Search PubMed⌕ Search

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.

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

At least 289 records · Page 16Linked to original sources
PubMed1989

Stability of esmolol hydrochloride and sodium nitroprusside in intravenous admixtures.

The stability of esmolol hydrochloride and sodium nitroprusside in an admixture containing both drugs was studied. Solutions containing sodium nitroprusside in a final concentration of approximately 200 micrograms/mL and esmolol hydrochloride in a final concentration of 10 mg/mL in 5% dextrose injection were prepared in a 250-mL volumetric flask. The flask was wrapped with a light-protective cover, stored at ambient room temperature (15-30 degrees C), and protected from light. All experiments were conducted in triplicate with samples taken at 0, 2, 4, 8, and 24 hours. Testing included measurement of pH and absorbance at 400 and 600 nm. High-performance liquid chromatography was used to measure esmolol hydrochloride and sodium nitroprusside concentrations. No changes were observed in the physical appearance, pH, or absorbance of the admixtures. Neither the esmolol hydrochloride nor the sodium nitroprusside concentrations varied by more than 4% during the study. Under the conditions studied, esmolol hydrochloride is compatible with sodium nitroprusside in an admixture containing both drugs.

Adrenergic beta-Antagonists↗
PubMed1987

Further investigations regarding the toxicity of sodium nitroprusside.

Sodium nitroprusside is a valuable vasodilator, but its use has been curtailed because of numerous reports that, in the presence of blood, nitroprusside decomposes with release of toxic cyanide. We have examined the release of cyanide in terms of the known chemistry of nitroprusside and suggest that photochemical decomposition of nitroprusside and (or) its metabolism in vivo invalidates the analytical procedure used by previous workers. We also present evidence for the stability of nitroprusside in blood, based on 13C nuclear magnetic resonance studies.

Ferricyanides↗
PubMed1979

Efficacy of nitroprusside therapy in postcardiotomy low-output syndrome necessitating intra-aortic balloon counterpulsation.

Serial hemodynamic measurements were obtained before, during, and after nitroprusside therapy over a 24 hour period in 19 patients requiring intra-aortic balloon pumping (IABP) for successful weaning from cardiopulmonary bypass. Nitroprusside, administered in doses ranging from 0.5 to 5 micrograms/kg/min, effected significant reductions in mean aortic pressure and systemic vascular resistance within 20 to 30 minutes. Mean aortic pressure decreased from 108 +/- 22 mm Hg to 85 +/- 27 mm Hg (p less than 0.005). Systemic vascular resistance decreased from 2,705 +/- 1,072 to 1,942 +/- 823 dynes sec cm-5 (p less than 0.005). 2n response to nitroprusside-induced decreases in left venticular afterload, cardiac indes increased from 1.83 +/- 0.58 to 2.04 +/- 0.54 L/min/m2 (p less than 0.025). Pulmonary capillary wedge pressure (PCW), right atrial pressure, right and left ventricular minute work indices, and the rate-pressure products did not change, indicating that nitroprusside administration during IABP further increased cardiac output without increasing ventricular filling pressure, ventricular work, or indices of myocardial oxygen consumption. The data suggest that nitroprusside, in conjunction with volume loading to optimal preload levels (PCW = 15 to 18 mm Hg), augments ventricular performance in postcardiotomy low-output syndrome by lowering impedance to left ventricular ejection through a direct dilator effect on vascular smooth muscle, without a direct effect on cardiac muscle. Thus it is a valuable pharmacologic adjunct during mechanical (IABP) support of the failing circulation.

Blood Pressure↗
PubMed1983

Lack of correlation between cyclic GMP elevation and relaxation of nonvascular smooth muscle by nitroglycerin, nitroprusside, hydroxylamine and sodium azide.

Recent reports have suggested that the smooth muscle relaxant effects of drugs such as nitroprusside and nitroglycerin are mediated by increases in tissue levels of cyclic GMP. This hypothesis was examined by comparing the effects of nitroprusside, nitroglycerin, hydroxylamine and sodium azide on tension and cyclic GMP levels in rat vas deferens, rat myometrium and guinea-pig taenia coli. All four of the agents were capable of increasing cyclic GMP levels in these tissues but there did not appear to be a good correlation between cyclic GMP elevation and muscle relaxation in any of the tissues studied. For example, nitroprusside markedly elevated cyclic GMP levels in rat vas deferens and myometrium but had no relaxant effect on either tissue. Nitroglycerin was less effective than nitroprusside in elevating cyclic GMP levels, but was an effective relaxant in both tissues. Significant increases in myometrial cyclic GMP were seen with 0.1, 1 and 5 mM concentrations of hydroxylamine but only the highest concentration had a definite relaxant effect on the muscles. A similar concentration of nitroprusside produced a greater elevation of cyclic GMP than did hydroxylamine, but had no relaxant effect in this preparation. In guinea-pig taenia coli, significant increases in cyclic GMP levels were obtained with concentrations of sodium azide and hydroxylamine which had no effect on the contractile activity of the preparations. These results, together with previous results from this laboratory, suggest that the relaxant effects of this group of drugs in rat vas deferens, rat myometrium and guinea-pig taenia coli are not mediated by increases in tissue levels of cyclic GMP. Further experiments are necessary to determine whether a causal relationship exists between cyclic GMP elevation and relaxation in other types of smooth muscle.

Animals↗
PubMed1982

Use of sodium nitroprusside in complications of gestational hypertension.

Sodium nitroprusside is a potent and ultrafast-acting antihypertensive agent. Limited clinical experience and uncertainty about toxicity have restricted its use in obstetrics. The authors have used nitroprusside concomitantly with hemodynamic monitoring in 4 obstetric patients with severe pregnancy-induced hypertension unresponsive to conventional therapy. The patients with acute congestive heart failure and pulmonary edema responded rapidly and dramatically to nitroprusside. No signs of fetal distress associated with lowering of the arterial pressure were observed, and significant cyanide levels were not detected in a fetal cord blood sample. Nitroprusside should be reserved for refractory hypertensive emergencies in pregnancy. Hemodynamic monitoring is required for adjusting nitroprusside administration and fluid balance. In short-term usage, the authors' experience suggests that maternal and fetal toxicity may not be serious concerns.

Acute Disease↗
PubMed1980

Nitroprusside and mitral stenosis.

The cardiovascular effects of an intravenous nitroprusside infusion were evaluated intraoperatively in seven patients with pure mitral stenosis and seven patients with predominant mitral stenosis. Prior to therapy the adverse hemodynamic consequences of light anesthesia and surgical stimulation were evident in all patients: systemic and/or pulmonary hypertension were present, systemic vascular resistance was twice normal, and cardiac function was depressed. Nitroprusside consistently reduced systemic vascular resistance and systemic arterial as well as pulmonary arterial and wedge pressures, but cardiac index increased only when severe pulmonary hypertension and/or some mitral regurgitation coexisted with mitral stenosis. In the group with predominant mitral stenosis, cardiac index increased from 1.8 to 2.1 L/min/m2 with nitroprusside (p < 0.05). In three individuals who demonstrated severe pulmonary hypertension (one with pure mitral stenosis and two with predominant mitral stenosis), nitroprusside induced an increase of almost 50% in cardiac index and stroke volume. In contrast, patients with pure mitral stenosis and mild pulmonary hypertension showed little change in cardiac index or stroke volume. It is concluded that nitroprusside can safely be used to control systemic or pulmonary hypertension during anesthesia and surgery in patients with mitral stenosis and that if severe pulmonary hypertension and/or mitral regurgitation coexist with mitral stenosis, cardiac function will also improve.

Ferricyanides↗
PubMed1994

Isolation and characterization of HL-60 cells resistant to nitroprusside-induced differentiation.

Sodium nitroprusside and sodium nitrite, which generate nitric oxide and increase the intracellular cGMP concentration, and 8-bromo-cGMP, a membrane-permeable cGMP analog, induce myelomonocytic differentiation of HL-60 cells (Boss, G. R. (1989) Proc. Natl. Acad. Sci. U. S. A. 86, 7174-7178). We have selected HL-60 cells resistant to nitroprusside-induced differentiation as assessed by acquisition of the OKM-1 antigen, reduction of nitro blue tetrazolium, and morphologic maturation. The variant cells were also resistant to differentiation induced by sodium nitrite and two cGMP analogs but still differentiated in response to other inducing agents such as dimethyl sulfoxide and cAMP analogs and showed the same changes in c-myc and c-fos expression in response to the latter drugs as occurred in parental cells. We studied the early steps of the NO/cGMP signal transduction pathway in the variant cells and found that basal and nitroprusside-stimulated guanylate cyclase activity was similar in parental and variant cell extracts and that nitroprusside increased the intracellular cGMP concentration to the same extent in parental and variant cells. As part of these studies we found that HL-60 cells expressed only alpha 2 and beta 2 guanylate cyclase mRNA; the abundance of these two mRNA species was similar in parental and variant cells. Neither nitroprusside nor 8-bromo-cGMP changed the intracellular calcium concentration in parental or variant cells. The data suggest that the defect in the variant cells is after guanylate cyclase activation in the NO/cGMP transduction pathway and that the cGMP and cAMP transduction pathways operate independently in inducing differentiation of HL-60 cells.

Cell Differentiation↗
PubMed1996

Electromyographic changes of corpus cavernosum due to papaverine and nitroprusside in veno-occlusive dysfunction.

PURPOSE: We compared electrical activity of the corpus cavernosum after intracavernous papaverine and nitroprusside injections. Some aspects of the androgen modulator system in patients with veno-occlusive dysfunction are discussed. MATERIALS AND METHODS: Electromyography of the corpus cavernosum was performed before and 1 day after intracavernous injection of 60 mg. papaverine and 400 micrograms. sodium nitroprusside in 22 patients with veno-occlusive dysfunction. Changes in duration and amplitude of electromyographic potentials were compared in groups with and without incoordination patterns. RESULTS: The decreases in electrical amplitude and duration in 15 patients with a negative incoordination pattern, and increases in 7 with a positive pattern were more significant with intracavernous sodium nitroprusside than with papaverine injections. CONCLUSIONS: Electromyographic changes were more prominent with nitroprusside than with papaverine, which demonstrates the use of nitroprusside when performing corpus cavernosum electromyography.

Electromyography↗
PubMed1996

Responses of internal mammary artery graft flow to nitroprusside: a duplex Doppler study in hypertensive hearts.

OBJECTIVE: To assess the response of internal mammary artery (IMA) flow of hypertensive hearts to nitroprusside infusion. METHODS: Fifteen patients were studied with a high-frequency duplex Doppler probe from the supraclavicolar approach. All the patients had undergone coronary artery bypass surgery with an IMA graft into the left anterior descending artery. The investigated patients were normotensives (controls, n = 5) and hypertensive with a normal (group 1, n = 5) or a hypertrophic (group 2, n = 5) left ventricle. Values of the left ventricular mass index were 102 +/- 11 g/m2 in controls, 115 +/- 18 g/m2 in group 1 and 153 +/- 8 g/m2 in group 2. The IMA flow volume was studied at baseline and continuously during nitroprusside infusion. The arterial blood pressure was measured each minute by a cuff sphygmomanometer. In each patient we considered the peak flow volume (percentage increment from baseline) and the flow volume at the end point (the lowest tolerated diastolic blood pressure). RESULTS: Nitroprusside infusion induced a comparable flow-volume increment in controls (38 +/- 27%) and in group 1 (24 +/- 11%). Conversely, the flow-volume increment was trivial in group 2 (6 +/- 6%). At the end point, the flow volume was similar to the baseline value in controls (with diastolic blood pressure 67 +/- 9 mmHg) and in group 1 (diastolic blood pressure 61 +/- 4 mmHg), whereas the flow volume declined significantly from baseline (by 23%) in group 2 at a perfusion pressure of 79 +/- 9 mmHg. CONCLUSION: Hypertensive patients with a normal left ventricular mass exhibit a coronary flow behaviour similar to that of normotensives in response to a nitroprusside infusion. Conversely, hypertrophic hypertensives show a blunted nitroprusside-induced coronary vasodilator response and are much more vulnerable to coronary flow reductions in the face of hypotension. This dynamic assessment of flow patterns can be obtained non-invasively by duplex Doppler monitoring of IMA graft flow.

Aged↗
PubMed1976

Effect of nitroprusside on smooth muscle and adrenergic nerve terminals in isolated blood vessels.

Experiments were designed to assess the mode of action of nitroprusside on isolated blood vessels and its relative potency on venous and arterial smooth muscle. Strips from dog blood vessels were mounted in an organ bath for isometric tension recording. Sodium nitroprusside (10(-5) M) depressed the contraction of saphenous vein strips caused by electric stimulation, tyramine, K+, Ba++, norepinephrine and acetylcholine. The depression of the norepinephrine-induced contractions also occurred in a Ca++- free medium and when Ca++ influx was inhibited by verapamil. Nitroprusside reduced the frequency of the spontaneous contractions of strips of portal-mesenteric veins. It depressed the contraction caused by norepinephrine in tibial artery strips more than in saphenous vein strips. Saphenous vein strips were incubated with (3H)norepinephrine and mounted for superfusion and isometric tension recording. Sodium nitroprusside (10(-5) M) had no effect on the basal efflux of 3H compounds. During electric stimulation, it did not change the output of (3H)norepinephrine but increased the outflow of deaminated and O-methylated metabolites. Thus sodium nitroprusside 1) has a direct effect on the smooth muscle cells which is independent of Ca++ influx, 2) depresses contractions of different types of vascular smooth muscle and 3) does not inhibit the release of norepinephrine from the nerve endings.

Animals↗
PubMed1976

Hemodynamic effects of nitroprusside infusion during coronary artery operation in man.

The hemodynamic response to vasodilator therapy with sodium nitroprusside has been assessed in 33 patients with severe coronary artery disease (CAD) during coronary artery operation. The patients were divided into three groups; Group 1 included seven patients with CAD and normal left ventricular filling pressure (LVFP less than 12 mm Hg); Group 2 included 18 patients with CAD and chronic left ventricular (LV) dysfunction (LVFP greater than 12 mm Hg) and Group 3 included eight patients with CAD and acute LV dysfunction (LVFP greater than 12 mm Hg) associated with an intraoperative hypertensive episode. Nitroprusside was administered intraoperatively at an initial infusion rate of 10-15 mcg/min and the rate was gradually increased thereafter until the criteria for effective therapy were satisfied. The effective dose ranged from 10-120 mcg/min with an average of 52 +/- 4 (SEM) mcg/min. In all three groups, pulmonary and systemic arterial pressure, right and left ventricular filling pressure, and pulmonary and systemic vascular resistance decreased significantly with nitroprusside infusion. Heart rate increased significantly in Group 1 and remained unchanged in Group 2 and 3. Heart rate X systolic arterial pressure decreased significantly in Group 1 and 3 and did not change in Group 2. Stroke index increased significantly in both groups of patients with elevated control LVFP (Group 2 and 3) and remained unchanged in patients with normal left ventricular function (Group 1). Left ventricular stroke work index decreased in Group 1, increased in Group 2, and remained unchanged in Group 3. Right ventricular stroke work index decreased significantly in all groups. These findings suggest that judicious intraoperative administration of sodium nitroprusside improves left ventricular function in patients with acute or chronic elevation of LVFP and LV dysfunction associated with severe CAD. Furthermore, nitroprusside is an effective drug for control of intraoperative hypertensive episodes in such patients.

Adult↗
PubMed1976

Nitroprusside therapy. Treatment of hypertensive patients with recurrent resting chest pain, ST-segment elevation, and ventricular arrhythmias.

Five hypertensive patients with acute myocardial infarction and persistent postinfarction hypertension who experienced severe and recurrent resting chest pain, ST elevations, and severe ventricular arrhythmias refractory to conventional treatment with bed rest, sedation, oxygen inhalation, nitrates, and antiarrhythmic agents received sodium nitroprusside by continuous intravenous infusion, titrated to reduce systolic blood pressure to 100 to 110 mm Hg. Treatment resulted in noticeable improvement in symptoms, reduction in ST elevations, and abolition of ventricular arrhythmias in all five patients. In four patients, cessation of nitroprusside infusion after 48 hours resulted in prompt recurrence of hypertension, chest pain, ST-segment elevations, and ventricular arrhythmias. These were all rapidly reversed following reinstitution of the nitroprusside therapy for seven to eight days, strongly suggesting a cause-and-effect relationship. Nitroprusside infusion in these patients suggests a potentially important use for such therapy in this clinical setting.

Acute Disease↗
PubMed1984

In vitro stability of sodium nitroprusside solutions for intravenous administration.

A sensitive high-performance liquid chromatographic assay for nitroprusside using an ion-exchange column and UV detection was developed to evaluate the stability of aqueous solutions of sodium nitroprusside in light-protected glass and plastic containers and during simulated infusions. The results showed that sodium nitroprusside is stable in 5% dextrose, normal saline, and lactated Ringer's solutions in light-protected glass or plastic containers. In addition, there was no decrease in the delivered potency of sodium nitroprusside solutions during simulated infusions lasting up to 24 h.

Chromatography, High Pressure Liquid↗
PubMed1993

Disinhibition of AVP release during noradrenaline and angiotensin II infusions in dogs by maintaining normotension with sodium nitroprusside.

Noradrenaline (NA) and angiotensin II (A II) were infused intravenously in conscious dogs without (series I) and with (series II) additional infusions of sodium nitroprusside at doses re-establishing normal levels of mean arterial pressure (MAP). In series I, NA infusion (1.6 micrograms/min per kg for 30 min) initially elevated MAP by some 25 mm Hg and lowered heart rate by some 30 beats/min. Plasma concentrations of arginine vasopressin (AVP) remained constant, while those of A II and atrial natriuretic factor were slightly, but significantly, increased. Infusion of A II (10 or 20 ng/min per kg for 30 min) induced similar rises in MAP and slight reductions of heart rate and increased plasma AVP by 70% and atrial natriuretic factor by 60%. In series II, sodium nitroprusside (1-4 micrograms/min per kg) was added for 30 min to infusions of NE (1.6 micrograms/min per kg) and A II (20 ng/min per kg) in order to maintain MAP at its control level. This resulted in an 11-fold increase in plasma AVP during NA infusion and a 19-fold increase during A II infusion. Infusing sodium nitroprusside (4 micrograms/min per kg) alone lowered MAP to clearly hypotensive levels, but the resulting rises in plasma AVP were less than, rather than equal to, those seen at normotensive MAP levels during the combined infusions of sodium nitroprusside with A II or NA, respectively. It is concluded that both NA and A II exert strong stimulatory actions on AVP release which are, however, counteracted by inhibitory influences arising from the hypertensive effects of NA and A II.

Angiotensin II↗
PubMed1986

Evaluation of two adaptive sodium nitroprusside control algorithms.

Computer control of sodium nitroprusside infusion may be safer and provide better control of arterial blood pressure than is achieved with manual control. In a series of test maneuvers in 20 mongrel dogs, the performance of two adaptive control algorithms (controllers) was compared and their safety tested. The controllers were set to infuse sodium nitroprusside to decrease mean arterial pressure and maintain it 20 to 30 mm Hg below the control pressure. Then, sequentially, the right atrium was paced to simulate a supraventricular tachydysrhythmia, the right ventricle was intermittently paced to simulate ventricular extrasystoles, large tidal volumes were given to simulate a respiratory-therapy maneuver, the catheter was clamped to simulate clotting, an air bubble was introduced, and the infused sodium nitroprusside concentrations were either doubled or halved. Next, 500 ml of blood was drawn. Then, in sequence, positive end-expiratory pressure was applied, the right atrium was paced, and large tidal volume breaths were given to cause the blood pressure to fluctuate. When the controllers were turned on, mean arterial pressure reached the set point and remained within 5 mm Hg of the target pressure after 8.6 +/- 0.9 minutes (mean +/- SEM). The controllers properly handled the differences in sodium nitroprusside sensitivity and the catastrophic challenges presented in the experiments. When the animals were not being disturbed, stability was maintained and the blood pressure was kept well within 5 mm Hg of the desired pressure. The controllers rejected all invalid pressure signals during testing.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Self-tuning adaptive control of induced hypotension in humans: a comparison of isoflurane and sodium nitroprusside.

Induced hypotension is commonly used during surgery to decrease arterial pressure. Sodium nitroprusside and isoflurane are well-known hypotensive agents. The use of self-tuning adaptive control of induced hypotension was assessed with the use of sodium nitroprusside and isoflurane as hypotensive agents. Nineteen surgical patients were studied during closed-loop control of hypotension induced with sodium nitroprusside. This group of patients was compared with 10 similar patients in whom infusions of sodium nitroprusside were controlled manually by an anesthesiologist. Although the results of the two studies varied, no conclusion could be drawn regarding the superiority of either manual or closed-loop control. When manual versus automatic control of isoflurane-induced hypotension was assessed in a similar fashion, the two methods of induction were found to be comparable.

Algorithms↗
PubMed1980

Vasodilator therapy after cardiac surgery: a review of the efficacy and toxicity of nitroglycerin and nitroprusside.

Eight-five patients who required vasodilator therapy in the postoperative period after cardiac surgery were studied to compare the haemodynamic effects of nitroglycerin and nitroprusside, to evaluate local and systemic toxicity, and to develop long-range dosage recommendations. Ninety-one per cent of the patients received the vasodilators for postoperative hypertension, while nine per cent had low output syndromes. Both drugs significantly decreased blood pressure and central venous pressure, and increased heart rate. Nitroglycerin decreased both right and left ventricular filling pressures more than nitroprusside. No local toxicity or methaemoglobinaemia was found with either drug. Elevated thiocyanate levels were detected in 44 per cent of the nitroprusside group; however, none of the patients developed progressive metabolic acidosis. For prolonged infusions we found that nitroprusside at 1 microgram.kg-1.min-1 and nitroglycerin at 0.5 microgram.kg-1.min-1 were without significant toxicity.

Blood Pressure↗
PubMed1986

Hypotensive actions of diltiazem and nitroprusside compared during fentanyl anaesthesia for total hip arthroplasty.

The potential for inducing hypotension during fentanyl anaesthesia by administering either diltiazem (n = 7) or sodium nitroprusside (n = 7) was investigated during total hip arthroplasty. Haemodynamic variables were obtained in the lateral position before, during and after administration of the hypotensive agent. Diltiazem 0.15 mg X kg-1 given as an IV bolus followed by a 12.5 +/- 3 micrograms X kg-1 X min-1 continuous infusion decreased mean arterial pressure (MAP) from 77 +/- 11 mmHg to 63 +/- 16 mmHg (p less than 0.05) while other haemodynamic parameters showed only minor and insignificant changes. Hypotension continued for at least 30 min after the cessation of diltiazem. With sodium nitroprusside MAP decreased immediately from 81 +/- 11 mmHg to 59 +/- 9 mmHg (p less than 0.01) and rapidly returned to its control value after cessation of the infusion. CI and Qs/Qt rose significantly (p less than 0.05) while the systemic vascular resistance index (SVRI) (p less than 0.01) and pulmonary vascular resistance index (PVRI) (p less than 0.05) fell significantly. The haemodynamic profile was significantly different between hypotensive agents for MAP (p less than 0.02), heart rate (HR) (p less than 0.01), SVRI (p less than 0.05), and PVRI (p less than 0.05). HR was lower with diltiazem than with nitroprusside. A bradycardia less than 50 beats/min was observed in five patients in the diltiazem group. MAP, SVRI and PVRI were lower with nitroprusside than with diltiazem. Diltiazem can induce and maintain moderate hypotension without tachycardia and decreased cardiac output in humans during fentanyl anaesthesia but the modulation of the level of arterial pressure and the depression of atrioventricular conduction are unpredictable.

Aged↗