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PubMed1992

Postoperative hypertension: a multicenter, prospective, randomized comparison between intravenous nicardipine and sodium nitroprusside.

OBJECTIVE: To compare the efficacy and safety of iv nicardipine with sodium nitroprusside in the treatment of postoperative hypertension after both cardiac and noncardiac surgery. DESIGN: Multicenter, prospective, randomized, open-label study. SETTING: Six tertiary referral medical centers (recovery rooms and surgical ICUs). PATIENTS: A total of 139 patients with postoperative hypertension: i.v. nicardipine (n = 71), sodium nitroprusside (n = 68). INTERVENTION: Administration of i.v. nicardipine or sodium nitroprusside. MEASUREMENTS: Vital signs (BP, heart rate), hemodynamic variables, medication dosage, total number of dose changes, and time to achieve BP control were recorded. MAIN RESULTS: Both medications were equally effective in reducing BP in both the cardiac and noncardiac surgical groups. Under the conditions of the study, i.v. nicardipine controlled hypertension more rapidly than sodium nitroprusside (i.v. nicardipine 14.0 +/- 1.0 mins and sodium nitroprusside 30.4 +/- 3.5 mins, p = .0029). The total number of dose changes required to achieve therapeutic BP response was significantly less in the i.v. nicardipine-treated patients (i.v. nicardipine 1.5 +/- 0.2 vs. sodium nitroprusside 5.1 +/- 1.4, p < .05). Adverse effects were observed with both drugs (i.v. nicardipine 7% [5/71] and sodium nitroprusside 18% [12/68] [NS]). CONCLUSIONS: Intravenous nicardipine is as effective as sodium nitroprusside in the therapy of postoperative hypertension. Specific advantages have been identified. The use of i.v. nicardipine should be considered in the therapy of postoperative hypertension.

Aged↗
PubMedDate not supplied

Influence of methylene blue and oxyhemoglobin on mammalian vascular responses to sodium nitroprusside and nitroglycerin.

Vasodilatory responses to sodium nitroprusside were compared with those to nitroglycerin in helical strips of blood vessels isolated from dogs, humans, monkeys, rats and guinea-pigs. Sodium nitroprusside relaxed arterial and venous strips contracted with prostaglandin F2 alpha in a dose-related manner, as did nitroglycerin. Relaxant responses to sodium nitroprusside and nitroglycerin were significantly greater in dog coronary arteries than in the mesenteric arteries. Tachyphylaxis developed upon repeated applications of nitroglycerin but not of sodium nitroprusside. In rat and guinea-pig aortae, relaxant responses to sodium nitroprusside and nitroglycerin were markedly suppressed by treatment with methylene blue or oxyhemoglobin. In dog arteries and veins, treatment with oxyhemoglobin significantly inhibited relaxant responses to sodium nitroprusside and nitroglycerin. On the other hand, treatment with methylene blue did not inhibit responses to sodium nitroprusside but markedly suppressed those to nitroglycerin in dog blood vessels as well as in human gastroepiploic and monkey mesenteric arteries. It is concluded that dog and primate blood vessels do not develop tolerance to repeated applications of sodium nitroprusside and that sensitivity of soluble guanylate cyclase to methylene blue may differ in blood vessels from different mammals (dog and primate vs rat and guinea-pig).

Animals↗
PubMed1980

Reflex responses to sodium nitroprusside and their control by cryptenamine.

In chloralose-anesthetized dogs the hypotensive and reflex cardiovascular responses to infusions of sodium nitroprusside were studied before and during halothane and enflurane, and before after divided doses of cryptenamine. The latter drug, a mixture of hypotensive veratrum alkaloids, lowers blood pressure reflexly by acting on afferent receptors (baroreceptors). Control infusions of nitroprusside, which caused 10% to 15% decreases im mean arterial blood pressure, markedly increased heart rate, myocardial contractility, cardiac output, rate-pressure product, and left ventricular minute work in spite of decreases in peripheral vascular resistance. Except for increases in contractility, these reflexly mediated effects were not blocked by the addition of 1% halothane or 2% enflurane. Cryptenamine, on the other hand, potentiated nitroprusside-induced hypotension, markedly diminished increases in heart rate, and eliminated increases in myocardial contractility, rate-pressure product, and left ventricular work. Measurements of cardiovascular function returned promptly to preinfusion values when the nitroprusside was stopped. We conclude that under conditions when a high degree of central vasomotor tone is present, homeostatic reflexes may counteract the direct vasodilator effect of nitroprusside, resulting in the need for a greater dose of nitroprusside and obviating the expected beneficial effects on myocardial oxygen supply/demand ratio. Combining cryptenamine with nitroprusside eliminates these problems and at the same time allows retention of the evanescent action of nitroprusside.

Anesthesia↗
PubMed1995

Sodium nitroprusside: physiologic effects as a nitric oxide donor in three species.

Recent in vitro and in vivo studies have suggested that nitric oxide may be the neurotransmitter responsible for cavernous smooth muscle relaxation and penile erection. Sodium nitroprusside, after combining with different kinds of thiols in the cellular cytoplasm, can effect nitric oxide release. We undertook this study to determine the physiologic response to sodium nitroprusside injection when used to induce and maintain penile erection in three species. Sodium nitroprusside was injected in increasing concentrations into the cavernous tissue of rats, dogs and monkeys. Dosages injected were 10(-4) M, 10(-3) M and 10(-2) M in 10 rats; 10(-4) and 10(-3) M in five dogs and five monkeys. The volume of drug injected was 0.05 ml for the rats and 0.5 ml for dogs and monkeys. The results show a dose-dependent erectile response to sodium nitroprusside injection (mean intracavernous pressure increase of 102.4 cm H2O in dogs, and 98.4 cm H2O in monkeys after injection of 10(-3) M nitroprusside). However, only a slight increase in intracavernous pressure (mean increase 28.4 cm H2O after injection of 10(-2) M of sodium nitroprusside) was noted in rats. The drop in blood pressure was > 15 mmHg in dogs and monkeys, while in rats it varied according to the dose studied. Sodium nitroprusside induced excellent erections in dogs and monkeys with minimal alteration in blood pressure. However, administration in rats resulted in hypotension. Nitroprusside may not be an acceptable nitric oxide donor for the treatment of male erectile dysfunction.

Animals↗
PubMed1996

Thrombin-stimulated phospholipase C activity is inhibited without visible delay by a rapid increase in the cyclic GMP levels induced by sodium nitroprusside.

Different drugs that elevate the cGMP levels inhibit the agonist-induced platelet activation. The mechanisms of action of cGMP probably include inhibition of both phospholipase C and the increase in intracellular Ca2+ concentration, and these effects seem to be mediated by cGMP-dependent protein kinases. However, in most studies, cells were preincubated with nitrovasodilators before stimulation. The effect of the preincubation with sodium nitroprusside before stimulation or the simultaneous addition of sodium nitroprusside and thrombin has been compared. The simultaneous addition of sodium nitroprusside and thrombin was able to inhibit without any significant delay the platelet aggregation. This rapid effect was correlated with an inhibition of both the maximum increase in intracellular Ca2+ concentration and the phospholipase C activity. Also, the simultaneous addition of sodium nitroprusside and thrombin clearly accelerated the decline in the Ca2+ signal, which was not observed in platelets preincubated with sodium nitroprusside. The rapid inhibition induced by sodium nitroprusside was correlated with a rapid and significant increase in the cGMP levels and reversed when platelets were pretreated with methylene blue. The inhibitor of cAMP-dependent protein kinase Rp-8-(4-chlorophenylthio)-adenosine-3',5'-cyclic monophosphorothioate was able to abolish nearly completely the inhibitory effect induced by sodium nitroprusside independent of the protocol used. Thus, the rapid inhibition induced by sodium nitroprusside seems to be induced by a rapid phosphorylation-dependent mechanism. In addition, both cGMP- and cAMP-dependent protein kinase seem to be involved; however, the cAMP-dependent protein kinase seems to be more important.

Calcium↗
PubMed1977

Reduction of pulmonary hypertension by nitroprusside.

The action of nitroprusside on pulmonary circulation was studied in patients with pulmonary hypertension due to mitral stenosis (group I) or to primary lung disease (group II) and in patients with normal pulmonary artery pressure (group III). Nitroprusside 20 microgram/min decreased systolic and mean pulmonary artery pressure in groups I and II while higher doses were necessary to produce a similar pressure reduction in group III. Diastolic pulmonary artery pressure was reduced by 40 microgram/min nitroprusside in all groups. Systemic arterial pressure declined during nitroprusside infusion similary in all groups in a dose-related manner; cardiac index remained unaltered. Pulmonary vascular resistance was reduced by 20 microgram/min nitroprusside in group I, not below 200 microgram/min nitroprusside in group II and remained unchanged in group III. Peripheral vascular resistance declined in all groups with nitroprusside infusion. The study suggests direct relaxation of the pulmonary vasculature by nitroprusside.

Adolescent↗
PubMed1997

Safety and efficacy of urapidil and sodium nitroprusside in the treatment of hypertensive emergencies.

OBJECTIVE: To assess the safety and efficacy of urapidil compared to sodium nitroprusside in the treatment of hypertensive emergencies. DESIGN: Randomized, prospective clinical study. SETTING: Emergency department in a 2000-bed inner city hospital. PATIENTS: Eighty-one patients with hypertensive emergencies defined as elevation of systolic blood pressure above 200 mmHg and/or diastolic blood pressure above 110 mmHg plus evidence of end-organ damage were included in the study protocol. The efficacy of therapy was defined as 1) blood pressure reduction below 180/95 mmHg within 90 min and 2) no re-elevation of blood pressure during a 4-h follow-up period in primary responders. The safety of both drugs was defined as the number of minor and major side effects during treatment. INTERVENTIONS: Patients received either sodium nitroprusside (n = 35; continuous intravenous administration with a starting dose of 0.5 microgram/kg per min; increase in increments of 0.5 microgram/kg per min every 15 min until response to treatment or a maximum of 3 micrograms/kg per min) or urapidil (n = 46; intravenous bolus; starting dose: 12.5 mg; repetitive administration of 12.5 mg every 15 min until response or a maximum dose of 75 mg). MEASUREMENTS AND RESULTS: Blood pressure was measured every 2.5 min by using a non-invasive oscillometric blood pressure measurement unit. Response to treatment within 90 min was observed in 75 (93%) patients (urapidil: n = 41 [89%]; nitroprusside: n = 34 [97%]; p = 0.18). During the follow-up period 8/34 (24%) patients in the nitroprusside group and 1/41 (2%) patients in the urapidil group exhibited blood pressure re-elevation. Major side effects were observed in seven patients receiving nitroprusside and two patients in the urapidil group (p = 0.04). CONCLUSION: Urapidil is equally effective, compared to sodium nitroprusside, in the treatment of hypertensive emergencies. Due to a smaller number of adverse events, urapidil is a reasonable alternative to nitroprusside in the treatment of hypertensive emergencies.

Adult↗
PubMed1984

Comparison of hemodynamic responses to nifedipine and nitroprusside in severe chronic congestive heart failure.

The hemodynamic effects of 20 to 40 mg of oral nifedipine were compared with those of intravenous nitroprusside in 11 patients with severe chronic congestive heart failure (CHF). In each patient, both drugs were administered to produce similar reduction of systemic vascular resistance (SVR) (29 +/- 13% with nifedipine and 29 +/- 12% with nitroprusside, difference not significant [NS]). At this comparable decrease in systemic vascular resistance, significant differences in hemodynamic responses to both drugs were noted: Nifedipine caused a smaller increase in cardiac index (20 +/- 20% vs 40 +/- 24%, p less than 0.02) and a larger decrease in mean blood pressure than nitroprusside (16 +/- 9% vs 8 +/- 10%, p less than 0.05). In addition, nifedipine produced a smaller decrease in mean pulmonary artery wedge pressure (13 +/- 24% vs 36 +/- 21%, p less than 0.001) and pulmonary vascular resistance than nitroprusside (6 +/- 42% vs 26 +/- 46%, NS). Mean right atrial pressure decreased with nitroprusside, from 10 +/- 7 to 5 +/- 3 mm Hg (p less than 0.05), but not with nifedipine (10 +/- 7 mm Hg before and after nifedipine administration, NS). Left ventricular stroke work index increased with nitroprusside (20 +/- 8 to 27 +/- 9 g-m/m2, p less than 0.05), but did not change with nifedipine (21 +/- 9 vs 21 +/- 10 g-m/m2, NS). These data show that nifedipine has an arteriolar dilatatory action in patients with CHF. However, compared with nitroprusside, nifedipine had a significantly larger hypotensive effect and had a lesser effect on right and left ventricular filling pressure, cardiac output and left ventricular function.

Administration, Oral↗
PubMed1985

Effects of atrial natriuretic factor, sodium nitroprusside, and acetylcholine on cyclic GMP levels and relaxation in rat aorta.

The purpose of this study was to investigate the mechanisms whereby an endothelium-dependent vasodilator, acetylcholine, a nitrovasodilator, sodium nitroprusside and atrial natriuretic factor (atriopeptin II), elevate cyclic GMP levels and induce relaxation in rat thoracic aorta. Methylene blue inhibited the elevated cyclic GMP levels and relaxation due to sodium nitroprusside and acetylcholine, but not those to atriopeptin II. Cyanide inhibited relaxations to all three vasodilators, but inhibited the elevated cyclic GMP levels in response to only nitroprusside and acetylcholine. The reducing agents sodium borohydride, dithiothreitol, sucrose and isoproterenol all inhibited the elevated cyclic GMP levels due to nitroprusside and acetylcholine, while the increased cyclic GMP levels with atriopeptin II were unaffected by sodium borohydride, sucrose and isoproterenol. The effects of the reducing agents on relaxation induced by the vasodilators were difficult to interpret due to their nonspecific contractile and relaxant properties. Agents and procedures known to inhibit the Na+, K+-pump and relaxation to endothelium-dependent vasodilators and nitroprusside, including ouabain, K+-free, Mg2+-free and low Na+ Krebs-Ringer bicarbonate solution, all partially inhibited relaxations to atriopeptin II. Relaxations to atriopeptin II were also inhibited in tissues contracted with KCl. The present results suggest that the mechanism of atrial natriuretic factor-induced increased cyclic GMP levels, in contrast to that of nitroprusside and acetylcholine, does not involve the formation of free radicals, a reducible species or interaction with heme. Furthermore, the cyclic GMP formed in response to nitroprusside, acetylcholine and atrial natriuretic factor mediates relaxation through a common mechanism that may be functionally antagonized by agents and procedures which result in membrane depolarization.

Acetylcholine↗
PubMed1990

Sodium nitroprusside potentiates the depressor response to the phosphodiesterase inhibitor zaprinast in rats.

To determine if the presence of an activator of guanylate cyclase alters the depressor response to a selective inhibitor of low Km cyclic GMP (cGMP) phosphodiesterase (PDE), zaprinast (3-30 mg/kg) was given i.v. to conscious, spontaneously hypertensive rats during a steady state of i.v. infusion of sodium nitroprusside (15 micrograms/kg per min). Sodium nitroprusside significantly increased the magnitude of the depressor response to zaprinast. In contrast, fenoldopam (20 micrograms/kg per min), an activator of adenylate cyclase, did not affect the depressor response to zaprinast. Zaprinast (10 mg/kg) significantly decreased mean arterial pressure (MAP) in rats given an infusion of sodium nitroprusside, an activator of soluble guanylate cyclase, at doses of 15 and 25 micrograms/kg per min but not at a dose of 5 micrograms/kg per min. However, in rats given atrial natriuretic peptide (ANP; 0.5, 1 and 2 micrograms/kg per min), an activator of particulate guanylate cyclase, zaprinast (10 mg/kg) did not affect MAP. In contrast to the potentiation of the depressor response to zaprinast, sodium nitroprusside (15 micrograms/kg per min) significantly attenuated the reductions in MAP produced by CI-930, a selective inhibitor of low Km cAMP PDE. It is concluded that sodium nitroprusside, but not ANP or fenoldopam, potentiates the depressor response to zaprinast. Furthermore, the potentiation of the depressor response to zaprinast is dependent upon the dose of sodium nitroprusside and is selective for zaprinast; the depressor response to CI-930 is attenuated by sodium nitroprusside.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

Programmed ventricular stimulation in patients with left ventricular dysfunction and ventricular tachycardia: effects of acute hemodynamic improvement due to nitroprusside.

To assess the electrophysiologic effects of acute hemodynamic improvement in patients with left ventricular systolic dysfunction, 12 patients with a left ventricular ejection fraction less than 0.40 and a history of sustained monomorphic ventricular tachycardia were studied. All patients had underlying coronary artery disease. Patients underwent programmed cardiac stimulation in random order during a baseline period and with nitroprusside infusion. Mean pulmonary capillary wedge pressure decreased from 20 +/- 8 mm Hg at baseline study to 8 +/- 3 mm Hg during nitroprusside infusion (p less than 0.0001). Pulmonary artery, right atrial and systemic arterial pressures also decreased with nitroprusside (p less than 0.01). Cardiac output did not change. Left ventricular dimensions, determined by two-dimensional echocardiography, decreased significantly during nitroprusside infusion. The right ventricular effective refractory period, measured during ventricular drive trains at cycle lengths of 400 and 600 ms, were similar during baseline and nitroprusside periods (271 +/- 30 versus 274 +/- 31 ms at 600 ms, and 249 +/- 25 versus 246 +/- 18 ms at 400 ms). In 2 patients no ventricular arrhythmias were induced during either study period; in the other 10, ventricular tachyarrhythmias were induced during both periods. The mean number of extrastimuli required to induce a ventricular tachyarrhythmia was similar during the baseline period (1.8 +/- 0.6) and during nitroprusside infusion (1.9 +/- 0.7). As well, the mean cycle length of ventricular tachycardia induced was similar during the baseline period (347 +/- 61 ms) and during nitroprusside infusion (342 +/- 70 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Nicardipine versus nitroprusside for deliberate hypotension during idiopathic scoliosis repair.

STUDY OBJECTIVE: To compare coagulation, blood loss, and transfusion requirements between patients receiving nicardipine and nitroprusside for deliberate hypotension during idiopathic scoliosis repair. DESIGN: Prospective, randomized study. SETTING: University hospital. PATIENTS: 51 ASA physical status I patients presenting for spine fusion for idiopathic adolescent scoliosis. INTERVENTIONS: Patients were randomized to two groups to receive nicardipine or nitroprusside to maintain mean arterial pressure (MAP) between 55 and 65 mmHg. MEASUREMENTS: Blood loss, blood transfusions, and coagulation studies (thromboelastogram and platelet aggregation) before starting vasodilator, 30 minutes and 90 minutes after starting vasodilator, and 30 minutes after stopping vasodilator, were all recorded. MAIN RESULTS: There was no difference between the groups in blood loss [nicardipine = 1,129 cc (893 to 1,480), nitroprusside = 960 cc (704 to 1,473)] and only one patient required a nonautologous transfusion. There were no differences in prothrombin time (pT, partial thromboplastin time (pTT), platelet count, or platelet aggregation between groups. There were more episodes of severe hypotension (MAP <45 mmHg) in the nitroprusside group (0% vs. 28%, p = 0.0175). On average, patients in the nicardipine group spent 21 minutes less in the recovery room than did the nitroprusside group (p = 0.043). CONCLUSIONS: Nitroprusside's effect on platelet aggregation produces no increase in blood loss compared with nicardipine. Nicardipine causes less transient severe hypotension than nitroprusside, although both drugs are acceptable choices for obtaining the goals of deliberate hypotension.

Adolescent↗
PubMed2003

Differential effects of sodium nitroprusside and hydralazine in a rat model of topical FeCl3-induced carotid artery thrombosis.

INTRODUCTION: In the rat model of topical ferric chloride-induced carotid artery thrombosis, a transient blood flow velocity (VEL) increase is observed immediately following ferric chloride application. The immediacy of the response suggested vasoconstriction, as thrombotic narrowing of the vessel lumen was hypothesized to be too slow to account for the rapidity of the response. METHODS: To explore this phenomenon, the effects of two mechanistically distinct vasodilators, sodium nitroprusside (SNP) and hydralazine (HYD), on velocity increase, ex vivo platelet aggregation and thrombosis, were assessed in the rat ferric chloride-induced thrombosis model. RESULTS: Sodium nitroprusside (10, 30 and 50 microg/kg/min i.v.) and hydralazine (0.1, 0.3 and 1.0 mg/kg/min i.v.) reduced the mean arterial pressure with the higher dose regimens eliciting equivalent hypotensive effects. Both sodium nitroprusside and hydralazine blunted the initial velocity increase, but only sodium nitroprusside significantly reduced the incidence of thrombotic occlusion. No differences in ex vivo platelet aggregation responses to adenosine diphosphate (ADP), collagen (COLL) and arachidonic acid (AA) were observed between the sodium nitroprusside and hydralazine treatment groups. However, platelet aggregation response to thrombin was significantly reduced in the 50 microg/kg/min i.v. sodium nitroprusside compared to the 1.0 mg/kg/min i.v. hydralazine and vehicle groups. CONCLUSIONS: Inhibition of the initial velocity increase by two mechanistically distinct vasodilators, and the dissociation between this velocity change and antithrombotic efficacy, support the hypothesis that the early velocity increase results from a change in vascular tone rather than due to enhanced platelet activation and thrombus formation. Inhibition of thrombin-induced platelet activation may contribute to the antithrombotic actions of sodium nitroprusside in this preparation.

Animals↗
PubMed2002

Sodium nitroprusside stimulates L-DOPA release from striatal tissue through nitric oxide and cGMP.

The effects of the nitric oxide (NO) donor, sodium nitroprusside, on L-DOPA and dopamine release from striatal tissue were evaluated using a static incubation system in which the striatal tissue released between three and six times more L-DOPA than DA, although the DA content was four times higher than that of L-DOPA. Sodium nitroprusside stimulated L-DOPA release in a time- and concentration-dependent (25, 50 and 100 microM) manner. This effect was not due to an increase in L-DOPA synthesis because sodium nitroprusside did not modify the tyrosine hydroxylase activity of striatal tissue. DA release was also stimulated by sodium nitroprusside but it required a higher concentration (500 microM) and longer incubation (60 min). Neither basal nor sodium nitroprusside-stimulated L-DOPA release was influenced by Ca(2+) deprivation (EGTA 5 mM) and/or the presence of nitrendipine (1 microM), a blocker Ca(2+) channel, in the incubation medium. However, cGMP (1 mM) increased L-DOPA release, and the soluble guanylate cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one (ODQ) (5 microM), partially blunted the stimulatory effect of sodium nitroprusside 100 microM. In addition, the presence of certain scavengers of free radicals, such as uric acid (300 microM) or melatonin (300 microM) but not of superoxide dismutase (1000 UI/ml) or salicylic acid (300 microM), completely blocked sodium nitroprusside (100 microM)-induced L-DOPA release. These results show that NO stimulates L-DOPA release from striatal tissue by an apparently Ca(2+)-independent mechanism, mediated by cGMP but also by peroxynitrite.

Animals↗
PubMed2001

Treatment of no-reflow and impaired flow with the nitric oxide donor nitroprusside following percutaneous coronary interventions: initial human clinical experience.

OBJECTIVES: The objective of this study was to test the hypothesis that the intracoronary administration of a direct donor of nitric oxide is a safe and effective method to treat impaired blood flow (no-reflow phenomenon) that occurs during percutaneous transluminal coronary interventions (PTCI). BACKGROUND: The absence of blood flow or decreased blood flow in a coronary artery following PTCI despite the presence of a patent epicardial vessel or graft is designated "no-reflow" or "impaired flow." This alteration in blood flow is a serious complication of percutaneous revascularization strategies that results in an increased incidence of morbidity, myocardial infarction and mortality. METHODS: Nineteen consecutive patients undergoing standard percutaneous revascularization procedures complicated by either no-reflow or impaired flow that received intracoronary nitroprusside treatment were studied. One patient had two procedures performed on two separate grafts on two successive days. Interventions were performed on either saphenous vein grafts or native vessels and utilized angioplasty, stent deployment or rotational atherectomy strategies. Following interventions that were associated with impaired flow, varying total doses (of nitroprusside 50 to 1,000 microg) were administered into the coronary artery or saphenous vein graft. The angiographic archives before and after intracoronary administration of nitroprusside were analyzed for TIMI grade flow and a frame count method was used to quantitate blood flow velocity. RESULTS: Following a PTCI that resulted in either no-reflow or impaired flow, nitroprusside (median dose 200 microg) was found to lead to a highly significant and rapid improvement in both angiographic flow (p < 0.01 compared with pretreatment angiogram) and blood flow velocity (p < 0.01 compared with pretreatment angiogram). No significant hypotension or other adverse clinical events were associated with nitroprusside administration. CONCLUSIONS: The direct nitric oxide donor nitroprusside is an effective, safe treatment of impaired blood flow and no-reflow associated with PTCI. The use of nitroprusside to treat syndromes secondary to microvascular dysfunction may provide a novel therapeutic strategy for treating no-reflow or impaired blood flow following percutaneous interventions.

Aged↗
PubMed2002

Relaxation and cGMP formation in response to sildenafil and sodium nitroprusside in saphenous veins from normotensive and hypertensive patients.

BACKGROUND: This study was designed to measure cyclic guanosine 3'5' monophosphate (cGMP) formation and relaxation response to sildenafil given either alone or in combination with sodium nitroprusside in saphenous veins obtained from normotensive and hypertensive patients. METHODS: Saphenous vein rings were obtained from 13 hypertensive and nine normotensive patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. The effect of sildenafil on sodium nitroprusside-induced cGMP formation was also assessed. RESULTS: Sildenafil (10 nmol/L to 100 micromol/L) and sodium nitroprusside (0.01 to 100 nmol/L) caused concentration-dependent relaxations that were of greater magnitude in veins from normotensive patients. Sildenafil (1 to 10 micromol/L) amplified the relaxation induced by sodium nitroprusside in both groups of veins, but this effect was more pronounced in veins from hypertensive patients. Levels of cGMP in response to sodium nitroprusside were significantly lower in veins from hypertensive subjects. However, in the presence of sildenafil, the increase in cGMP levels in response to sodium nitroprusside was significantly greater in the hypertensive as compared with the normotensive group. CONCLUSIONS: Although the relaxant effects of sildenafil are less pronounced in veins from hypertensive patients, the synergistic interaction sildenafil-sodium nitroprusside is more effective in veins from hypertensive patients, mainly due to an increase in cGMP accumulation.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2003

Comparison of clevidipine with sodium nitroprusside in the control of blood pressure after coronary artery surgery.

BACKGROUND AND OBJECTIVE: We set out to compare the efficacy of clevidipine and sodium nitroprusside infusions in the control of blood pressure and the haemodynamic changes they produce in hypertensive patients after operation for elective coronary bypass grafting. METHODS: Thirty patients were randomly allocated to receive either clevidipine or sodium nitroprusside after their mean arterial pressure (MAP) had reached > 90 mmHg for at least 10 min in the postoperative period. The MAP was continuously measured and related to time. Thus, the efficacy of the drugs in controlling arterial pressure could be inversely related to the total area under the MAP-time curve outside a target MAP range of 70-80 mmHg normalized per hour (AUC(MAP) mmHg min h(-1)). Haemodynamic variables and the number of dose-rate adjustments required to maintain MAP were also studied. RESULTS: There was no statistically significant difference in the efficacy (AUC(MAP) mmHg min h(-1)) of clevidipine (106 +/- 25 mmHg min h(-1)) compared with sodium nitroprusside (101 +/- 28 mmHg min h(-1)). Nor was any significant difference found in the total number of dose adjustments required to control MAP within the target range. The heart rate in patients receiving clevidipine increased less than in those given sodium nitroprusside. Stroke volume, central venous pressure and pulmonary artery pressure were significantly reduced upon administration of sodium nitroprusside but not of clevidipine. CONCLUSIONS: There was no significant difference between clevidipine and sodium nitroprusside in their efficacy in controlling MAP. The haemodynamic changes, including tachycardia, were less pronounced with clevidipine than with sodium nitroprusside.

Adult↗
PubMed1996

Intrinsic radiosensitivity of human pancreatic tumour cells and the radiosensitising potency of the nitric oxide donor sodium nitroprusside.

A panel of eight human pancreatic tumour cell lines displayed high intrinsic radioresistance, with mean inactivation doses between 2.4 and 6.5 Gy, similar to those reported for melanoma and glioblastoma. The radiosensitising potency of sodium nitroprusside, a bioreductive nitric oxide donor, was assessed in a model of metabolism-induced hypoxia in a cell micropellet. Sodium nitroprusside at 0.1 mM revealed a radiosensitising effect with an overall enhancement ratio of 1.9 compared with 2.5 for oxygen. Radiosensitising activity correlated with the enhancement of single-strand DNA breakage caused by radiation. In suspensions with cell densities of between 3% and 30% (v/v), the half-life of sodium nitroprusside decreased from 31 to 3.2 min, suggesting a value of around 1 min for micropellets. Despite this variation, the radiosensitising activity was similar in micropellets and in diluted cell suspensions. S-nitroso-L-glutathione was found to possess radiosensitising activity, consistent with a possible role of natural thiols in the storing of radiobiologically active nitric oxide adducts derived from sodium nitroprusside. As measured by a nitric oxide-specific microsensor, activation of sodium nitroprusside occurred by bioreduction, whereas S-nitroso-L-glutathione showed substantial spontaneous decomposition. Both agents appear to exert radiosensitising action through nitric oxide as its scavenging by carboxy phenyltetramethylimidazolineoxyl N-oxide (carboxy-PTI0) and oxyhaemoglobin resulted in attenuated radiosensitisation. Sodium nitroprusside was at least 10-fold more potent than etanidazole, a 2-nitroimidazole used as a reference. Our data suggest that sodium nitroprusside, a drug currently used for the treatment of hypertension, is a potential tumour radioresponse modifier.

Aerobiosis↗