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PubMed2005

Comparative analysis of the neuronal activation and cardiovascular effects of nitroglycerin, sodium nitroprusside and L-arginine.

In this study, we compare the biological effects, Fos expression and cardiovascular responses induced in the rat, of different nitric oxide modulators (nitroglycerin, sodium nitroprusside and L-arginine). Nitroglycerin and sodium nitroprusside induced a similar pattern of neuronal activation in several areas, which include the paraventricular and supraoptic nuclei of the hypothalamus, central nucleus of the amygdala, parabrachial nucleus, locus coeruleus, ventrolateral medulla and nucleus tractus solitarius. However, only nitroglycerin activated the periaqueductal grey and nucleus trigeminalis caudalis. L-arginine-induced neuronal activation was restricted to the paraventricular and supraoptic nuclei of the hypothalamus. As regards cardiovascular effect, both nitroglycerin and sodium nitroprusside induced moderate hypotension (nitroglycerin: -23.3%, sodium nitroprusside: -24.3%) that lasted 40 min in the case of sodium nitroprusside and 80 min in the case of nitroglycerin. L-arginine did not significantly influence blood pressure. These data suggest that nitroglycerin, sodium nitroprusside and L-arginine are associated with different biological effects on both the central nervous system and the cardiovascular system. Of the NO-related drugs tested in this study, only nitroglycerin confirmed its ability to activate brainstem areas implicated in nociception.

Analysis of Variance↗
PubMed2005

Hydralazine decreases sodium nitroprusside-induced rat aortic ring relaxation and increased cGMP production by rat aortic myocytes.

Association of hydralazine with nitrova-sodilators has long been known to be beneficial in the vasodilator treatment of heart failure. We previously found that hydralazine appeared to reduce the increase in cGMP induced by sodium nitroprusside in cultured rat aortic myocytes. In order to further explore this seemingly paradoxical interaction, we extended our initial observations in rat aortic myocytes and also determined the influence of hydralazine on sodium nitroprusside-induced relaxation of rat aortic rings. Hydralazine produced a concentration-dependent inhibition of sodium nitroprusside stimulation of cGMP production and caused a rightward shift of concentration-relaxation curves in aortic rings. A possible mechanism of the hydralazine-nitroprusside interaction could be the interference with bioactivation of the nitro-vasodilator to release nitric oxide. Recent evidence indicates that vascular NADH oxidase, an enzyme known to be inhibited by hydralazine, could be involved in this process. Accordingly, hydralazine was found to inhibit NADH oxidase activity in rat aortic myocytes at concentrations similar to those reducing sodium nitroprusside responses. It was concluded that antagonism of sodium nitroprusside action by hydralazine could be a consequence of interference with bioactivation of the former, apparently through inhibition of vascular NADH oxidase.

Animals↗
PubMed1983

Quantitative differences in the hemodynamic effects of captopril and nitroprusside in severe chronic heart failure.

The hemodynamic effects of oral captopril and intravenous nitroprusside were compared in 15 patients with severe chronic congestive heart failure. At doses of both drugs titrated so as to produce similar decreases in systemic vascular resistance in each patient, nitroprusside produced substantially greater increases in cardiac index (+0.67 versus +0.31 liters/min/m2, p less than 0.01) but smaller decreases in mean arterial pressure (-18.4 versus -11.0 mm Hg, p less than 0.01) than did captopril. This finding was due to a significant decrease in heart rate with captopril (-7 beats/min, p less than 0.01) which was not seen with nitroprusside, since changes in stroke volume index with both drugs were similar. Nitroprusside produced a decrease in pulmonary arteriolar resistance quantitatively similar to the decrease in systemic vascular resistance, but the decrease in pulmonary arteriolar resistance with captopril was not significant. Despite similar decreases in systemic resistance, captopril produced a greater decrease in left ventricular filling pressure (-10.2 versus -6.9 mm Hg, p less than 0.01) but a smaller decrease in mean right atrial pressure (-3.1 versus -5.3 mm Hg, p less than 0.01) than did nitroprusside. Thus, captopril has actions independent of its systemic vasodilator effects which account for the quantitative differences observed in its hemodynamic responses compared with those of nitroprusside in patients with severe chronic heart failure. These differences support experimental evidence that angiotensin, in addition to its direct systemic arterial vasoconstrictor actions, exerts positive chronotropic effects and alters ventricular compliance but has minimal direct effects on the limb venous circulation and on the pulmonary vasculature.

Adult↗
PubMed1995

Inhibitory effect of nitroglycerin and sodium nitroprusside on platelet activation across the coronary circulation in stable angina pectoris.

This study assessed the inhibitory effect of nitroglycerin and sodium nitroprusside on platelet aggregation in a model of platelet activation across coronary circulation. Platelet aggregation is believed to contribute to the precipitation of acute ischemic syndromes. We previously showed that rapid atrial pacing in patients with stable coronary artery disease (CAD) causes platelet hyperaggregability during blood passage in coronary circulation. Because nitroglycerin and sodium nitroprusside have been shown to inhibit platelet aggregation, we examined the effect of these drugs on this model of platelet activation. During catheterization of 19 patients with CAD (> 50% diameter narrowing of epicardial coronary arteries), we measured platelet aggregation (using whole blood platelet aggregometry) on blood samples obtained simultaneously from the coronary sinus and aorta at rest, and 2 minutes after onset of rapid atrial pacing. This procedure was repeated during an intravenous infusion of either nitroglycerin (n = 9) or sodium nitroprusside (n = 10). There was no arteriovenous difference in platelet aggregation under resting conditions. Atrial pacing caused an increase in platelet aggregation in coronary sinus blood (+64 +/- 9%; p < 0.01), but not in arterial blood (15 +/- 12% decrease; p = NS). This increase was transient and returned toward baseline 10 minutes after termination of pacing. Although resting platelet aggregation was not affected by nitroglycerin or sodium nitroprusside, activation of platelets with atrial pacing across the coronary bed was stopped by pretreatment with therapeutic doses of nitroglycerin or sodium nitroprusside. When coronary blood flow increases in patients with CAD, platelets are activated and aggregate more easily. This activation can be blunted by pretreatment with nitroglycerin or sodium nitroprusside.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1982

Effect of sodium nitroprusside during the payback period of cardiopulmonary bypass on the incidence of postoperative arrhythmias.

This study was designed to determine whether a sodium nitropruside infusion during the reperfusion (payback) period of cardiopulmonary bypass would minimize arrhythmias during the early postoperative period of coronary artery bypass surgery. A double-blind randomized study was carried out in 38 patients with no previous history of ventricular arrhythmias. Seventeen received 5% dextrose in water (D5W) and 21 received sodium nitroprusside at the rate of 2 microgram per kilogram per minute during the payback period. The pump flow was kept constant at 2.2 liters per square meter per minute, and mean pressure was maintained at greater than 50 mm Hg. There was a statistically significant difference between the two groups in the number of patients who developed ventricular arrhythmias (13 of 17, or 76%, in the D5W group versus 6 of 21, or 29%, in the sodium nitroprusside group; p less than 0.005). Twelve of the 13 patients in the D5W group experienced arrhythmias (6 ventricular tachycardia and 6 ventricular premature depolarization) within the first 24 hours, compared to 5 of 12 patients in the nitroprusside group (3 ventricular tachycardia and 2 ventricular premature depolarization). Only 1 patient in each group developed ventricular arrhythmia after the first postoperative day. One patient in each group experienced atrial arrhythmia during the first 24 hours. After 24 hours, atrial arrhythmias developed in 5 patients in the D5W group (35%) and 3 patients in the sodium nitroprusside group (17%) (p greater than 0.05). The arterial pH ranged from 7.35 to 7.55, with a Po2 greater than 70 torr and a serum potassium of 3.7 +/- 0.36 mEq per liter in the D5W group and 3.4 +/- 0.34 mEq per liter in the nitroprusside group during the period of arrhythmias. Sodium nitroprusside given during the payback period of cardiopulmonary bypass appears to minimize ventricular arrhythmias in the early postoperative period of coronary artery bypass surgery.

Arrhythmias, Cardiac↗
PubMed1985

A comparison of nitroglycerin and nitroprusside: I. Treatment of postoperative hypertension.

Nitroglycerin improves perfusion to ischemic myocardial regions and therefore has theoretical advantages over sodium nitroprusside to treat hypertension (mean arterial pressure [MAP] greater than 95 mm Hg) following coronary bypass operation. Thirty-three hypertensive patients were randomized to an initial infusion of either nitroglycerin or nitroprusside in a crossover trial designed to reduce MAP to 85 mm Hg. Thermodilution cardiac output measurements permitted calculation of left ventricular stroke work index (LVSWI), and nuclear ventriculograms permitted estimation of left ventricular ejection fraction, left ventricular end-diastolic volume index (LVEDVI), and left ventricular end-systolic volume index (LVESVI). Coronary sinus blood flow was measured by the continuous thermodilution technique, and arterial and coronary sinus lactate measurements permitted calculation of myocardial lactate flux (MVL). Both nitroglycerin and nitroprusside reduced MAP (-25 +/- 12 mm Hg and -20 +/- 10 mm Hg, respectively; not significant [NS]). Nitroglycerin reduced LVSWI more than did nitroprusside (-15 +/- 13 gm-m/m2 and -7 +/- 9 gm-m/m2, respectively; p less than 0.01). Both agents increased left ventricular ejection fraction (nitroglycerin, +8 +/- 8%, and nitroprusside, +10 +/- 7%; NS), and decreased LVEDVI (-20 +/- 22 ml/m2 and -11 +/- 17 ml/m2, respectively; NS) and LVESVI (-13 +/- 14 ml/m2 and -10 +/- 12 ml/m2, respectively; NS). Coronary sinus blood flow decreased with both drugs (NS), but MVL increased with nitroglycerin (+0.02 +/- 0.14 mmol/min) and decreased with nitroprusside (-0.02 +/- 0.02 mmol/min) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1985

A comparison of nitroglycerin and nitroprusside: II. The effects of volume loading.

The treatment of postoperative hypertension with nitroglycerin or nitroprusside reduces cardiac filling, and volume loading is required to maintain hemodynamic and metabolic stability. Postoperative hypertension (mean arterial pressure greater than 95 mm Hg) developed in 33 patients who were randomized to an initial infusion of nitroglycerin or nitroprusside in a crossover trial. Volume loading (a rapid infusion of 250 to 500 ml of colloid to raise the left atrial pressure 2 to 4 mm Hg) was instituted prior to hypertension and again following the crossover trial during the infusion of nitroglycerin (11 patients) and nitroprusside (13 patients). Volume loading increased left ventricular end-diastolic volume index (LVEDVI) as documented by nuclear ventriculography, cardiac index (CI), and left ventricular stroke work index (LVSWI). Although CI was higher (p less than 0.01) with nitroprusside at any level of LVEDVI, myocardial performance (the relation between LVSWI and LVEDVI) was not different. Diastolic compliance (the relation between left atrial pressure and LVEDVI) was increased (p less than 0.01) with nitroglycerin. Myocardial metabolism was assessed by calculating myocardial lactate flux (MVL), the product of myocardial lactate extraction and coronary sinus blood flow by the thermodilution technique. Volume loading increased MVL during nitroglycerin therapy and decreased (p less than 0.01) MVL during nitroprusside therapy. Volume loading restored preload and increased CI with both nitroglycerin and nitroprusside. Only nitroglycerin improved myocardial lactate utilization. Nitroglycerin is the preferred vasodilator when ischemia is suspected after coronary bypass operations.

Cardiac Volume↗
PubMed1996

Nitroprusside ameliorates lung allograft reperfusion injury.

BACKGROUND: Nitric oxide is believed to play a critical role in the maintenance of vascular integrity through its interaction with neutrophils, platelets, and cellular components of the vessel wall. It has been reported that endogenous nitric oxide level was depressed after ischemia, reperfusion, or both. Furthermore, exogenous as well as endogenous nitric oxide decreases reperfusion-induced vascular dysfunction. We hypothesized that nitroprusside, a potent nitric oxide donor, might enhance lung preservation and reduce posttransplantation lung allograft dysfunction. METHODS: Ten dogs underwent left lung allotransplantation. Donor lungs were flushed with modified Euro-Collins solution and stored for 21 hours at 1 degree C. Immediately after transplantation, the contralateral right main pulmonary artery and bronchus were ligated to assess isolated allograft function. Hemodynamics and arterial blood gas analysis (inspired oxygen fraction, 1.0) were assessed for 6 hours before sacrifice. Allograft myeloperoxidase activity and wet-to-dry weight ratio were assessed. Group 1 (n = 5) animals received no nitroprusside. In group 2 (n = 5), the donor lung received nitroprusside in the flush solution (10 mg/L) and recipient animals received 0.2 mg/kg just before reperfusion as well as a continuous infusion (0.11 +/- 0.01 mg.kg-1. h-1) during the assessment period. RESULTS: Superior gas exchange and hemodynamics were noted in lungs receiving nitroprusside. Although allograft myeloperoxidase activity and the total amount of fluid suctioned from the allograft were significantly reduced in group 2, protein levels in bronchoalveolar lavage fluid were not statistically different. CONCLUSIONS: Nitroprusside administration in the flush solution and during reperfusion improves lung allograft function and blood flow, and reduces pulmonary vascular resistance and myeloperoxidase activity in the transplanted lung. Nitroprusside reduces lung allograft reperfusion injury.

Animals↗
PubMed2001

Sodium nitroprusside-induced seizures and adenosine release in rat hippocampus.

In the present study, we examined the effects of nitric oxide (NO)-related compounds, i.e. sodium nitroprusside (NO donor), diethyldithiocarbamate (NO trapper) and dithiothreitol (superoxide radical scavenger) on release of aspartate and adenosine from rat hippocampus using electrophysiological and microdialysis methods. Perfusion with 0.05 or 0.5 mM sodium nitroprusside significantly reduced high K(+)-evoked release of aspartate during high K(+) perfusion. Perfusion with 0.5 mM sodium nitroprusside always induced seizures and significantly increased release of aspartate and adenosine during washout of sodium nitroprusside. Diethyldithiocarbamate (5 mM) reversed the effects of sodium nitroprusside. Dithiothreitol (1 mM) significantly reduced the increase in adenosine release by sodium nitroprusside. These findings indicate that adenosine release is closely related to development of seizures, which are triggered by an increase in both NO itself and in part peroxynitrite, which results in reaction with superoxide radicals.

Adenosine↗
PubMed2001

Effects of sildenafil citrate, acetylcholine, and sodium nitroprusside on the relaxation of rabbit cavernosal tissue in vitro.

OBJECTIVES: To investigate the effect of sildenafil together with the influence of sodium nitroprusside and acetylcholine and further discuss its mechanism of action in vitro. METHODS: Isolated strips of rabbit corpus cavernosum were stimulated isometrically with phenylephrine. Graded relaxations were induced using increasing concentrations of acetylcholine, sodium nitroprusside, and sildenafil alone and in combination. RESULTS: The agents all relaxed the rabbit corpus cavernosal strips in a dose-dependent manner. The inhibitory potentials of the test agents were ranked (from least inhibitory to most inhibitory) as follows: sildenafil, acetylcholine plus sildenafil, sodium nitroprusside, sodium nitroprusside plus sildenafil, acetylcholine. The presence of sodium nitroprusside in the medium reduced the median effective dose for the sildenafil-induced relaxation of the cavernosal tissue from 3.65 x 10(-5) M to 2.73 x 10(-7) M, and the presence of acetylcholine reduced it to 9.79 x 10(-6) M. CONCLUSIONS: Sildenafil enhances the relaxing effect of both sodium nitroprusside and acetylcholine on the phenylephrine-induced contraction of rabbit cavernosal tissue.

Acetylcholine↗
PubMed1984

Effect of sodium nitroprusside on ventilation-perfusion mismatching in heart failure.

Sodium nitroprusside has been shown to lower arterial partial pressure of oxygen (PaO2) in patients with congestive heart failure and respiratory failure. The multiple inert gas elimination technique was used to evaluate the effect of sodium nitroprusside infusion on pulmonary gas exchange in five patients with congestive heart failure. During sodium nitroprusside infusion, mean values of cardiac output increased and mean values of arterial pressure, pulmonary artery pressure, pulmonary artery wedge pressure and pulmonary vascular resistance decreased. Cardiac output increased in each patient and PaO2 decreased in all but one patient (mean 75.6 +/- 15.1 to 68 +/- 17.5 mm Hg, p = 0.032). Distributions of ventilation and perfusion showed increased perfusion of lung units with low (less than or equal to 0.1) ventilation-perfusion ratios in all subjects during sodium nitroprusside infusion (mean 3.89 +/- 1.52 to 11.33 +/- 7.42% of cardiac output, p = 0.027, paired t test). The amount of shunt (fractional perfusion of lung units with ventilation-perfusion ratio = 0) increased in the two patients with some shunt present in the baseline measurements. The mean total low ventilation-perfusion perfusion (shunt plus ventilation-perfusion less than or equal to 0.1) was significantly increased from 4.38 +/- 1.54 to 14.7 +/- 9.37% (p = 0.023) during sodium nitroprusside infusion. Total low ventilation-perfusion perfusion was negatively correlated with mean pulmonary artery pressure and pulmonary artery wedge pressure (r = -0.949 and -0.946, respectively). Although sodium nitroprusside infusion increased cardiac output and overall oxygen transport in all patients, it worsened ventilation-perfusion mismatching. The mechanism is probably pulmonary vasodilation or increased cardiac output, or both.

Aged↗
PubMed1987

Myocardial metabolism, catecholamine balance, and left ventricular function during coronary artery surgery: effects of nitroprusside and nifedipine.

The effects of nitroprusside and nifedipine on myocardial oxygen consumption (MVO2), catecholamine release, and left ventricular (LV) function (using 2D transesophageal echocardiography) were compared. Thirty-seven patients undergoing coronary artery surgery, anesthetized with fentanyl, 100 micrograms/kg, were studied. All had good LV function and had been receiving long-term oral beta-blocking therapy. Patients were randomly allocated to one of three groups. Group C (n = 12) received no vasodilator and served as control. Group S (n = 13) received nitroprusside at an initial rate of 1 microgram/kg/min. Group N (n = 12) received nifedipine at an initial rate of 0.7 microgram/kg/min. Baseline measurements were obtained ten minutes after intubation. Vasodilator therapy was then started in groups S and N. Infusion rates were adjusted to maintain systolic blood pressure (SBP) between 80% and 120% of baseline values. Additional measurements were made ten minutes after the start of the infusion, ie, before surgery (in group C immediately before surgery), and after sternotomy when the pericardium was opened. The mean (+/- SD) total dose requirements were 1.9 +/- 0.5 micrograms/kg/min for nitroprusside and 1.1 +/- 0.2 micrograms/kg/min for nifedipine. The mean (+/- SD) total infusion time was 31 +/- 5 minutes for nitroprusside and 32 +/- 11 minutes for nifedipine. After sternotomy, heart rate increased in all groups. At this time arterial blood pressure and systemic vascular resistance (SVR) increased in group C. SVR was decreased after the first ten minutes of nitroprusside infusion and after sternotomy in group S. Coronary sinus blood flow, MVO2, and myocardial norepinephrine release increased in group N, but not in groups C or S. After sternotomy, LV percentage area reduction increased in groups S and N, but not in group C. In group N there was a significant correlation (r = 0.65; P less than .05) between the increases in MVO2 and LV percentage area reduction, an estimate of myocardial function. Lactate production occurred in two patients in group C after sternotomy. This was not associated with ECG changes, but in one patient regional wall motion abnormalities developed. No evidence of myocardial ischemia was observed in groups S and N. However, in contrast to nitroprusside, the use of nifedipine was associated with increases in MVO2, myocardial norepinephrine release, and inotropy.

Blood Pressure↗
PubMed1999

Acetylcholine but not sodium nitroprusside exerts vasodilation in pulmonary hypertension secondary to chronic congestive heart failure.

BACKGROUND: Reduced endothelium-dependent vasodilation contributes to the development of pulmonary hypertension in chronic congestive heart failure (CHF). We investigated pulmonary endothelium-dependent and independent vasodilation in patients with CHF. METHODS: We studied 42 patients with CHF (age 55 +/- 10, NYHA Classes II-III, left ventricular ejection fraction 27 +/- 10%, mean PAP 29 +/- 12 mmHg). The endothelial vasodilator capacity of pulmonary resistance vessels was assessed by the infusion of acetylcholine into a pulmonary artery branch while measuring the blood flow velocity with a Doppler flow wire. For comparison endothelium-independent vasodilation was measured with the response to sodium nitroprusside. The conductance vessel diameter (4.4 +/- 0.2 mm) was determined by intravascular ultrasound. Acetylcholine was administered at concentrations of 10(-6) to 10(-4) mol/l, sodium nitroprusside was administered at concentrations of 0.125 and 0.25 microg/kg per min. The effects on conductance vessel diameter were investigated in 12 patients by the measurement of diameter and flow velocity following the administration of acetylcholine and sodium nitroprusside. RESULTS: Acetylcholine markedly increased blood flow velocity (+39 +/- 7% at 10(-4) mol/l; p < .05). This correlated with the baseline PAP (r = 0.58; p < .05) and pulmonary vascular resistance (r = 0.58; p < .05). Sodium nitroprusside caused a small increase in the flow velocity (5 +/- 2% at 0.125, 12 +/- 4% at 0.25 microg/kg per minute; p < .05) that was accompanied by systemic vasodilation. The conductance vessel diameter was unchanged after acetylcholine was administered and was only marginally decreased after the administration of sodium nitroprusside. CONCLUSIONS: In CHF acetylcholine reveals preserved receptor-mediated endothelial vasodilation, that is positively correlated to pulmonary hypertension, and cannot be reproduced by sodium nitroprusside.

Acetylcholine↗
PubMed2002

Haemodynamic and splanchnic organ blood-flow responses to hypotension induced by the calcitonin gene-related peptide and sodium nitroprusside in dogs.

BACKGROUND AND OBJECTIVE: To elucidate the effects of various degrees of hypotension induced by the calcitonin gene-related peptide (CGRP) on the splanchnic circulation, we investigated the renal and hepatic blood flow during hypotension induced by either the calcitonin gene-related peptide or sodium nitroprusside in the isoflurane-anaesthetized dog. METHODS: Anaesthesia was maintained with 1.3% isoflurane in oxygen. After the baseline period, mean arterial pressure was reduced to 60 mmHg in the CGRP60 and nitroprusside groups, and to 50 mmHg in the CGRP50 group. The splanchnic organ blood flow was measured by hydrogen clearance. RESULTS: The cardiac index in the CGRP60 group increased (P < 0.01), but in the CGRP50 group it decreased (P < 0.01), and in the nitroprusside group it remained unchanged during hypotension. Mean pulmonary artery and pulmonary capillary wedge pressures in the CGRP60 group remained unchanged, but in the CGRP50 and nitroprusside groups they decreased (P < 0.01) during hypotension. Cardiac contractility in the CGRP60 group remained unchanged, whereas in the CGRP50 and nitroprusside groups it was reduced (P < 0.01) during hypotension. Renal blood flow in the CGRP60 group was relatively well maintained but in the CGRP50 and nitroprusside groups it was reduced (P < 0.01) throughout the observation. Hepatic blood flow in all three groups was reduced (P < 0.01) during hypotension. The reductions in hepatic blood flow between the Calcitonin gene-related peptide groups were associated with a dose-dependent decrease in mean arterial pressure. CONCLUSIONS: The results suggest that calcitonin gene-related peptide acts as an arteriolar vasodilator at low doses but as a vasodilator of the arteriolar and venous systems at higher doses, and that profound hypotension induced by the calcitonin gene-related peptide may impair splanchnic circulation.

Analysis of Variance↗
PubMed1996

Effects of dobutamine on the relationship between oxygen consumption and delivery in healthy volunteers: comparison with sodium nitroprusside.

1. Dobutamine has been used to study the relationship between oxygen consumption (VO2) and oxygen delivery (DO2) in critically ill patients, but this has led to concerns that it could consistently increase VO2 in all patients. Although a direct thermogenic effect of the catecholamine has been primarily implicated in this increase in VO2, an increase in blood flow may contribute significantly by increasing the oxygen requirements of the heart and other organs such as the kidney and the liver. If this mechanism is predominant, it should also be observed when blood flow increases during the infusion of non-adrenergic agents. To separate the two mechanisms, we compared the effects of dobutamine with those of sodium nitroprusside on VO2/DO2 relationships in healthy volunteers. 2. Eight healthy volunteers received infusions of dobutamine at doses of 2, 4 and 6 micrograms min-1 kg-1 and nitroprusside at doses of 0.5, 1 and 2 micrograms min-1 kg-1 in an alternate order. 3. VO2 was determined by indirect calorimetry and cardiac output by electrical bioimpedance. Data were analysed by analysis of variance for repeated measurements and individual VO2/DO2 slopes were determined by linear regression. 4. VO2 increased more with dobutamine than with nitroprusside (from 138 +/- 14 to 149 +/- 20 ml min-1 m-2, P < 0.001, and from 131 +/- 14 to 138 +/- 17 ml min-1 m-2, P < 0.001, respectively). However, DO2 also increased more with dobutamine than with nitroprusside (from 531 +/- 186 to 702 +/- 274 ml min-1 m-2, P < 0.001, and from 523 +/- 107 to 610 +/- 122 ml min-1 m-2, P < 0.001, respectively). Individual VO2/DO2 slopes were similar with dobutamine and nitroprusside (6.5 +/- 3.5 compared with 7.1 +/- 4.6%, P not significant). 5. At the doses used, DO2 and VO2 increased more with dobutamine than with nitroprusside in healthy volunteers. However, the VO2/DO2 slopes were similar for both substances. Thus, an increase in VO2 is not exclusively observed with catecholamines. Studies of the effects of therapeutic interventions on oxygen-derived variables should report not only changes in VO2 but also VO2/DO2 slopes.

Adult↗
PubMed1995

Sodium nitroprusside induces internalization of muscarinic receptors stably expressed in Chinese hamster ovary cell lines.

We have characterized the internalization of muscarinic acetylcholine receptors induced by the nitric oxide (NO)-generating compound sodium nitroprusside. When Chinese hamster ovary cells, stably transfected with the human m4 muscarinic receptor subtype, were incubated for 1 h in the presence of 700 microM sodium nitroprusside, the number of receptors measured in intact cells with the hydrophilic ligand N-[3H]methylscopolamine was reduced by 30%. The effect was dose dependent, beginning with a concentration of sodium nitroprusside as low as 45 microM. Removal of sodium nitroprusside from the incubation medium did not result in a recovery of the binding sites. The phenomenon was temperature dependent and was blocked by the muscarinic antagonist atropine. No receptor diminution was detected when the number of binding sites was evaluated with the lipophilic antagonist [3H]quinuclidinyl benzilate. This indicates that sodium nitroprusside induces a redistribution of the muscarinic receptors between the plasma membrane and an internal compartment of the cell. Receptor loss was readily reversed by treatment with the sulfhydryl reducing agent diethyldithiocarbamate. Our data provide evidence that muscarinic receptors are internalized by sodium nitroprusside through the oxidation of sulfhydryl groups; they also suggest that NO could play a role in muscarinic receptor desensitization.

Animals↗
PubMed2003

Nitroprusside in critically ill patients with left ventricular dysfunction and aortic stenosis.

BACKGROUND: Vasodilators are considered to be contraindicated in patients with severe aortic stenosis because of concern that they may precipitate life-threatening hypotension. However, vasodilators such as nitroprusside may improve myocardial performance if peripheral vasoconstriction is contributing to afterload. METHODS: We determined the response to intravenous nitroprusside in 25 patients with severe aortic stenosis and left ventricular systolic dysfunction. Patients were included in the study if they had been admitted to the intensive care unit for invasive hemodynamic monitoring of heart failure and if they had a depressed ejection fraction (<or=0.35), severe aortic stenosis (aortic-valve area, <or=1 cm2), and a depressed cardiac index (<or=2.2 liters per minute per square meter). Patients were excluded if they had hypotension, defined as either the need for intravenous inotropic or pressor agents or a low mean systemic arterial pressure (<60 mm Hg). Patients were enrolled irrespective of other, coexisting valve disease or coronary artery disease. RESULTS: At base line, the mean (+/-SD) ejection fraction was 0.21+/-0.08; the aortic-valve area was 0.6+/-0.2 cm2, with peak and mean gradients of 65+/-37 and 39+/-23 mm Hg, respectively; and the cardiac index was 1.60+/-0.35 liters per minute per square meter. After six hours of therapy with nitroprusside (at which time the dose had been increased to a mean of 103+/-67 microg per minute), the cardiac index had increased to 2.22+/-0.44 liters per minute per square meter (P<0.001 for the comparison with base line). After 24 hours of nitroprusside infusion (dose, 128+/-96 microg per minute), the cardiac index had increased further, to 2.52+/-0.55 liters per minute per square meter (P<0.001 for the comparison with base line). Nitroprusside was well tolerated and had minimal side effects. CONCLUSIONS: Nitroprusside rapidly and markedly improves cardiac function in patients with decompensated heart failure due to severe left ventricular systolic dysfunction and severe aortic stenosis. It provides a safe and effective bridge to aortic-valve replacement or oral vasodilator therapy in these critically ill patients.

Aged↗
PubMed1982

Sodium nitroprusside-induced protein phosphorylation in intact rat aorta is mimicked by 8-bromo cyclic GMP.

The effects of sodium nitroprusside, 8-bromo cyclic GMP, 8-bromoguanosine 5'-monophosphate, 8-bromo cyclic AMP, dibutyryl cyclic AMP, and isoproterenol on incorporation of (32)P into proteins in intact rat thoracic aorta were studied. Aortas were incubated in [(32)P]orthophosphate in order to label endogenous adenosine triphosphate. Agents were then added for various times and the tissues were homogenized and fractionated (100,000 x g for 60 min) into soluble and particulate fractions. Soluble and particulate fractions were subjected to isoelectric focusing followed by sodium dodecyl sulfate/polyacrylamide gel electrophoresis and autoradiographs were made. Nitroprusside induced a concentration-dependent increase in incorporation of (32)P into nine proteins and a decrease in (32)P incorporation into two proteins. Some of these proteins appeared in both the soluble and particulate fractions of homogenates; others appeared only in the soluble fraction. The pattern of (32)P incorporation was identical after 2- or 15-min exposure to nitroprusside and was mimicked by exposure to 50-500 muM 8-bromo cyclic GMP. 8-Bromoguanosine 5'-monophosphate did not alter (32)P incorporation. Dibutyryl cyclic AMP at 50 muM had no effect upon (32)P incorporation whereas a higher concentration (0.5 mM) caused increased or decreased (32)P incorporation into some, but not all, of the same proteins. 8-Bromo cyclic AMP (5 mM) produced only small changes in (32)P incorporation. The pattern of (32)P incorporation induced by a relatively high concentration of isoproterenol 0.1 mM was similar but not identical to that seen with 0.5 mM dibutyryl cyclic AMP. The present study indicates that the incorporation of (32)P into endogenous proteins of intact rat aorta can be regulated by nitroprusside. These effects can be mimicked by cyclic GMP analogues and only partially by cyclic AMP analogues or isoproterenol. Presumably, these effects of nitroprusside are mediated through a cyclic GMP-dependent process (protein kinase or phosphatase) which may play a role in the relaxant properties of nitroprusside and cyclic GMP.

8-Bromo Cyclic Adenosine Monophosphate↗