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At least 19 recordsLinked to original sources
PubMed1991

Nitric oxide generation from nitroprusside by vascular tissue. Evidence that reduction of the nitroprusside anion and cyanide loss are required.

Nitric oxide (NO) was produced from sodium nitroprusside in the presence of vascular tissue but was not released spontaneously from the nitroprusside anion. In the absence of tissue in the dark nitroprusside did not release NO. When solutions of nitroprusside alone were irradiated with visible light, nitric oxide was released at rates linearly proportional to nitroprusside concentration and light intensity. Nitric oxide was produced from solutions of nitroprusside in the dark after the addition of vascular tissue, including lengths of rabbit aorta, subcellular fractions of aorta, and human plasma. NO was also released from nitroprusside after reaction with various reducing agents including cysteine and other thiols, ascorbic acid, sodium dithionite, ferrous chloride, hemoglobin, myoglobin, and partially purified cytochrome P450 with an NADPH-regenerating system. HCN was simultaneously produced in these solutions, and addition of KCN blocked NO release. Iodine oxidized intermediate cyanoferrates and blocked nitric oxide release. KCN or iodine also blocked NO production by tissue, but had no effect upon photochemical NO release. These results show that, apart from photolysis which makes no physiological contribution, release of nitric oxide from nitroprusside, in simple solutions and in biological tissue, occurs after nitroprusside has undergone reduction and lost cyanide.

Animals↗
PubMed1989

[Comparison of effects on carbohydrate metabolism of hypotension induced by sodium nitroprusside and a nitroprusside-trimetaphan mixture in rabbits].

Effects on carbohydrate metabolism of hypotension induced by sodium nitroprusside and a nitroprusside-trimetaphan mixture were studied in 29 male rabbits under halothane anesthesia. They were randomly divided into three groups; Nitroprusside (Group N; n = 10), A Nitroprusside-Trimetaphan Mixture (Group M; n = 10), Control (Group C; n = 9). No changes were noted in blood glucose, blood lactate, blood pyruvate and lactate/pyruvate ratio in Group C throughout the experiment. During induced hypotension, blood glucose, blood lactate, blood pyruvate and L/P ratio of group N were significantly higher than the control value. On the other hand, in group M, blood glucose and blood pyruvate tended to increase slightly but not significantly. In contrast, in group M, L/P ratio remained unchanged. The results suggest that sodium nitroprusside tended to cause tissue hypoxia more markedly than a nitroprusside-trimetaphan mixture. The mechanism may be that a mixture of nitroprusside and trimetaphan maintained the carbohydrate metabolism (including gluconeogenesis, glucogenolysis) during induced hypotension. In conclusion, our results suggest that a nitroprusside-trimetaphan mixture is a safe method for hypotensive anesthesia.

Animals↗
PubMed1988

Comparison of intravenous nitroprusside, nitroprusside-captopril, and nitroglycerin for deliberate hypotension during posterior spine fusion in adults.

Three techniques for deliberate hypotension (mean arterial pressure, 60 to 70 mmHg) were prospectively compared in adults undergoing posterior spine fusion. Patients received either IV sodium nitroprusside, sodium nitroprusside with oral captopril pretreatment, or IV nitroglycerin. Patient groups were comparable in age, sex, weight, baseline hemodynamic and laboratory parameters, duration of surgery, and duration of hypotension. Absolute blood loss was significantly less in the group receiving nitroglycerin; however, there were no differences between groups when corrected for operative exposure (milliliter per spine segment exposed). Nitroprusside was effective in producing target blood pressure in all patients. Nitroglycerin was ineffective in two patients and two other patients required greater than 20 micrograms/kg/min. Both groups receiving nitroprusside developed significant postinfusion increases in arterial pressure. Blood pressure fell significantly after induction of anesthesia in patients receiving captopril. Cardiac index, heart rate, pulmonary capillary wedge pressure, intrapulmonary shunt, and arterial blood gases were comparable and did not change significantly in any group. Systemic vascular resistance fell during infusion in all groups and remained depressed after infusion in patients receiving nitroglycerin. Plasma renin activity was significantly increased in the group receiving captopril due to loss of feedback inhibition of renin release and rose significantly during infusion in those patients receiving nitroprusside alone. There were no complications. Nitroprusside with and without captopril pretreatment was associated with postoperative increases in arterial pressure, although not to hypertensive levels, probably due to loss of captopril activity after single-dose administration. The use of nitroglycerin was limited by lack of potency. There was no demonstrable clinical advantage for any of the three techniques.

Administration, Oral↗
PubMed1989

[Comparison of endocrine effects of hypotension induced by sodium nitroprusside, trimetaphan camsylate and a nitroprusside-trimetaphan mixture in rabbits].

Endocrine effects of hypotension induced by nitroprusside, trimetaphan and a nitroprusside-trimetaphan mixture were studied in 34 male rabbits under halothane anesthesia. They were randomly divided into four groups; nitroprusside (group N; n = 8), trimetaphan (group T; n = 10), a nitroprusside-trimetaphan mixture (group M; n = 8) and controls (group C; n = 8). No change was noted in plasma catecholamines measured in group C throughout the experiment, but plasma renin activity decreased progressively. During induced hypotension, plasma catecholamines and plasma renin activity of group N were significantly higher than the control value. In contrast, in group T plasma epinephrine decreased significantly. On the other hand, in group M, plasma renin activity showed a slight but not significant increase, while plasma catecholamines remained unchanged. This may have occurred since a mixture of nitroprusside and trimetaphan produced the dissociation of renin-angiotensin-sympathoadrenal loop. In conclusion, these results suggest that a nitroprusside-trimetaphan mixture is a useful method for hypotensive anesthesia by inhibiting the excessive activation of renin-angiotensin-sympathetic system.

Animals↗
PubMed1985

Nitroprusside vs. a nitroprusside-trimethaphan mixture for induced hypotension: hemodynamic effects and cyanide release.

Changes in hemodynamic variables and whole blood cyanide and plasma thiocyanate concentrations associated with the infusion of sodium nitroprusside were compared with those during administration of a mixture of sodium nitroprusside (25 mg) and trimethaphan camsylate (250 mg) in a solution of 5% dextrose in water in twenty subjects who required deliberate hypotension for major orthopedic procedures. Subjects were randomly assigned to receive nitroprusside alone (group 1; n = 10) or the nitroprusside-trimethaphan mixture (group 2; n = 10). All subjects received a similar anesthetic technique, consisting of 5 mg/kg thiopental, 1 mg/kg succinylcholine, 1% halothane, 0.2 mg/kg metocurine, and 60% nitrous oxide in oxygen. Mean arterial pressure decreased and was maintained at 55 mm Hg for 258 +/- 4 and 266 +/- 8 minutes in groups 1 and 2. Arterial hypotension was associated with a rise in cardiac output and heart rate in group 1 but not in group 2. Subjects in group 2 required less nitroprusside than did those in group 1 (1.39 +/- 0.3 and 5.82 +/- 0.63 micrograms/kg/min) because of the synergistic or additive action of the combination. After 4 hours of hypotension, the whole blood cyanide level rose from 3.5 +/- 1.1 to 96.6 +/- 14.0 micrograms/dl (1.35 +/- 0.27 to 37.2 +/- 5.4 mumol/L) in group 1 and from 3.7 +/- 1.1 to 22.7 +/- 4.2 micrograms/dl (1.42 +/- 0.4 to 8.7 +/- 1.6 mumol/L) in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Plasma and red blood cell cyanide concentrations during hypotension induced by sodium nitroprusside or by a nitroprusside-trimetaphan mixture in rabbits].

Plasma and red blood cells cyanide concentrations during hypotension induced by sodium nitroprusside and a nitroprusside-trimetaphan mixture were studied in 29 male rabbits under halothane anesthesia. They were randomly divided into three groups; Nitroprusside (group N; n = 10), A nitroprusside-trimetaphan mixture (group M; n = 10), Controls (group C; n = 9). No changes were noted in plasma and red blood cells cyanide concentrations in group C throughout the experiment. During and after induced hypotension, in group N, plasma cyanide concentration was significantly higher than the control value. The maximum increase occurred 60min after induction of hypotension and the highest concentration of plasma cyanide was six times the control value. In contrast, in group M, plasma cyanide concentration was unchanged from the control value. However, during and after induced hypotension, red blood cells cyanide concentrations of group N and group M were significantly higher compared with the control values. Red blood cells concentrations of cyanide increased for 30 and 60 min during induced hypotension in group N (27.11 +/- 3.9 micrograms.ml-1, P less than 0.001, 46, 73 +/- 4.7 micrograms.ml-1, P less than 0.001, respectively) and in group M (0.31 +/- 0.05 micrograms.ml-1, P less than 0.05, 0.29 +/- 0.03 micrograms.ml-1, P less than 0.05, respectively). In conclusion, the data suggest that a nitroprusside-trimetaphan mixture is a safe method for hypotensive anesthesia.

Animals↗
PubMed1986

Comparative effects of combined dopamine and nitroprusside versus dobutamine and nitroprusside infusions for computer-controlled management of low-output cardiac failure after open heart surgery.

In order to evaluate the possible differences in response to two currently preferable inotropic-vasodilator drug combinations, the hemodynamic effects of automated infusions of nitroprusside-dobutamine and nitroprusside-dopamine were studied in two clinically similar groups of patients with low-output syndrome after aorto-coronary bypass surgery. Nitroprusside, when infused in combination with dopamine, was effective in lowering filling pressures of both ventricles and systemic and pulmonary arterial pressures reflecting the reversal of deleterious rise of these parameters including determinants of myocardial oxygen consumption (mean arterial pressure rate by +6%, heart rate by +20%) caused by dopamine (6 micrograms/kg/min) infused alone. The combination of the more cardioselective catecholamine dobutamine with nitroprusside brought about similar increase in cardiac output by 50%, but derived its hemodynamic efficiency from the sum of separate effects of components and produced less in the way of elevation of determinants of oxygen consumption. Dobutamine when infused alone (6 micrograms/kg/min) has not affected systemic and pulmonary arterial pressures and stroke index rose more markedly (+9%) as a result of more moderate heart rate increase (+13%). Nitroprusside contributed in an additive manner to the achieved overall reduction of SVR and PVR by 43% and 50%, resp., the automated infusion being helpful in maintaining these values within close tolerances.

Cardiac Output, Low↗
PubMed1984

Inhibition of superoxide dismutase by nitroprusside and electron spin resonance observations on the formation of a superoxide-mediated nitroprusside nitroxyl free radical.

Nitroprusside appears to inhibit the known types of superoxide dismutases irrespective of their metal prosthetic group and regardless of the source from which the enzymes were isolated. Thus the copper-zinc enzyme from bovine erythrocyte or Neurospora crassa behaved identically as did the manganese enzymes from Escherichia coli or red alga and the iron enzyme from E. coli and a blue-green alga. The inhibition was dose dependent with a Ki = 2.5 X 10(-5) for nitroprusside. Nitroprusside does not bind to the copper moiety of copper-zinc enzyme and seems to compete with O2- for superoxide dismutase. These inhibitions by nitroprusside, which were elicited not only in purified enzymes but also in crude soluble extracts of biological samples, were rapidly reversible. Nitroprusside was found to react with O2- to form a paramagnetic species with three absorption lines of equal width with a separation AN = 15.0 G and a g value of 2.028. The spin adduct appears to be a nitroxide radical and was stable for several minutes.

Cyanobacteria↗
PubMed1981

Propranolol alters renin release during nitroprusside-induced hypotension and prevents hypertension on discontinuation of nitroprusside.

Ten patients who received hypotensive anesthesia for surgical correction of a cerebral aneurysm were pretreated for 1 day with propranolol. In the awake state, before start of anesthesia, mean arterial pressure was 91 +/- 3 torr and plasma renin activity 3.0 +/- 0.1 ng/ml/hr. Thirty minutes after the induction of anesthesia mean arterial pressure decreased to 79 +/- 2 torr and plasma renin activity increased to 3.5 +/- 0.1 ng/ml/hr. There was no further significant change in either measurement with surgical stimulation. During sodium nitroprusside-induced hypotension (the dose used was 0.35 +/- 0.02 mg/kg) mean arterial pressure was reduced to 53 +/- 2 torr, and plasma renin activity increased to 8.8 +/- 0.9 ng/ml/hr. Heart rate did not change. Discontinuation of sodium nitroprusside resulted in a gradual reduction of plasma renin activity to the awake level and concurrent gradual increase in mean arterial pressure to its basal anesthetic value. When compared with previous work, these results indicate that propranolol attenuates nitroprusside-induced renin release, reduces the dosage of nitroprusside required to induce hypotension, suppresses reflex tachycardia, and prevents overshoot hypertension on discontinuation of nitroprusside.

Adult↗
PubMed1981

[Haemodynamic effects of dopamine, sodium nitroprusside and the association dopamine-sodium nitroprusside. Comparison of their effects after extra-corporeal circulation under deep hypothermia for congenital heart defects in infants and small children (author's transl)].

Heart rate, cardiac index measured by thermodilution, systolic diastolic and mean arterial pressure, mean left and right atrial pressures, were measured immediately before and after 30 minutes of dopamine infusion at a rate of 7 micrograms/kg/minute, then after 30 minutes of nitroprusside infusion at a rate of 0.5 micrograms/kg/minute, and after 30 minutes of association dopamine-nitroprusside at the same doses. The statistical analysis shows that the best enhancement in the cardiac output is observed (P less than 0.01) after the association dopamine-nitroprusside, with a diminution of systemic vascular resistance (P less than 0.05) however less important than that observed with sodium nitroprusside alone (P less than 0.025).

Child, Preschool↗
PubMed1983

The acute response of plasma norepinephrine, renin activity, and arginine vasopressin to short-term nitroprusside and nitroprusside withdrawal in patients with congestive heart failure.

Activation of the sympathetic nervous system, manifested by an increase in heart rate and circulating plasma norepinephrine, can occur in normal subjects when they are given vasodilators. The extent to which this activation occurs in patients with congestive heart failure (CHF) and whether this activation could account for the hemodynamic rebound sometimes observed following abrupt withdrawal of nitroprusside in such patients are unclear. We prospectively and retrospectively studied the effects of nitroprusside on plasma norepinephrine in 38 patients with CHF to determine if acute vasodilator therapy activates this vasoconstrictor system during or following such treatment. Thirty-six of these patients also had plasma renin activity (PRA) measured and plasma arginine vasopressin was measured in 12 patients. Baseline supine plasma norepinephrine (714 +/- 72 pg/ml, +/- SEM), PRA (15 +/- 2 ng/ml/hr), and arginine vasopressin (10 +/- 1 pg/ml) were increased at least twofold in the CHF patients. Nitroprusside (96 +/- 11 micrograms/min) was infused for 63 +/- 5 minutes after achieving an optimal hemodynamic response: cardiac index increased (2.01 +/- 0.08 to 2.67 +/- 0.1 L/min/m2, p less than 0.001), pulmonary artery wedge pressure decreased (25 +/- 1 to 16 +/- 1 mm Hg, p less than 0.001), mean arterial pressure decreased (83 +/- 1 to 72 +/- 1 mm Hg, p less than 0.001), and heart rate was unchanged. Plasma norepinephrine (632 +/- 43 pg/ml), PRA (18 +/- 3 ng/ml/hr), and arginine vasopressin (11 +/- 1 pg/ml) did not change significantly for the group during peak effect of the vasodilator.(ABSTRACT TRUNCATED AT 250 WORDS)

Arginine Vasopressin↗
PubMed1977

Sodium nitroprusside as a coronary vasodilator in man. I. Effect of intracoronary sodium nitroprusside on coronary arteries, angina pectoris, and coronary blood flow.

The effect of the intra-arterial injection of 5 to 10 microng of sodium nitroprusside on the caliber of normal and diseased coronary arteries was evaluated in 21 patients during diagnostic cardiac catheterization. In addition, the effect of intra-graft injection of 5 microng of the same agent on the blood flow in aorta-right coronary artery saphenous vein bypass grafts was also evaluated intra-operatively in two patients. The compound induced an increase in the caliber of both normal and stenosed coronary arteries as well as an increase of flow in the grafts. Consistent with measurements of coronary flow response to sodium nitroprusside, angina pectoris which developed in four patients during cardiac catheterization was immediately relieved and the ischemic ST-segment depression significantly reversed after injection of 5 to 10 microng of the drug into the left main coronary artery. Within the dose range used, the drug caused no significant effect on systemic blood pressure or apparently deleterious electrophysiologic changes. No side effects were observed. We conclude that the primary direct action of sodium nitroprusside in the human coronary artery is vasodilatory.

Adult↗
PubMed1976

Sodium nitroprusside as a coronary vasodilator in man: a comparison of the effects of sodium nitroprusside and papaverine hydrochloride on aortocoronary saphenous vein graft flow.

Blood flow in aortocoronary saphenous vein grafts was studied in response to intragraft injection of sodium nitroprusside and papaverine hydrochloride. Following injection of 50 mug of sodium nitroprusside, mean graft flow increased from 40.1 +/- 4.5 to 81.3 +/- 8.5 ml per minute. Administration of 30 mg of papaverine hydrochloride caused mean graft flow to rise from 35.4 +/- 3.9 to 70 +/- 7.9 ml per minute. Sodium nitroprusside increases aortocoronary graft flow, the doubling effect of 50 mug of the drug being of the same order of magnitude as that induced by 30 mg of papaverine hydrochloride.

Adult↗
PubMedDate not supplied

Effect of cyanide on the reaction of nitroprusside with hemoglobin: relevance to cyanide interference with the biological activity of nitroprusside.

The reaction of sodium nitroprusside (SNP) with deoxyhemoglobin (Hb) results in two distinct EPR-detectable species, the one-electron-reduced nitroprusside ion [(CN)5FeNO]3- and nitrosylhemoglobin (HbNO). In the presence of excess cyanide (CN-) only the signal for [(CN)5FeNO]3- is observed. Thus, while free CN- does not interfere with Hb reduction of SNP, it prevents transfer of the NO moiety to Hb. Electrolytic reduction of SNP under similar conditions, however, leads to [(CN)5FeNO]3- and a small amount of [(CN)4FeNO]2- resulting from loss of the CN- trans to the NO. Excess free CN- shifts the equilibrium between these two species toward [(CN)5FeNO]3-, thereby reducing the concentration of [(CN)4FeNO]2-. Thus, [(CN)4FeNO]2- appears to be responsible for the transfer of NO to Hb. Consistent with this mechanism, both [(CN)5FeNO]3- and [(CN)4FeNO]2- are observed when SNP is added to erythrocyte lysates. Under these conditions HbNO is formed more rapidly due to the higher concentration of the latter species with the labile NO. This observation suggests that red blood cell constituents capable of binding CN- shift the equilibrium between the reduced SNP ions toward [(CN)4FeNO]2-. In the reaction of reduced glutathione (GSH) with SNP, [(CN)5FeNO]3- is formed as well as low concentrations of an EPR-detectable GSH-SNP adduct. Excess free CN- introduces a lag in the appearance of these signals, suggesting that GSH mediates SNP reduction by a different mechanism from that of Hb, although it too is inhibited by CN-.(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive Agents↗
PubMed1988

Cardiovascular actions of trimetaphan nitroprusside. Comparison with sodium nitroprusside in greyhounds.

Trimetaphan nitroprusside (TNP) is a new potent hypotensive agent developed to induce and maintain decreases in arterial pressure unaccompanied by resistance. This study investigated its properties and compared them with those of sodium nitroprusside (SNP) in anaesthetized greyhounds. The mean dose response to TNP was obtained by measuring haemodynamic changes in five dogs. With increasing doses, stepwise decreases in mean arterial pressure and progressive increases in heart rate occurred: cardiac index did not change significantly. In a further six greyhounds, SNP and TNP were alternately infused to induce and maintain a 30% reduction in arterial pressure for 30 min. Both drugs were short-acting, decreased systemic vascular resistance and caused tachycardia. Infusion of TNP produced lower plasma and red cell cyanide concentrations; SNP maintained hypotension with significantly less tachycardia. We conclude that there was no outstanding advantage of TNP over SNP when given as a short-term infusion in greyhounds.

Anesthesia, General↗
PubMed1982

The interaction of sodium nitroprusside with human endothelial cells and platelets: nitroprusside and prostacyclin synergistically inhibit platelet function.

Sodium nitroprusside (NP) is a potent vasodilator that also inhibits platelet aggregation. To test the hypothesis that NP causes both of these effects by altering the balance between prostacyclin (PGI2) produced by endothelial cells and thromboxane A2 (TXA2) produced by platelets, we incubated each of these cell types with NP for 5 minutes and assayed the PGI2 and TXA2 produced. NP at pharmacologically achieved doses (0.01--30 micrograms/ml) inhibited platelet aggregation and resultant TXA2 synthesis in a dose- and time-dependent manner (p less than 0.001). The inhibition was not dependent on cAMP production, external calcium concentration, or suppression of TXA2 synthesis. NP did not alter the production of PGI2 by cultured human endothelial cells as measured by radioimmunoassay for 6-Keto-PGF1 alpha, the stable hydrolysis product of PGI2. However, supernates of NP-treated endothelial cells containing low, noninhibitory concentrations of NP unexpectedly inhibited platelet aggregation. This inhibition of platelet aggregation was due to synergy between PGI2 (0.1--3 nM) and NP (p interaction less than 0.03). The synergistic inhibition by NP and PGI2 of platelet aggregation and TXA2 synthesis in vivo may explain some of the beneficial actions of NP in the treatment of hypertension and congestive heart failure.

Calcium↗
PubMed1996

Effect of sodium nitroprusside on complement activation induced by cardiopulmonary bypass: a clinical and experimental study.

Complement activation and leukocyte stimulation were prospectively studied during and after cardiopulmonary bypass in 16 children receiving sodium nitroprusside--a nitrovasodilator releasing nitric oxide--for vasodilation during the cooling and rewarming periods of extracorporeal circulation. Results were compared with those in 29 patients who were not treated with sodium nitroprusside during the operation. Patients treated with sodium nitroprusside had significantly less C3 conversion during cardiopulmonary bypass as measured by the ratio C3d/C3 (p <0.05) and significantly less C5a liberation immediately after cardiopulmonary bypass (p < 0.005) than patients not treated with sodium nitroprusside. C4 was not overtly consumed in our series. Leukocyte count during the rewarming period of cardiopulmonary bypass, but not leukocyte elastase release during cardiopulmonary bypass, was significantly reduced in patients treated with sodium nitroprusside (p <0.05). In vitro experiments were conducted to analyze the effect of sodium nitroprusside on complement hemolytic activity initiated by the classic and the alternate pathways and on zymosan-induced C3 conversion by the activation of the alternate pathway. The in vitro experiments clearly demonstrate inhibition of complement hemolytic activity by sodium nitroprusside in the sera tested. The 50% inhibitory concentration of sodium nitroprusside on the available complement hemolytic activity was less through the alternate pathway than through the classic one (4.2 +/- 0.8 mmol/L and 14.0 +/- 2.88 mmol/L, respectively). The decrease of complement hemolytic activity measured was dose-dependent and was enhanced by the sodium nitroprusside preincubation of the sera tested. This effect was related to the duration of preincubation. Sodium nitroprusside photodegradation (enhancing nitric oxide release) increased the anticomplementary effect of the drug, reducing the 50% inhibitory concentration on complement hemolytic activity to 0.24 to 0.02 mmol/L for the alternate pathway and 2.74 o 0.3 mmol/L for the classic pathway. the zymosan-induced C3 conversion was inhibited by sodium nitroprusside. Nitroglycerin and isosorbide dinitrate (other nitric oxide donors) had in vitro effects on complement hemolytic activity similar to those of nonphotodegraded sodium nitroprusside at similar concentrations (1 mmol/L). Our results suggest that sodium nitroprusside, both in vitro and in vivo, has an inhibiting effect on complement activation initiated by both classic and alternate pathways and that this effect is mediated by nitric oxide release from sodium nitroprusside. This is the first report on the anticomplementary effect of sodium nitroprusside by nitric oxide release.

Cardiopulmonary Bypass↗