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PubMed1975

A sudden death associated with the use of sodium nitroprusside for induction of hypotension during anaesthesia.

A death from cyanide poisoning during operation was attributable to the use of approximately 400 mg (10 mg per Kg) sodium nitroprusside as an hypotensive agent. Autopsy cyanide levels of 0.5 mg per cent in blood and 0.3 mg per cent in urine and thiocyanate levels too low to measure in either, suggest an abnormality of cyanide metabolism. The lethal dose of sodium nitroprusside appears to be 7 mg per Kg. A safe regimen would be 3.5 mg per Kg as the anticipated total dose for the period of hypotension. Patients resistant to the full hypotensive effects of sodium nitroprusside, or unable to maintain the level of hypotension, or requiring more than 3.5 mg per Kg to achieve the required effect for the anticipated time, may accumulate toxic levels of cyanide in the blood. Patients with Leber's optic atrophy, tobacco amblyopia and possibly those with other nerve atrophies should not receive sodium nitroprusside or any other cyanide precursor.

Adolescent↗
PubMed2003

Protection of rat pancreatic islets by potassium channel openers against alloxan, sodium nitroprusside and interleukin-1beta mediated suppression--possible involvement of the mitochondrial membrane potential.

AIMS/HYPOTHESIS: We aimed to study the effects of two K(ATP) channel openers (KCO), diazoxide and the more potent compound NNC 55-0118, on beta-cell suppression and/or toxicity induced by alloxan, sodium nitroprusside and IL-1beta. METHODS: Islets from rats were exposed to 0.3 mmol/l diazoxide or NNC 55-0118 for 30 min and either alloxan (0.5 mmol/l), sodium nitroprusside (0.5 mmol/l) or IL-1beta (12.5 or 25 U/ml) were added and the incubation continued for 30 min. Islets were then washed and incubated for 24 h before examination. RESULTS: After exposure to alloxan, islets showed reduced glucose oxidation rate and impaired glucose-stimulated insulin release. NNC 55-0118 counteracted the effects of alloxan, while diazoxide was less effective. After treatment with sodium nitroprusside, islet glucose oxidation rates were reduced and this was prevented by pretreatment with NNC 55-0118. In short-term experiments the potassium channel openers (KCOs) did not influence the IL-1beta effect on insulin secretion. However, long-term addition (24 h) of NNC 55-0118 counteracted IL-1beta induced inhibition of the glucose oxidation rate. It was shown, using the fluorescent probe JC-1, that the mitochondrial membrane potential was reduced by the potassium channel openers (KCOs), most strongly by NNC 55-0118. Nevertheless culture with KCOs for 72 h did not cause irreversible damage to the islets. CONCLUSION/INTERPRETATION: Potassium channel openers (KCOs), in particular NNC 55-0118, prevented the toxic effects of alloxan and sodium nitroprusside. IL-1beta mediated suppression was reduced by NNC 55-0118 provided the long-term addition of the potassium channel opener (KCO). The protective mechanism of potassium channel openers (KCOs) might involve a decrease of the mitochondrial membrane potential.

Alloxan↗
PubMed2005

Elevated carboxyhemoglobin associated with sodium nitroprusside treatment.

OBJECTIVE: To report four cases of carboxyhemoglobinemia associated with high doses of sodium nitroprusside after cardiac transplant in children. PATIENTS: Four children in the pediatric care unit of a university hospital aged 6 months-4 years. Carboxyhemoglonemia developed at levels of 5.5-7.7% in patients receiving high doses of sodium nitroprusside (7-16 microg/kg per minute and no other medication that could caused elevated carboxyhemoglobin). One patient died, and three recovered with no sequelae after discontinuation of sodium nitroprusside. CONCLUSIONS: High doses of sodium nitroprusside can induce carboxyhemoglobinemia in children after heart transplant, probably by inducing hemeoxygenase, with no other secondary effects.

Carboxyhemoglobin↗
PubMed1983

Effects of nitroprusside-induced reduction of elevated preload and afterload on global and regional ventricular function in acute myocardial infarction.

To evaluate the effects of nitroprusside infusion on left and right ventricular ejection fractions and left ventricular regional wall motion, radionuclide ventriculography with simultaneous hemodynamic assessment was performed before and during nitroprusside infusion in 20 patients with acute myocardial infarction complicated by left ventricular failure and/or systemic arterial hypertension. Nitroprusside produced significant reductions in pulmonary capillary wedge pressure (21 +/- 6 to 13 +/- 5 mm Hg; -38%; p less than 0.001), mean arterial pressure (107 +/- 19 to 90 +/- 13 mm Hg; -15.9%; p less than 0.001), left ventricular end-diastolic volume index (84 +/- 28 to 75 +/- 23 ml/m2; -10.7%; p less than 0.001), and right ventricular end-diastolic volume index (77 +/- 30 to 67 +/- 27 ml/m2; -13.0% p less than 0.007), and significant increases in left ventricular ejection fraction (0.32 +/- 0.12 to 0.37 +/- 0.13; +15.6%; p less than 0.0001), right ventricular ejection fraction (0.37 +/- 0.11 to 0.45 +/- 0.14; +21.6%; p less than 0.001), and stroke volume index (25 +/- 7 to 27 +/- 7 ml/beat m2; +8.0%; p less than 0.03). These beneficial changes in global ventricular performance were accompanied by no change in the regional contractile function of 90% of the abnormally contracting infarct-related left ventricular segments and improved regional wall motion of 34% of noninfarcted but abnormally contracting left ventricular segments. We conclude that nitroprusside-induced reduction of elevated preload and afterload in acute myocardial infarction results in salutary effects on global ventricular function and improved regional function of noninfarcted left ventricular segments but with less prominent effects on regional function of infarcted segments.

Adult↗
PubMed1988

Intravenous fenoldopam in heart failure: comparing the hemodynamic effects of dopamine1 receptor agonism with nitroprusside.

Dopamine1 receptors mediate hemodynamic effects that may be beneficial in patients with congestive heart failure. We infused the selective dopamine1 receptor agonist, fenoldopam mesylate (SKF 82526 J), to evaluate hemodynamic and neurohumoral changes during continuous intravenous infusion in patients with congestive heart failure and compared them with the effects of nitroprusside, a traditional vasodilator that works by a distinctly different mechanism. In 15 patients with a mean radionuclide ejection fraction of 17%, the agents were infused in a random-ordered, double-blinded, crossover, active drug-controlled protocol after optimal dosing was determined during a titration period. Hemodynamic changes were induced in minutes with both drugs during a mean (+/- standard deviation) infusion dose of 1.45 +/- 1.66 micrograms/kg/min for fenoldopam and 2.99 +/- 1.59 micrograms/kg/min for nitroprusside. At 1 hour, mean blood pressure decreased and cardiac index rose with both drugs, and the effect lasted throughout the 6-hour infusion period. Nitroprusside, but not fenoldopam, reduced right heart filling pressures (including mean pulmonary capillary wedge, mean right atrial, and mean pulmonary artery pressures) during the infusion period. Both drugs caused significant reduction in systemic vascular and pulmonary arteriolar resistances. No significant change occurred in plasma norepinephrine levels. Fenoldopam ameliorates some of the adverse hemodynamic changes that occur during heart failure but does not reduce right heart filling pressures as does nitroprusside. Because of fenoldopam's unique characteristics, it may benefit certain patients with heart failure.

Adult↗
PubMed1985

Acute hemodynamic effects of nitroprusside in children with isolated mitral regurgitation.

The acute hemodynamic responses to nitroprusside during cardiac catheterization were evaluated in 12 children with isolated mitral regurgitation (MR) of congenital origin. The patients were classified into 2 groups. Group I consisted of 5 patients who received digitalis or diuretic drugs and group II consisted of 7 patients who received no medication. Hemodynamic measurements were performed using a multisensor catheter system during infusion of nitroprusside at a dose of 2.0 micrograms/kg/min. With nitroprusside, the mean right atrial pressure decreased an average of 50% in group I (from 6 +/- 1 to 3 +/- 1 mm Hg) and 75% in group II (from 4 +/- 1 to 1 +/- 1 mm Hg), and the mean decrease of pulmonary artery wedge pressure was 50% in group I (from 14 +/- 3 to 7 +/- 3 mm Hg) and 56% in group II (from 9 +/- 2 to 4 +/- 1 mm Hg). Administration of nitroprusside also caused a significant reduction in systemic vascular resistance by 40% in both groups (from 25 +/- 6 to 15 +/- 5 U/m2 in group I and from 25 +/- 2 to 15 +/- 3 3 U/m2 in group II), whereas forward cardiac output increased markedly, by an average of 48% in group I (from 3.3 +/- 0.5 to 4.9 +/- 0.9 liters/min/m2) and 58% in group II (from 3.3 +/- 0.3 to 5.2 +/- 0.8 liters/min/m2). No significant differences in hemodynamic response between groups I and II were noted.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗
PubMed1986

Alterations in regional myocardial blood flow after nitroprusside and nitroglycerin in patients with and without significant coronary artery disease.

To evaluate vasodilator-induced redistribution of regional myocardial blood flow, intravenous sodium nitroprusside and nitroglycerin were administered in doses producing matched reductions (15%) in mean arterial pressure at constant heart rate. Anterior left ventricular great cardiac vein blood flow (thermodilution) was measured in 14 patients without angiographic anterior collateral supply. Global coronary sinus blood flow remained constant with both nitroprusside and nitroglycerin administration, despite significant reductions in mean arterial pressure. However, nitroglycerin reduced great vein flow by 25 +/- 17% and nitroprusside by 10 +/- 16% (p less than 0.01). Subgroup analysis indicated that the nitroglycerin-nitroprusside regional blood flow differences were more pronounced in patients without significant left anterior descending coronary artery narrowing. Neither vasodilator produced significant differences in arterial-coronary sinus oxygen or lactate contents, calculated myocardial oxygen consumption, left ventricular dP/dt, or electrocardiographic or clinical signs of myocardial ischemia. Despite qualitatively similar hemodynamic effects, comparisons of vasodilator-induced relative reductions in normally supplied anterior left ventricular regional coronary blood flow suggest a mechanism of the reported beneficial effects of nitroglycerin on potentially ischemic myocardial regions.

Adult↗
PubMed1981

Nitroprusside-induced hemodynamic alterations in normotensive and hypertensive pregnant sheep.

It has been suggested that sodium nitroprusside, a potent vasodilator, be used in the management of an acute hypertensive crisis during pregnancy. The present study was designed to evaluate the hemodynamic effects of this agent in the same group of chronically instrumented, unanesthetized pregnant sheep during two experimental periods: (a) normotension with intact kidneys, and (b) one-kidney hypertension. The results demonstrate that (1) nitroprusside is a potent vasodilator which lowers mean arterial pressure; (2) nitroprusside-induced tachycardia was greater in the hypertensive animal; (3) uterine blood flow decreased with the development of hypertension; (4) the hypertensive-induced reduction in uterine blood flow was increased by the infusion of nitroprusside.

Animals↗
PubMed1975

Effect of sodium nitroprusside on myocardial performance and venous tone.

The action of sodium nitroprusside upon the mechanical performance of the isolated, working rat heart and on isolated bull veins has been studied. Cumulative concentrations of 1--1000 ng sodium nitroprusside per ml had no effect on left ventricular pressure, end-diastolic left ventricular pressure, dp/dtmax, cardiac output and calculated wall stiffness of isolated rat hearts with constant rate, preload and afterload. Isolated strips of bull veins contracted with noradrenaline showed a dose dependent relaxation by sodium nitroprusside in concentrations of 5--1000 ng per ml. This study shows that sodium nitroprusside has no direct effect on myocardial contractility and causes venous relaxation.

Animals↗
PubMed1991

Comparative effects of a selective adenosine A2 receptor agonist, CGS 21680, and nitroprusside in vascular smooth muscle.

CGS 21680 (2-[p-(2-carboxyethyl)phenylethylamino]-5'-N-ethyolcarboxamidoa denosine) is an adenosine agonist that has been reported recently to bind selectively to adenosine A2 receptors in rat brain. This adenosine agonist, and the parent compound NECA (5'-N-ethylcarboxamidoadenosine), were found to be potent vasorelaxants of prostaglandin F2 alpha (PGF2 alpha) precontracted porcine coronary smooth muscle with EC50s of 4.5 and 9.7 nM, respectively. Schild analysis of the inhibition of CGS 21680, NECA and 2-chloroadenosine induced relaxation of the porcine coronary artery by CGS 15943 (9-chloro-2-(2-furanyl)[1,2,4]triazolo[1,5-C]quinazolin-5-amine), an A2 receptor antagonist, yielded identical pA2 values for the antagonist (approximately 9.3). This indicates that the same receptor mediates the effects of these three adenosine agonists. NECA and CGS 21680 were equipotent in most vascular preparations except in the canine coronary artery. Porcine coronary arterial rings contracted with PGF2 alpha were relaxed by NECA or CGS 21680 as well as by nitroprusside; those contracted with KCl (40 mM) were relaxed only by nitroprusside. In rabbit aorta, contractions induced by phenylephrine or PGF2 alpha were inhibited by nitroprusside but not by NECA or CGS 21680. Thus, the adenosine A2 receptor agonists, NECA and CGS 21680, are potent vasorelaxants that display regional vascular and species variations that differ from those of nitroprusside.

Adenosine↗
PubMed1992

Effects of K+ channel blockers on the relaxant action of dihydralazine, cromakalim and nitroprusside in isolated rabbit femoral arteries.

The relaxant responses to dihydralazine and the influence of different K+ channel blockers were studied in isolated rabbit femoral arteries. The prototype K+ channel opener, cromakalim, and nitroprusside, which does not produce relaxation by K+ channel activation were used for comparison. Dihydralazine was most effective on contractions induced by noradrenaline (EC50 = 1.1 microM; Emax = 95%) and relaxed the contractions elicited by 20 mM K+ (EC50 = 2.0 microM; Emax = 81% in preference to 124 mM K(+)-induced contractions (EC50 = 30.1 microM; Emax = 54%). Cromakalim, but not nitroprusside, also selectively relaxed 20 mM K(+)-induced contractions. In noradrenaline-contracted arteries, glibenclamide (10 microM) completely suppressed the relaxant response to cromakalim but did not influence the vasorelaxation produced by dihydralazine or nitroprusside. Tetraethylammonium (8 mM) and Cs+ (4 mM) shifted the concentration-relaxation curve for dihydralazine 2-fold to the right, whereas Ba2+ (0.1 mM), 4-aminopyridine (5 mM) and procaine (0.1 mM) failed to influence dihydralazine-induced responses. Tetraethylammonium (8 mM) shifted the concentration-relaxation curve for cromakalim and nitroprusside 6-fold to the right and suppressed the maximal relaxant effects by about 30%. It is concluded that dihydralazine produces vascular smooth muscle relaxation by a mechanism different from the opening of glibenclamide- and ATP-sensitive K+ channels.

Animals↗
PubMed1984

Cyclic GMP-dependent protein kinase activation in canine tracheal smooth muscle by methacholine and sodium nitroprusside.

Methacholine (3 microM) and sodium nitroprusside (300 microM) increased cGMP-dependent protein kinase activity ratios (activity without cGMP divided by activity with 2 microM cGMP) in canine tracheal smooth muscle from a control value of 0.47 to 0.55 and 0.71, respectively. This correlates with 3-fold and 6-fold increases in cGMP concentrations in response to methacholine and sodium nitroprusside, respectively. Addition of charcoal to the homogenizing buffer prior to homogenization had no significant effect on the cGMP-dependent protein kinase response to either agent, suggesting that activation of the enzyme was not occurring as a result of cGMP release during homogenization. In order to limit cGMP dissociation from cGMP-dependent protein kinase during the assay procedure, it was necessary to perform assays at a reduced temperature (0 degree C) and with an abbreviated incubation time (2.5 min). When assayed at 30 degrees C, activated cGMP-dependent protein kinase rapidly lost activity. This inactivation occurred whether the enzyme had been activated exogenously, by exposing a supernatant fraction of canine trachealis to 0.1 microM cGMP, or endogenously, by treating intact canine trachealis with methacholine or sodium nitroprusside. By assaying instead at 0 degree C, the inactivation of cGMP-dependent protein kinase was minimized. Therefore, the activity ratio obtained by this new modified assay provided an estimate of the endogenous activation state of cGMP-dependent protein kinase. The data indicate that cGMP responses in canine trachealis to both methacholine and sodium nitroprusside are functionally linked to activation of cGMP-dependent protein kinase and are consistent with the hypothesis that cGMP, via cGMP-dependent protein kinase activation, regulates smooth muscle contractility.

Animals↗
PubMed1984

A comparison of the effects of sodium nitroprusside and insulin on the control of metabolism in rat isolated adipocytes.

Sodium nitroprusside, a known activator of guanylate cyclase within cells, was used as a probe to investigate the possible role of cyclic GMP in the control of metabolism within rat isolated white adipocytes. Over the concentration range 0-0.1 mM, it increased intracellular cyclic GMP concentrations up to 6-fold within 2 min. Over the same concentration range, it increased the incorporation of 14C from D-[U-14C]glucose into triacylglycerol and of L-[14C]leucine into protein. It also inhibited adrenalin -stimulated lipolysis in the cells, but had no effect on the transport of glucose into the cells. The effects of sodium nitroprusside were compared with those elicited by insulin under identical conditions, as this hormone was shown to cause a similar, but transient, rise in intracellular cyclic GMP concentrations within these cells. Nor insulin, neither sodium nitroprusside were able to increase cyclic AMP levels in adipocytes, whereas adrenalin (0.3 microM) stimulated this production. It is suggested that cyclic GMP may have a role in the control of some part of metabolism 'glucose or amino acids' in adipocytes, and that sodium nitroprusside is a useful probe to investigate this. The limitation of its use are discussed.

Adipose Tissue↗
PubMed1987

Effect of nitroprusside-induced fall in systemic pressure on coronary stenoses.

A fall in coronary pressure increases resistance across compliant coronary stenoses, probably because of passive collapse of the stenotic segment. The effects of a mechanically induced fall in coronary pressure were compared with the effects of a similar fall in pressure caused by intravenous sodium nitroprusside, a systemic and large coronary artery vasodilator. Seventeen dogs were studied in which a compliant circumflex coronary stenosis was produced by inflating an intracoronary balloon with saline. When coronary pressure was lowered from 105 +/- 3 to 78 +/- 3 mm Hg (P less than 0.001) by tightening a snare proximally on the circumflex coronary artery, the stenosis pressure gradient increased (9 +/- 1 to 17 +/- 3 mm Hg, P less than 0.005), flow fell (21 +/- 2 to 15 +/- 2 ml/mm, P less than 0.001) and stenosis resistance increased (0.67 +/- 0.15 to 2.06 +/- 0.68 units, P less than 0.05). When nitroprusside caused pressure to fall from 112 +/- 4 to 81 +/- 4 mm Hg (P less than 0.001), the stenosis pressure gradient did not change (16 +/- 1 to 16 +/- 1 mm Hg), flow increased (42 +/- 5 to 62 +/- 6 ml/min, P less than 0.001), and stenosis resistance decreased (0.46 +/- 0.07 to 0.32 +/- 0.06 units, P less than 0.01). These findings demonstrate that nitroprusside prevented passive collapse of the compliant stenoses as pressure fell, possibly by nitroprusside actively dilating the stenotic segment. Therefore a moderate fall in systemic pressure caused by a coronary vasodilator may not have deleterious effects on stenosis severity.

Animals↗
PubMed1995

Dietary nitroprusside alleviates atherosclerosis in hypercholesterolemic Japanese quail (Coturnix coturnix japonica).

Male Japanese quail (Coturnix coturnix japonica), susceptible to cholesterol-induced atherosclerosis, were rendered hypercholesterolemic by feeding a diet containing 0.5% cholesterol in two experiments. Half the animals also received a dietary supplement of sodium nitroprusside ranging in concentration from 0.005% to 0.015%. After 10 weeks on the diets, serum was obtained for cholesterol analysis, the animals were killed, and the aortae removed and examined for the presence of atherosclerotic lesions. The number of animals having lesions and the severity of the lesions was reduced in a dose dependent manner among those animals receiving nitroprusside. Serum cholesterol was also reduced in response to increasing levels of dietary nitroprusside. These findings indicate that, in this model, dietary nitroprusside, a source of nitric oxide, can reduce the appearance and severity of atherosclerotic lesions in the aorta.

Animals↗
PubMed1993

The interaction of sodium nitroprusside with peripheral white blood cells in vitro: a rationale for cyanide release in vivo.

Isolated monocytes and polymorphonuclear leukocytes release the cyanide anion from the hypotensive agent, sodium nitroprusside. The proposed mechanism involves the production of hydrogen peroxide which oxidizes the substitution inert d6 iron(II) transition metal complex to a labile d5 iron(III) complex. Consequently, the release of cyanide becomes more favoured. This mechanism is supported by the chemical release of the cyanide anion from sodium nitroprusside in vitro by hydrogen peroxide and the demonstrated ability of monocytes and polymorphonuclear leukocytes to generate hydrogen peroxide ex vivo when chemically stimulated by the nitroprusside anion. The results suggest that within a clinical environment white cell counts and cell activation induced as a consequence of disease processes may be important for predicting the toxicity of sodium nitroprusside.

Cells, Cultured↗
PubMed1990

Comparison of isoflurane with sodium nitroprusside for controlling hypertension during thoracic aortic cross-clamping.

The aims of this randomized study were (1) to determine if isoflurane is effective in controlling blood pressure during thoracic aortic cross-clamping, and (2) to compare its effects on hemodynamics and oxygen transport to those of sodium nitroprusside. Sodium nitroprusside (SNP group, n = 10) or isoflurane (ISO group, n = 10) was started 2 minutes before cross-clamping and was adjusted to maintain systolic arterial pressure as near as possible to preinduction values. The duration of thoracic aortic cross-clamping was 26 +/- 4 minutes in the SNP group and 30 +/- 4 minutes in the ISO group. Administration of isoflurance and sodium nitroprusside was stopped 2 minutes before unclamping. The same anesthetic technique using fentanyl, 6 micrograms/kg, flunitrazepam, 0.02 mg/kg, pancuronium, 0.1 mg/kg, and 50% N2O was used for all patients. At the time of clamping, either isoflurance (maximal expired concentration, 2.5% +/- 0.3%) or sodium nitroprusside (cumulative dose, 11.1 +/- 1.0 mg) was effective in maintaining the systolic blood pressure below 160 mm Hg, whereas the pulmonary capillary wedge pressure did not change. However, only SNP was able to bring the arterial pressure above the cross-clamp back to postinduction levels. During clamping, stroke index values were similar in both groups, but cardiac index increased only in patients receiving SNP. In both groups, at clamping and unclamping, PvO2 was higher than postinduction values, indicating that throughout the study the oxygen needs of the perfused area were adequately met. There was no evidence of acute left ventricular decompensation because pulmonary capillary wedge pressures did not abruptly increase, nor did pulmonary edema occur.(ABSTRACT TRUNCATED AT 250 WORDS)

Aorta, Abdominal↗
PubMed1989

A randomized comparison of labetalol and nitroprusside for induced hypotension.

In a randomized study, labetalol-induced hypotension and nitroprusside-induced hypotension were compared in 20 patients (10 in each group) scheduled for major orthopedic procedures. Each patient was subjected to an identical anesthetic protocol and similar drug-induced reductions in mean arterial blood pressure (BP) (50 to 55 mmHg). Nitroprusside infusion was associated with a significant (p less than 0.05) increase in heart rate and cardiac output; rebound hypertension was observed in three patients after discontinuation of nitroprusside. Labetalol administration was not associated with any of these findings. Arterial PO2 decreased in both groups. It was concluded that labetalol offers advantages over nitroprusside.

Adult↗