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.

SourceResearch connectionFrom yearThrough year

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

At least 127 records · Page 7Linked to original sources

PubMed1992

Reduced relaxant potency of nitroprusside on pulmonary artery preparations taken from rats during the development of hypoxic pulmonary hypertension.

1. Relaxant responses to nitroprusside were examined on U46619-contracted pulmonary artery ring preparations from rats exposed to hypoxia, in chambers containing 10% oxygen, for 1, 3, or 14 days, or for 14 days followed by 12 days in room air. Control rats were housed in room air. 2. After 3 days of hypoxia (but not 1 day), rats had elevated pulmonary artery pressure, right ventricular hypertrophy and polycythemia. After 14 days of hypoxia there was, in addition, hypertrophy of the pulmonary artery. In rats returned to room air for 12 days after 14 days of hypoxia, there was still some right ventricular and vascular hypertrophy but no increase in pulmonary artery pressure or polycythemia. 3. The potency (neg log EC50) of nitroprusside on pulmonary arteries taken from rats after 3 or 14 days of hypoxia was significantly less than on preparations from control rats (3 and 11 fold, respectively). This was not seen after 1 day of hypoxia or after 14 days of hypoxia followed by 12 days in room air. Removal of the endothelium from the preparations had no effect on the potency of nitroprusside in control or hypoxic rats (14 days). 4. In preparations from hypoxic, but not control, rats (14 days), the maximum response to nitroprusside was > 100% (177% reversal of the U46619 contraction) in the absence, but not in the presence, of the endothelium, indicating that pulmonary arteries from hypoxic rats had inherent tone which could be counteracted by a relaxing factor from the endothelium. 5. Exposure of rats to hypoxia (14 days) did not affect the potency of nitroprusside on aorta or trachea.6. It is concluded that exposure of rats to hypoxia results in reversible desensitization of the vascular smooth muscle of pulmonary artery to nitroprusside. The time course of this desensitization suggests that it is probably associated with the elevated pulmonary artery pressure or maintained hypoxaemia rather than with the vascular hypertrophy.7. It is postulated that the increase in pulmonary artery pressure and/or the maintained hypoxaemia may cause chronic release of nitric oxide from the pulmonary vascular endothelium or smooth muscle resulting in desensitization of soluble guanylate cyclase to the action of nitroprusside.

Animals↗

PubMed1994

The interaction of alpha-human atrial natriuretic peptide (ANP) with salbutamol, sodium nitroprusside and isosorbide dinitrate in human bronchial smooth muscle.

1. Contractions in human bronchial rings evoked by methacholine (10(-6) M) were reversed by single contractions of alpha-human atrial natriuretic peptide (10(-6) M), salbutamol (10(-6) M), sodium nitroprusside (10(-6) M) or isosorbide dinitrate (4.2 x 10(-5) M) and the extent of the relaxations compared. The activity of combinations of ANP with salbutamol, sodium nitroprusside and isosorbide dinitrate were compared with those for each agonist alone. 2. ANP and salbutamol were equipotent in reversing methacholine-evoked contraction and, in combination these agonists evoked an additive response. ANP and sodium nitroprusside also evoked similar degrees of relaxation and were additive, as were ANP and isosorbide dinitrate; however, with isosorbide dinitrate a higher concentration was required to evoke the same degree of relaxation as ANP, sodium nitroprusside or salbutamol. 3. Cumulative concentration-response curves to methacholine (10(-9)-3 x 10(-4) M) were examined in the presence and absence of the above bronchodilator substances, alone and in combination allowing their abilities to protect against contraction to be compared. ANP (10(-6) M) and salbutamol (10(-6) M) each attenuated subsequent contractions evoked by methacholine, an ability not shared with sodium nitroprusside (10(-6) M) or isosorbide dinitrate (4.2 x 10(-5) M). Indeed at lower concentrations of methacholine (< 3 x 10(-7) M), sodium nitroprusside evoked a paradoxical enhancement of methacholine-evoked contractions. 4. In combination, ANP and salbutamol attenuated contractions evoked by methacholine to a significantly greater degree than that seen with either agonist alone, whilst a combination of ANP and sodium nitroprusside evoked no greater effect than that seen with ANP alone. By contrast, isosorbide dinitrate and ANP together evoked a greater inhibition than ANP alone.5 These results suggest that a combination of agents such as ANP and salbutamol evokes a greater effect than either alone, both in reversing and protecting against methacholine-evoked contractions.Such combinations may be of benefit in the treatment of patients, allowing lower doses of drug to be used. Combinations of ANP and isosorbide dinitrate may likewise be of interest; however, the mechanism underlying the enhancement of ANP responses by isosorbide dinitrate requires further study.

Albuterol↗

PubMed1979

Resistance and volume changes caused by nitroprusside in the dog.

Changes in vascular volume caused by a pharmacologic agent are frequently inferred rather than directly measured. We investigated the effects of nitroprusside in 8 dogs divided into 2 groups: control and splenectomized. We anesthetized the dogs using pentobarbital, and surgically prepared a veno-right atrial bypass preparation whose controlled cardiac output and external reservoir allowed measurement of both changes in vascular resistance and changes in vascular volume. In both groups, blood pressure (mean +/- SD) decreased at each successive level of nitroprusside: 114 +/- 24 mmHg (base line), 101 +/- 19 mmHg (45 microgram/min), 90 +/- 16 mmHg (90 microgram/min), 81 +/- 17 mmHg (180 microgram/min), 68 +/- 18 mmHg (360 microgram/min). Nitroprusside caused a large and similar decrease in vascular resistance in both groups. In the control group, vascular volume increased above base line 5.5 +/- 2.7, 8.3 +/- 3.2, 11.6 +/- 2.9, and 14.7 +/- 3.5 ml/kg at each successive level of nitroprusside infusion, whereas in the splenectomized group vascular volume increased above base line 0.9 +/- 0.3, 2.5 +/- 1.0, 3.3 +/- 1.1, and 4.0 +/- 1.3 ml/kg at each successive level of nitroprusside infusion, but increased significantly less than the control group. We concluded that nitroprusside decreases vascular resistance and increases vascular volume and that the spleen is the major site of changes in vascular volume caused by nitroprusside.

Animals↗

PubMed1977

Comparative responses to dobutamine and nitroprusside in patients with chronic low output cardiac failure.

The acute hemodynamic effects of dobutamine and nitroprusside were compared in 19 patients with low output cardiac failure. At dosage levels yielding similar increases in cardiac index (12 patients), nitroprusside resulted in significantly lower arterial systolic and wedge pressures and did not increase heart rate suggesting advantages over dobutamine when reduction in myocardial oxygen requirement or pulmonary congestion is a major goal. Systemic arterial mean and diastolic pressures were minimally changed with dobutamine, but fell significantly with nitroprusside suggesting advantages of dobutamine over nitroprusside in patients where hypotension could limit coronary blood flow or perfusion of other vital organs. Reduction in pulmonary arteriolar resistance occurred only with nitroprusside. Arterial hypoxemia developed in three patients during nitroprusside infusion suggesting the possibility of increased right-to-left intrapulmonary shunting resulting from a direct vasodilating effect of nitroprusside on pulmonary arteriole smooth muscle. Although both inotropic and vasodilator drugs can result in hemodynamic improvement when administered to patients with chronic low output cardiac failure, significant differences of potential clinical importance exist between these two modes of therapy.

Adult↗

PubMed1978

Hemodynamic effects of nitroprusside and hydralazine in experimental cardiac tamponade.

Cardiac tamponade is associated with decreased cardiac output and increased systemic vascular resistance. Thus, vasodilator drugs might lower systemic resistance and increase cardiac output. Three groups of dogs were studied during tamponade. Group I received nitroprusside only; group II received blood transfusion and then nitroprusside; group III received hydralazine. In group I, nitroprusside lowered right artrial pressure and systemic resistance; cardiac output was unchanged. In group II, transfusion raised right atrial pressure but not cardiac output. Then nitroprusside raised cardiac output significantly. Hydralazine decreased right atrial pressure less than nitroprusside but decreased vascular resistance and raised cardiac output. Both nitroprusside and hydralazine decreased systemic vascular resistance during tamponade, but only hydralazine raised cardiac output probably because of its lesser effect upon the capacitance vessels. Nitroprusside maintained cardiac output during tamponade despite lowered right atrial pressure but increased cardiac output only after transfusion.

Animals↗

PubMed1981

Hemodynamic effects of nitroprusside in infants with a large ventricular septal defect.

To evaluate the effect of acute vasodilator therapy, nitroprusside was administered at cardiac catheterization to five infants (ages 10 days to 6 months) with isolated ventricular septal defect and congestive heart failure. Intravenous nitroprusside was begun at a dose of 0.5 micrograms/kg/min and was increased by increments of 0.5 micrograms/kg. Hemodynamic measurements were made before nitroprusside, after 5 minutes at each dose, and 10 minutes after nitroprusside was discontinued. Baseline data were obtained before nitroprusside administration and compared with data obtained at maximal nitroprusside dose. The pulmonary-to-systemic flow ratio increased from 2.2 +/- 0.2 to 3.4 +/- 0.2 (mean +/- SEM, p less than 0.05) as a consequence of a marked decrease in systemic blood flow (5.3 +/- 0.7 to 3.6 +/- 0.51/min/m(2), p less than 0.05). Pulmonary flow did not change significantly. Mean pulmonary capillary wedge and right atrial pressures decreased by 53% (10.2 +/- 1.4 to 4.8 +/- 1.4 mm Hg [p less than 0.01] and 6.0 +/- 1.4 to 2.8 +/- 1.1 mm Hg [p less than 0.05], respectively). Decreases in mean aortic (63.6 +/- 3.0 to 54.6 +/- 2.1 mm Hg, p less than 0.05) and mean pulmonary artery pressure (41.4 +/- 6.2 to 32.0 +/- 6.7 mm Hg, p less than 0.05) were also observed. An apparently paradoxical increase in systemic resistance occurred (11.7 +/- 1.6 to 15.4 +/- 2.4 U, p less than 0.05. Our data show that nitroprusside causes a marked decrease in systemic blood flow and an increase in the pulmonary-to-systemic flow ratio in infants with a large ventricular septal defect. These findings may be related to the hemodynamic profile of these infants, in whom ventricular function, cardiac output and systemic resistance are normal.

Blood Circulation↗

PubMed1976

Effects of sodium nitroprusside and nitroglycerin on tension prolongation of cat papillary muscle during recovery from hypoxia.

Because of recent studies suggesting that vasodilators affect ventricular compliance, we studied the effect of sodium nitroprusside and nitroglycerin on the mechanical performance of 21 isolated cat papillary muscles. The muscles were stimulated isometrically at 36 beats/min. Sixteen of the muscles were made hypoxic (95% N2, 5% CO2) for 50 minutes and then reoxygenated. Sodium nitroprusside (10(-5) M) added to four of these muscles prior to hypoxia substantially diminished the tension prolongation (both the time to peak tension, TTP, and time for tension to fall to 1/2 its peak value, RT 1/2) that characterizes recovery from hypoxia. TTP and RT 1/2 measured 2 minutes after reoxygenation were 300 +/- 20 msec and 528 +/- 26 msec for the control muscles compared to 208 +/- 13 msec and 248 +/- 22 msec for the muscles pretreated with nitroprusside. Nitroprusside had no effect on the fall and recovery of peak developed force or on the rise and fall of resting force. Furthermore, nitroprusside had no effect on the above parameters in nonhypoxic muscles. We also found that nitroprusside in concentrations of 10(-7) M and nitroglycerin in concentrations of 10(-5) M had little or no effect on tension prolongation. The results of the study indicate that nitroprusside is capable of blocking the tension prolongation that occurs during recovery from hypoxia and may prevent the incomplete myocardial relaxation thought to characterize this phenomenon. Since nitroglycerin had no effect on tension prolongation, it is possible that other factors also may be important in the apparent increase in left ventricular compliance associated with administration of vasodilators to patients.

Animals↗

PubMed1992

Cyanide toxicity from sodium nitroprusside: risks and management.

OBJECTIVE: To review the risks, manifestations, and treatment of cyanide toxicity from nitroprusside therapy. DATA SOURCES: All English case reports identified in Index Medicus (MEDLINE) of cyanide intoxication related to nitroprusside from 1970 to the present were reviewed. In addition, literature regarding the incidence, risks, and treatment of cyanide toxicity from nitroprusside is presented. CONCLUSIONS: Numerous cases of cyanide toxicity associated with nitroprusside have been reported. The overall incidence appears to be infrequent; however, certain patients may be at high risk. Risk factors may include hypoalbuminemia, cardiopulmonary bypass procedures, or the administration of moderate to high doses of nitroprusside. Treatment of cyanide toxicity requires the cessation of nitroprusside and, for severe toxicity, use of the cyanide antidote kit. Cyanide toxicity from nitroprusside may be prevented by concomitant administration of sodium thiosulfate infusions.

Adolescent↗

PubMed1997

Nitroprusside treatment of erythromelalgia in an adolescent female.

OBJECTIVE: To report a case of erythromelalgia in an adolescent patient successfully treated with nitroprusside. CASE SUMMARY: A 15-year-old girl with erythromelalgia resistant to aspirin therapy received an infusion of nitroprusside. The response of the erythromelalgia to nitroprusside was dramatic, with complete pain resolution within 17 hours after the start of therapy. No relapse of erythromelalgia was seen when nitroprusside was discontinued and the patient remained well after 6 months. DISCUSSION: This case adds to existing literature substantiating the benefit of nitroprusside for the treatment of erythromelalgia in pediatric patients. Erythromelalgia in children may represent a different disease entity than that seen in adults, which is commonly responsive to aspirin therapy. The pathogenesis of erythromelalgia is unclear and precludes formulating a proposed mechanism by which nitroprusside has benefit in children. CONCLUSIONS: Nitroprusside is valuable for erythromelalgia resistant to aspirin therapy in pediatric patients. Because of unanswered questions regarding the disease, aspirin remains the agent of first choice in all patients with this rare disease.

Adolescent↗

PubMed1990

A comparison of labetalol and nitroprusside for inducing hypotension during major surgery.

The hemodynamic and intrapulmonary shunt effects of intravenous labetalol and nitroprusside were compared during induced hypotension for major spinal surgery. A randomized, double-blind protocol was used in which 20 patients, ASA physical status I or II, received either nitroprusside infusion (n = 10) or labetalol bolus injections of 10 mg every 10 min (n = 10) until mean arterial blood pressure was reduced to 55-60 mm Hg. Pulmonary artery pressures were measured and mixed venous samples obtained via a pulmonary artery catheter. Nitroprusside increased heart rate significantly more than labetalol during the period of hypotension. When compared with prehypotension baseline values, nitroprusside increased heart rate significantly with a concomitant significant decrease in systemic vascular resistance. Cardiac output increased significantly 60 min after hypotension was achieved in patients treated with nitroprusside. Systemic vascular resistance decreased significantly below baseline levels in patients treated with labetalol but without changes in cardiac output, heart rate, or mean pulmonary artery pressure. There was a 122% increase in intrapulmonary shunt with nitroprusside administration, compared with an 11% increase with labetalol. Labetalol was effective for inducing hypotension and was not associated with an increase in heart rate, intrapulmonary shunt, or cardiac output as seen with nitroprusside.

Adult↗

PubMed2004

Fenoldopam versus nitroprusside for the treatment of hypertensive emergency.

BACKGROUND: While sodium nitroprusside remains first-line therapy for hypertensive emergency (HEM), fenoldopam is increasingly being used because of its benign safety profile and potential renal protective effects. OBJECTIVE: To compare the efficacy, safety, and cost of sodium nitroprusside versus fenoldopam for the treatment of HEM. METHODS: This study was a retrospective analysis of consecutive patients with HEM admitted to a university-affiliated, level 1 trauma center from 1999 to 2001 and treated with either nitroprusside (n = 21) or fenoldopam (n = 22) for >30 minutes. Time to reach mean arterial pressure (MAP) goal, change in MAP over time, time to initiation of oral antihypertensive therapy, change in renal function, incidence of cyanide toxicity, and cost of therapy were compared between groups. RESULTS: Demographic parameters were similar between groups, except renal failure, which was more prevalent in the fenoldopam group (10% vs 46%; p = 0.009). Neither the mean +/- SD pretreatment MAP (nitroprusside 168 +/- 19; fenoldopam 163 +/- 19; p = 0.45), time to reach MAP goal (3.6 [0.4-30] vs 4 [1-22] h; p = 0.51), nor infusion duration (18 [0.7-113] vs 18 [3-74] h; p = 0.45) differed between the patient groups. Time to initiation of oral antihypertensive therapy was similar between nitroprusside--(4.5 h [0.5-22] and fenoldopam--(6.5 h [1-100] treated patients; p = 0.65). Additional intravenous antihypertensives were administered to 16 patients in each group (p = 0.80). Change in creatinine clearance and incidence of tachycardia did not differ between groups. No symptoms of cyanide toxicity were detected. Cost of drug therapy was greater with fenoldopam (597.60 dollars, 199.20-6675.20 dollars); than nitroprusside (2.66 dollars, 1.68-3.48 dollars; p < 0.001). CONCLUSIONS: Treatment of HEM with fenoldopam appears to result in patient outcomes equivalent to those with nitroprusside but at a substantially higher cost. Further study is required to delineate the exact role of fenoldopam for treatment of HEM.

Antihypertensive Agents↗

PubMed2000

Local 42 degrees C hyperthermia improves vascular conductance of the R3230Ac rat mammary adenocarcinoma during sodium nitroprusside infusion.

The effect of sodium nitroprusside-induced hypotension on the perfusion of the R3230 adenocarcinoma during local 42 degrees C hyperthermia was studied using a combination of intravital microscopy and laser Doppler flowmetry. Fischer 344 rats were implanted with dorsal skin flap window chambers containing the R3230Ac tumor and allocated to three treatment groups (34 degrees C with nitroprusside, 42 degrees C with nitroprusside, and 42 degrees C with 0.9% saline). After baseline observation at 34 degrees C, tumors were locally heated to 42 degrees C using a water bath and either 0.9% saline or nitroprusside sufficient to reduce blood pressure 20% below pretreatment baseline was infused. Nitroprusside at 34 degrees C decreased tumor vascular conductance 40% with no effect on the diameter of arterioles entering the tumor. The diameter of arterioles entering 42 degrees C heated tumors increased 35% independent of blood pressure change. Saline at 42 degrees C had no effect on tumor vascular conductance; however, nitroprusside at 42 degrees C increased tumor vascular conductance 55%. Local 42 degrees C tumor heating, combined with a moderate reduction in blood pressure with nitroprusside, overrides the vascular steal effect associated with reduced perfusion pressure alone and results in improved tumor perfusion. Observations of the effect of vasodilator substances on normothermic tumor perfusion cannot be extrapolated to situations where moderate hyperthermia is used.

Adenocarcinoma↗

PubMed2002

Intracisternal sodium nitroprusside fails to prevent vasospasm in nonhuman primates.

OBJECTIVE: Hemoglobin contributes to vasospasm after subarachnoid hemorrhage. One mechanism may involve binding of nitric oxide, destruction of nitric oxide, or both. Support for this mechanism would be evidence that nitric oxide donors prevent vasospasm. This study attempted to provide such evidence. METHODS: A randomized, blinded study was conducted in which 13 monkeys underwent cerebral angiography and creation of a right subarachnoid hemorrhage. Subcutaneous osmotic pumps were implanted to deliver sodium nitroprusside (n = 7) or vehicle (n = 6) via catheters into the right basal cisterns. Seven days later, angiography was repeated, and the animals were humanely killed. Levels of cyclic nucleotides, hemoglobins, and thiocyanate were measured. RESULTS: Significant vasospasm of the right middle cerebral artery was present in animals treated with sodium nitroprusside (35 +/- 22% reduction in diameter, P < 0.05, paired t test) and placebo (28 +/- 20% reduction, P < 0.05, not significantly different from nitroprusside group by unpaired t test). Adequate delivery of sodium nitroprusside was supported by the finding of a significant increase in cyclic guanosine monophosphate levels in the cerebral arteries of treated animals compared with placebo (P < 0.05, unpaired t test). Thiocyanate was not present in significantly increased amounts in animals treated with nitroprusside, although this group did display elevated concentrations of nitrosyl hemoglobin (measured by electron paramagnetic resonance spectroscopy) and cyanomethemoglobin (measured by spectrophotometry) in the cerebrospinal fluid on Day 7. CONCLUSION: The lack of effect of sodium nitroprusside was not the result of inadequate drug delivery because cyclic guanosine monophosphate levels were significantly increased in vasospastic arteries. Vasospasm may not have been prevented because of a toxic effect of sodium nitroprusside metabolites, involvement of smooth muscle relaxation or contraction processes downstream of cyclic guanosine monophosphate, or both.

Animals↗

PubMed1991

Age-dependent effects of sodium nitroprusside and dopamine in lambs.

Vasodilators and cardiotonic agents are frequently used in hypoxemic newborn infants with persistent pulmonary hypertension. We studied the effects of sodium nitroprusside and dopamine on hypoxia-induced pulmonary hypertension in seven newborn (0-3 d) and seven young (10-14 d) lambs under chloralose anesthesia. Pulmonary blood flow, pulmonary arterial pressure, systemic arterial pressure, and left atrial pressure were measured during the experimental states of hypoxia, hypoxia plus nitroprusside, and hypoxia plus both nitroprusside and dopamine. Pulmonary and systemic arterial pressure and cardiac output all decreased significantly when hypoxemic newborn lambs were given nitroprusside; in contrast, when hypoxemic young lambs were given nitroprusside, cardiac output did not change, whereas both pulmonary and systemic arterial pressure decreased significantly. Calculated pulmonary vascular resistance was unchanged in the newborn lambs but fell in the young lambs, implying that active pulmonary vasodilation by nitroprusside occurred only in the latter group. Systemic vascular resistance was not significantly affected by nitroprusside in either group. The addition of dopamine resulted in qualitatively similar changes in both groups of lambs, with increased pulmonary blood flow and no significant change in pulmonary or systemic arterial pressures. Maturation in vascular smooth muscle responsiveness to nitrovasodilators may explain the age-related differences that we found in lambs, and could also account for the variable clinical responses to vasodilators observed in hypoxemic human infants.

Age Factors↗

PubMed1986

Mechanism of inhibitory action of sodium nitroprusside in vascular smooth muscle of rabbit aorta.

Mechanism of inhibitory action of sodium nitroprusside in vascular smooth muscle of rabbit aorta was examined. Sodium nitroprusside inhibited the 1 X 10(-6) M norepinephrine-induced contraction with IC50 (concentration to induce 50% inhibition) of 1.40 X 10(-7) M, but had little effect on the 65.4 mM K-induced contraction. In contrast, verapamil had little effect on the norepinephrine-induced contraction at the concentration needed to inhibit the high K-induced contraction. The inhibitory effect of sodium nitroprusside on the norepinephrine-induced contraction did not change in the verapamil-treated aorta. In the high K-solution with verapamil, norepinephrine induced a sustained contraction with similar magnitude as that in normal solution. Sodium nitroprusside also inhibited this contraction although the inhibitory effect was slightly less compared to that in the polarized aorta (IC50 = 2.90 X 10(-7) M, p less than 0.01). In a Ca-deficient solution, norepinephrine induced a transient contraction due to release of cellular Ca. Sodium nitroprusside inhibited the norepinephrine-induced transient contraction at slightly higher concentrations than those which inhibit the sustained contraction (IC50 = 5.55 X 10(-7) M). In a high K, Ca deficient solution, norepinephrine also induced a transient contraction. The inhibitory effect of sodium nitroprusside on the transient contraction was reduced in the depolarized aorta (IC50 = 9.50 X 10(-6) M). It is suggested that the inhibition of norepinephrine-induced sustained contraction by sodium nitroprusside is mainly due to the direct inhibitory effect on the receptor linked-Ca channels whereas the inhibition of norepinephrine-induced transient contraction is attributable mainly to membrane hyperpolarization and, at higher concentrations, to a direct inhibition of Ca release.

Animals↗

PubMed1979

Relaxation of bovine coronary artery and activation of coronary arterial guanylate cyclase by nitric oxide, nitroprusside and a carcinogenic nitrosoamine.

The principal objective of this study was to test the hypothesis that nitroprusside relaxes vascular smooth muscle via the reactive intermediate, nitric oxide (NO), and that the biologic action of NO is associated with the activation of guanylate cyclase. Nitroprusside, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and NO elicit concentration-dependent relaxation of precontraced helical strips of bovine coronary artery. Nitroprusside, MNNG and NO also markedly activate soluble guanylate cyclase from bovine coronary arterial smooth muscle and, thereby, stimulate the formation of cyclic GMP. Three heme proteins, hemoglobin, methemoglobin and myoglobin, and the oxidant, methylene blue, abolish the coronary arterial relaxation elicited by NO. Similarly, these heme proteins, methylene blue and another oxidant, ferricyanide, markedly inhibit the activation of coronary arterial guanylate cyclase by NO, nitroprusside and MNNG. The following findings support the view that certain nitroso-containing compounds liberate NO in tissue:heme proteins, which cannot permeate cells, inhibit coronary arterial relaxation elicited by NO, but not by nitroprusside or MNNG; the vital stain, methylene blue, inhibits relaxation by NO, nitroprusside and MNNG; heme proteins and oxidants inhibit guanylate cyclase activation by NO, nitroprusside and MNNG in cell-free mixtures. The findings that inhibitors of NO-induced relaxation of coronary artery also inhibit coronary arterial guanylate cyclase activation suggest that cyclic GMP formation may be associated with coronary arterial smooth muscle relaxation.

Animals↗

PubMed1981

Effect of nitroprusside on end-diastolic pressure-diameter relations of the human left ventricle after pericardiotomy.

Although studies in human beings have suggested that sodium nitroprusside may increase the diastolic compliance of the left ventricle, animal models have provided contradictory evidence following pericardiotomy. The effect of nitroprusside on the human left ventricle after pericardiotomy has not been reported. Accordingly, we studied the effects of intravenous sodium nitroprusside in eight patients during cardiac operations. Curves relating left ventricular end-diastolic pressure (EDP) to echocardiographically determined end-diastolic diameter (EDD) were determined during the transfusion of volume from the reservoir of the heart-lung machine (EDP varied from 5 to 35 mm Hg) before and during nitroprusside administration (1 to 4 mcg/kg/min). An average relation (EDP = 0.41 +/- 0.40 [SD] e1.18 +/- 0.58 EDD was obtained for eight patients by exponential curve fitting (r = 0.80 +/-08). Nitroprusside decreased systolic left ventricular pressure (118 +/- 16 to 100 +/- 13 mm Hg, p less than 0.001, paired t test) but did not alter the control curve relating EDP to EDD. We conclude that EDD-EDP relations of the human left ventricle are not altered by nitroprusside administration in the absence of the restraining influence of the pericardium. This suggests that nitroprusside has no significant direct effect on diastolic properties of the human myocardium.

Adult↗

PubMed1995

Preliminary results of a comparative study with intracavernous sodium nitroprusside and prostaglandin E1 in patients with erectile dysfunction.

We compared the effect of intracavernous administration of sodium nitroprusside, a nitric oxide donor and, therefore, stimulator of the cyclic guanosine monophosphate pathway, with the activity of prostaglandin E1, which is a stimulator of the cyclic adenosine monophosphate pathway. To date 105 patients with erectile dysfunction have entered the study. As part of the diagnostic evaluation every patient received an intracavernous injection of 20 micrograms prostaglandin E1 and a second injection of sodium nitroprusside at different concentrations (100 micrograms in 10 patients, 300 micrograms in 60 and 400 micrograms in 35). Sodium nitroprusside at a dose of 100 micrograms was not effective for inducing erections. Prostaglandin E1 induced better responses overall than sodium nitroprusside at 300 and 400 micrograms (p < 0.001). The overall duration of erections was also significantly longer with prostaglandin E1 (mean 88.5 minutes) than with 300 micrograms sodium nitroprusside (mean 50.8 minutes, p < 0.001) but did not reach statistical significance compared to 400 micrograms sodium nitroprusside (mean 42.2 minutes). Side effects were minimal with both drugs. Although sodium nitroprusside has several benefits over prostaglandin E1 for intracavernous use (such as lower cost, absence of local pain and shorter action, allowing detumescence after orgasm and decreasing the risk of priapism), prostaglandin E1 still remains the agent of choice for intracavernous use.

Alprostadil↗