, whereas nitroprusside appears to elicit greater LA contribution to LV filling by reducing the LA workload.

Animals↗
PubMed1976

Reduction of S-T segment elevation with infusion of nitroprusside in patients with acute myocardial infarction.

The effect of infusion of sodium nitroprusside on S-T segment elevation was evaluated in 12 patients with acute anterior myocardial infarction. Precordial 35 lead S-T segment maps were obtained in each patient immediately before and 10 minutes after infusion of 53 mug/min (range 20 to 100 mug/min) of nitroprusside. The following measurements were made from each S-T map: sigmaST (total S-T elevation in all leads), NST (number of leads with S-T elevation greater than 1 mm) and ST (average (S-T elevation in leads with more than 1 mm elevation). After administration of mitroprusside, evidence of myocardial ischemic injury as assessed by S-T mapping decreased in association with reduction of the myocardial oxygen consumption index of pressure-time per minute. Group mean values diminished significantly for sigmaST (41.7 to 28.6 mm, P less than 0.001), NST (20.3 to 14.6, P less than 0.001) and ST (1.6 to 1.2 mm, P less than 0.005). Pressure-time per minute decreased from 2,690 to 2,372 mm Hg-sec/min (P less than 0.001). Because there was no significant relation (P less than 0.05) between reductions in S-T elevation and lower indexes of myocardial oxygen consumption, it is suggested that nitroprusside may possess a separate action of augmenting regional blood flow to ischemic myocardium. Evaluation with the precordial S-T mapping technique suggested that intravenous administration of nitroprusside was associated with evidence of reduced ventricular ischemic injury in patients with acute myocardial infarction. This effect appears to be related to reduction of myocardial oxygen demand by the peripheral cardiac unloading mechanisms of nitroprusside as well as to a possible direct action of the drug in improving regional blood flow to ischemic heart muscle.

Acute Disease↗
PubMed1984

Nitroprusside infusion in experimental acute myocardial infarction with systemic hypertension: effects on systemic hemodynamics and regional myocardial blood flows.

The effects of graded doses of nitroprusside on regional myocardial blood flow were studied in awake, acutely hypertensive dogs with acute myocardial infarction. Acute systemic hypertension was produced by infusing a mixture of norepinephrine and epinephrine for 80 minutes after coronary artery occlusion. The increase in aortic pressure produced by catecholamine infusion was accompanied by increases in heart rate, left ventricular (LV) end-diastolic pressure, first derivative of LV pressure (dP/dt), dP/dt at an LV developed pressure of 50 mm Hg (dP/dt/P) and pressure-rate product, but total peripheral vascular resistance did not change significantly. Two graded doses of nitroprusside were then infused, each for 25 minutes, beginning 30 minutes after the onset of coronary artery occlusion. The smaller dose of nitroprusside returned aortic pressure to control levels and significantly reduced total peripheral vascular resistance and LV end-diastolic pressure, but did not affect cardiac output, heart rate, LV dP/dt, dP/dt/P and pressure-rate product. Regional blood flow increased to both the ischemic and normal myocardium. The larger dose of nitroprusside further reduced aortic pressure and total peripheral vascular resistance and LV end-diastolic pressure and significantly increased heart rate and cardiac output. However, LV dP/dt, dP/dt/P and pressure-rate product remained unchanged. Regional blood flow to normal myocardium increased, but the increase in ischemic endocardial blood flow produced by the smaller dose of nitroprusside was no longer significant when the larger dose was administered. These changes were not produced by administration of normal saline solution.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Combined hemodynamic and scintigraphic assessment of piroximone (MDL 19,205) and comparison with dobutamine and nitroprusside.

The acute hemodynamic responses to intravenous infusion of piroximone (MDL 19,205), a nonglycoside, noncatecholamine agent with positive inotropic activity in vitro, were compared with those of intravenous dobutamine and sodium nitroprusside, respectively, in 2 groups of patients with New York Heart Association class III or IV symptoms. Each drug was titrated to optimal dosage (dobutamine, 12.5 +/- 3.9 micrograms/kg/min; nitroprusside, 2.5 +/- 0.6 micrograms/kg/min; piroximone 1.4 +/- 0.6 mg/kg) and simultaneous hemodynamic and scintigraphic values were measured. In group 1, the increase in cardiac index was slightly greater with piroximone than with dobutamine (from 1.6 +/- 0.5 to 2.7 +/- 0.6 vs 2.4 +/- 0.6 liters/min/m2, p less than 0.025) and only piroximone significantly decreased left ventricular (LV) filling pressure (from 29 +/- 7 to 22 +/- 8 mm Hg, p less than 0.05). Both agents increased heart rate and systolic blood pressure. In group 2, cardiac index increased similarly with nitroprusside and piroximone (1.5 +/- 0.6 to 2.6 +/- 0.8 and 1.6 +/- 0.5 to 2.6 +/- 0.5 liters/min/m2, difference not significant), whereas LV filling pressure decreased slightly less with piroximone (29 +/- 7 to 24 +/- 10 vs 30 +/- 7 to 20 +/- 11 mm Hg, difference not significant). Only nitroprusside reduced mean arterial pressure (88 +/- 13 to 72 +/- 12 mm Hg, p less than 0.001 between drugs). In group 1, systolic blood pressure to end-systolic volume ratio increased in 9 of 10 patients taking both piroximone and dobutamine, whereas in group 2, this ratio increased in 7 of 8 patients taking piroximone and declined in 7 of 8 taking nitroprusside.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Comparative effects of fenoldopam mesylate and nitroprusside on left ventricular performance in severe systemic hypertension.

To compare the effects of fenoldopam (n = 15), a selective dopamine-1 agonist, and nitroprusside (n = 14) on left ventricular (LV) function in severely hypertensive subjects (diastolic blood pressure (BP) greater than 120 mm Hg), both agents were infused to reduce diastolic BP by 40 mm Hg (or less than 110 mm Hg). Indexes of LV systolic and diastolic functions were obtained using gated radionuclide angiography before the initiation of treatment and after targeted BP was achieved. Both fenoldopam and nitroprusside effectively reduced systolic and diastolic BP to target levels. Changes in heart rate, peak filling rate and relative end-diastolic volume were similar with both agents. Baseline ejection fraction increased after infusion of both drugs. The magnitude of the increase in ejection fraction was far greater with fenoldopam than with nitroprusside (+22% vs +8%; p = 0.04), despite a lesser reduction in systolic BP (-12 vs -22%, p = 0.002). Furthermore, the reduction in relative end-systolic volume (-35 vs -20%; p = 0.04), and increase in the ratio of peak systolic pressure to relative end-systolic volume (+43 vs +6%; p = 0.007) were greater after fenoldopam than after nitroprusside. The greater increment in parameters of LV systolic function produced by fenoldopam than by nitroprusside suggests an effect on LV performance that is independent of afterload reduction.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Fenoldopam, but not nitroprusside, improves renal function in severely hypertensive patients with impaired renal function.

PURPOSE: Patients with hypertensive crises often experience reduced renal function that may worsen as the elevated blood pressure is treated. Fenoldopam, a novel, peripherally acting dopamine-1 agonist, lowers blood pressure through arteriolar vasodilation, with particularly prominent effects on the renal vascular bed. This study was conducted to examine the effects of fenoldopam on blood pressure and renal function compared to those of sodium nitroprusside in severely hypertensive patients with impaired renal function. PATIENTS AND METHODS: Renal function and systemic hemodynamics were studied in 19 severely hypertensive patients (diastolic blood pressure greater than or equal to 120 mm Hg) with impaired renal function (creatinine clearance less than or equal to 70 mL/min) enrolled in clinical trials of fenoldopam and sodium nitroprusside. For comparison, an additional 22 severely hypertensive patients with nonimpaired renal function were studied under the same conditions. Blood pressure and heart rate were measured at baseline before treatment and periodically during treatment. Renal function was determined before and during drug infusion by collection of timed urine specimens and blood samples. Creatinine clearance, urine flow rate, and sodium and potassium excretions were measured and compared. RESULTS: In patients with impaired renal function, blood pressure (mean +/- SEM) was reduced successfully in both groups (fenoldopam: 214 +/- 8/139 +/- 6 mm Hg to 176 +/- 8/107 +/- 3 mm Hg, p < 0.001 for systolic and diastolic comparisons; nitroprusside: 226 +/- 4/145 +/- 5 mm Hg to 171 +/- 6/108 +/- 2 mm Hg, p < 0.001 for systolic and diastolic comparisons). Results of renal function studies showed significant increases in creatinine clearance (from 39 +/- 7 mL/min to 75 +/- 16 mL/min, p < 0.05), urine flow (from 119 +/- 37 mL/h to 275 +/- 84 mL/h, p < 0.01), and sodium excretion (from 75 +/- 22 microEq/min to 227 +/- 60 microEq/min, p < 0.01) in patients with impaired renal function treated with fenoldopam. No significant changes were seen in patients treated with nitroprusside. In patients with nonimpaired renal function, blood pressure was reduced by both agents, but only patients who received fenoldopam experienced significant increases in creatinine clearance, urine flow rate, and sodium excretion. CONCLUSION: Fenoldopam, but not nitroprusside, improved renal function in severely hypertensive patients at all levels of baseline renal function while lowering blood pressure. Because of these effects, fenoldopam may be particularly useful in treating severely hypertensive patients with impaired renal function.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1988

Response of lamb ductus arteriosus to nitroglycerin and nitroprusside.

In certain forms of congenital heart disease, patency of the ductus arteriosus is critical for survival. Since the administration of prostaglandin is associated with adverse side effects, this study was undertaken to evaluate the effects of nitroglycerin and nitroprusside on ductal blood flow during oxygen-induced ductal closure. Fifteen near-term fetal lambs were instrumented acutely. Ductal blood flow and pre- and post-ductal pressures were monitored continuously. After obtaining control data, intravenous bolus injections of nitroglycerin (250 micrograms), nitroprusside (250 micrograms), or prostaglandin E1 (5 micrograms) were administered during ventilation with either 100% nitrogen or 100% oxygen. All three agents significantly increased ductal blood flow during nitrogen ventilation (PO2 = 15 +/- 1 mm Hg). When the lambs were ventilated with 100% oxygen, the arterial PO2 increased to 107 +/- 14 mm Hg, and this was associated with a marked decrease in ductal blood flow from 275 +/- 44 to 83 +/- 11 ml/min (P less than 0.05). When nitroglycerin was administered during oxygen-stimulated ductal closure, ductal blood flow increased 184%, from 79 +/- 18 to 225 +/- 18 ml/min (P less than 0.05); nitroprusside increased ductal blood flow 126%, from 86 +/- 20 to 195 +/- 25 ml/min (P less than 0.05); prostaglandin E1 increased ductal blood flow 110%, from 84 +/- 18 to 178 +/- 17 ml/min (P less than 0.05). These data demonstrate that both nitroglycerin and nitroprusside are potent vasodilators of the ductus arteriosus and, like prostaglandin E1, can markedly attenuate the oxygen-induced ductal vasoconstriction. These results imply that nitroglycerin and nitroprusside may be useful clinically in maintaining ductal patency.

Alprostadil↗
PubMed1991

Nitroprusside in vitro inhibits platelet aggregation and intracellular calcium translocation. Effect of haemoglobin.

The biologically final active compound of nitrovasodilators is now supposed to be nitric oxide (NO), a labile substance identical to EDRF. The effects of nitroprusside on platelet functions were studied in vitro. Platelet aggregation induced by several stimuli (ADP, collagen, arachidonic acid and PAF) was inhibited by increasing concentrations of the drug (1-50 uM); interestingly, the potency of nitroprusside is higher when PAF is employed as stimulating agent in comparison with the other agonists (ED50 = 2 uM for ADP, 2.5 uM for A.A., 4.5 uM for collagen and 0.3 uM for PAF-induced aggregations). The concomitant addition of haemoglobin is able to reverse the inhibitory effect of nitroprusside, according to the view that haemoglobin possesses a high affinity for NO, thus antagonizing the effect of this compound. Nitroprusside was also able to inhibit intracellular calcium translocation, as studied with the Quin 2 technique, induced by PAF and arachidonic acid. Fron these observations the hypothesis may be suggested that nitroprusside inhibits platelet functions by mimicking the endogenous NO, and that the intracellular calcium metabolism is involved in the inhibitory activity of the drug.

Adenosine Diphosphate↗
PubMed1983

A comparison of the cardiovascular and orofacial blood flow changes resulting from hypotension induced by sodium nitroprusside and adenosine triphosphate in the rat.

These experiments compared the cardiovascular effects and the alterations in orofacial blood flow resulting from hypotension induced with sodium nitroprusside and adenosine triphosphate infusions in 30 male rats. The authors found that sodium nitroprusside did not significantly change heart rate or cardiac output, while adenosine triphosphate caused a significant decrease in heart rate associated with a small increase in cardiac output. Both hypotensive agents produced similar profound decreases in total peripheral resistance. Blood flows to orofacial structures were qualitatively similar with both agents. Both adenosine triphosphate and sodium nitroprusside caused decreased flows to the maxilla and mandible. Sodium nitroprusside increased flows to masseter and suprahyoid muscles. Adenosine triphosphate caused increased flows to suprahyoid muscles but masseter muscle flows were not significantly changed. Tongue flows responded similarly to both agents, initially decreasing, then returning to normotensive levels. Finally, sodium nitroprusside-induced hypotension was associated with the development of tachyphylaxis in some animals, whereas no similar problem was observed with use of adenosine triphosphate. The demonstration of reduced blood flows to orofacial bony structures and the absence of resistance or tachyphylaxis during adenosine triphosphate-induced hypotension support its usefulness as a hypotensive agent during orthognathic and other surgery.

Adenosine Triphosphate↗
PubMed1988

Effects of ethacrynic acid and cystamine on sodium nitroprusside-induced relaxation, cyclic GMP levels and guanylate cyclase activity in rat aorta.

1. Ethacrynic acid, an agent that alkylates sulfhydryl residues, inhibited sodium nitroprusside- and 8-bromo cyclic GMP-induced relaxations. 2. Sodium nitroprusside-induced increased levels of cyclic GMP were unaltered by ethacrynic acid. 3. Concentrations of ethacrynic acid that inhibited sodium nitroprusside-induced relaxation did not affect sodium nitroprusside-activation of crude soluble and particulate fractions of guanylate cyclase, while a higher concentration of ethacrynic acid did inhibit the activation. 4. Cystamine, an agent that oxidizes sulfhydryl residues, inhibited sodium nitroprusside-activation of crude soluble and particulate fractions of guanylate cyclase. Exposure of intact rat aorta to cystamine inhibited basal guanylate cyclase activity in the particulate fraction but, in general, not in the soluble fraction. 5. These results are consistent with the hypothesis that vascular smooth muscle relaxation requires sulfhydryl groups. The sulfhydryl groups that presumably are alkylated by ethacrynic acid are not contained within guanylate cyclase and are involved at a regulatory step after the formation of cyclic GMP. The sulfhydryl groups altered by cystamine may be located on particulate guanylate cyclase and a role for particulate guanylate cyclase in nitrovasodilator-induced relaxation needs to be examined further.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

Dobutamine and nitroprusside infusion in patients with severe congestive heart failure: hemodynamic improvement by discordant effects on mitral regurgitation, left atrial function, and ventricular function.

OBJECTIVES: In patients with severe heart failure additional therapeutic support with intravenous inotropic or vasodilator drugs is frequently used in the attempt to obtain hemodynamic control. The nature and extent to which diastolic filling, atrial function, and mitral regurgitation are modified by these drugs have not been fully explored. The aim of this study was to compare the acute adaptations of the left ventricular performance, left atrial function, and mitral regurgitation that accompanied hemodynamic improvement during intravenous dobutamine and nitroprusside infusions in patients with severe chronic heart failure. METHODS: Forty consecutive patients with severe heart failure were evaluated by simultaneous echo-Doppler and hemodynamic investigations at baseline and during nitroprusside and dobutamine administration. Mitral flow velocity variables, left atrial and ventricular volumes, left atrial reservoir, conduit and pump volumes, and mitral regurgitation jet area were compared by analysis of variance for repeated measurements. RESULTS: Nitroprusside increased cardiac output (2.1 +/- .5 vs 2.6 +/- .5 L/min/m2, p < 0.004), reduced left ventricular filling pressure (25 +/- 6 vs 14 +/- 4 mm Hg, p < 0.0001), and improved left atrial pump volume (19 +/- 3 vs 26 +/- 12 ml, p < 0.02) without variations in left atrial reservoir and conduit volume. The restoration of preload reserve and improvement of the atrial contribution to left ventricular diastolic filling were demonstrated by the Doppler mitral flow pattern, which moved from a restrictive to a normal pattern. Furthermore mitral regurgitation decreased in all patients (9 +/- 4.6 vs 4.6 +/- 3.4 cm2, p < 0.0001). Dobutamine increased cardiac output (2.1 +/- .5 vs 2.8 +/- .6 L/min/m2), but the effects on pulmonary wedge pressure and mitral regurgitation were variable and unpredictable. Left atrial reservoir and conduit volumes increased, whereas left atrial pump volume did not change (19 +/- 13 vs 22 +/- 14 ml, p = NS). Furthermore Doppler mitral flow showed a persistent restrictive pattern. CONCLUSIONS: In patients with advanced congestive heart failure both nitroprusside and dobutamine improve cardiac output, with different adaptations of left ventricular performance and left atrial function. Nitroprusside seems to restore both atrial and ventricular pump function better. Careful echo-Doppler monitoring during drug infusion provides information relevant to the clinical treatment of individual patients.

Atrial Function, Left↗
PubMed1999

Sodium nitroprusside during coronary artery bypass grafting: evidence for an antiinflammatory action.

BACKGROUND: It was the aim of the present study to investigate whether a nitric oxide donor can reduce systemic inflammation and the cardiac inflammatory response during coronary artery bypass grafting with cardiopulmonary bypass. METHODS: Patients undergoing elective coronary artery bypass grafting (n = 22) were randomly assigned to treatment with either sodium nitroprusside (0.5 microg x kg(-1) x min(-1)) or placebo (controls), both for the first 20 minutes of reperfusion. Interleukin-6 and interleukin-8 levels, the adhesion molecules CD41 and CD62 on platelets and CD41 on monocytes and PMN (as markers for coaggregate formation), CD11b on monocytes and PMN, as well as platelet and leukocyte counts were determined in radial artery and coronary sinus blood before cardiopulmonary bypass and during reperfusion (1, 5, 10, 25, and 35 minutes). RESULTS: A reduction of systemic interleukin-6 levels (15.4+/-3.5 pg/mL, 36.7+/-5.9 pg/mL, and 46.8+/-8.0 pg/mL versus 33.4+/-7.7 pg/mL, 76.7+/-13.2 pg/mL, and 106.0+/-26.5 pg/mL, respectively, at 1, 25, and 35 minutes of reperfusion) and interleukin-8 (29.6+/-4.5 pg/mL versus 54.0+/-9.4, pg/mL, resp., at 35 minutes of reperfusion) resulted from treatment with sodium nitroprusside. No intracardiac production of interleukin-8 in sodium nitroprusside-treated patients (-1.1+/-0.4 pg/mL and -2.8+/-2.2 pg/mL, resp., for the coronary sinus-radial artery difference at 5 and 25 minutes of reperfusion) was observed, whereas cardiac production of interleukin-8 was present in controls (2.5+/-1.5 pg/mL and 5.5+/-2.8 pg/mL, resp.). Retention of platelet/leukocyte coaggregates occurred during coronary passage in controls (coronary sinus-radial artery difference for CD41-positive monocytes at 1 and 10 minutes of reperfusion, -16.3%+/-8.5% and -8.8%+/-2.6%, resp.). This was reduced in sodium nitroprusside-treated patients (with 5.8%+/-5.2% and 0.0%+/-3.2%). Retention of platelets in controls (ratio of coronary sinus to radial artery platelet count at 5 and 10 minutes of reperfusion, 88%+/-6% and 91%+/-5%) was compared to washout in treated patients (108%+/-6% and 113%+/-7%). CONCLUSIONS: In patients undergoing routine coronary artery bypass grafting, administration of sodium nitroprusside during early reperfusion alleviates systemic inflammation and the cardiac inflammatory response.

Aged↗