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PubMed1984

Propranolol prevents hemodynamic and humoral events after abrupt withdrawal of nitroprusside.

Hemodynamic and humoral events after intraoperative discontinuation of nitroprusside were studied in subjects without and with pretreatment with intravenous propranolol, 0.1 mg X kg-1. Nitroprusside-induced hypotension was associated with increases in heart rate, cardiac output, plasma renin activity (PRA), and catecholamine levels; these changes were prevented by propranolol. In subjects pretreated with propranolol, dose requirements of nitroprusside for hypotension of comparable degree and duration decreased 40%. On discontinuation of nitroprusside, mean systemic pressure rose to 100.2 mm Hg--a level higher than prehypotension and awake values--because of increased systemic vascular resistance. Hemodynamic events were associated with persistent elevations of PRA and catecholamine levels. These rebound changes were maximal 15 min after nitroprusside withdrawal and returned to control levels 30 to 60 min later. Pretreatment with propranolol completely prevented rebound hemodynamic events after nitroprusside. Persistent elevations of PRA and catecholamine levels after nitroprusside action subsided were responsible for the effects of withdrawal.

Adolescent↗
PubMed1996

Inhibition of excitatory amino acid-induced phosphoinositide hydrolysis as a possible mechanism of nitroprusside neurotoxicity.

Inclusion of sodium nitroprusside (Na2[Fe(2+)-(CN)5NO]) into the culture medium is toxic to cultured rat cerebellar granule neurons. A possible underlying mechanism may be the inhibition of phosphoinositide (PI) response to excitatory amino acids (EAAs) because activation of glutamate receptors can be neuroprotective and neurotrophic in differentiating neurons. Sodium nitroprusside selectively inhibited the PI response to EAAs (NMDA > glutamate = quisqualate > kainate) without affecting that to carbachol or KCl. In contrast, S-nitroso-N-acetyl-penicillamine (SNAP), another nitric oxide (NO) donor, potentiated NMDA-induced PI hydrolysis. Hemoglobin reversed the effects of nitroprusside and SNAP. However, NO may not be involved because NO solution was without effect and N-acetylpenicillamine, a SNAP analogue that does not contain a NO moiety, also potentiated NMDA-induced PI hydrolysis in a hemoglobin-sensitive manner. Furthermore, the metabolites of NO (nitrate and nitrite), L-arginine, reduced glutathione, 8-bromo-cyclic guanosine 3':5'-cyclic monophosphate (8-Br-cGMP), and atrial natriuretic peptide, which accelerates the production of cGMP independent of NO, were ineffective as modulators. However, potassium ferrocyanide (K4[Fe2+(CN)6]), but not potassium ferricyanide (K3[Fe3+(CN)6]), inhibited NMDA-induced PI hydrolysis as effectively as nitroprusside, but this inhibition was not reversed by hemoglobin. Cyanide, a product from the disintegration of nitroprusside, potentiated rather than inhibited NMDA-induced PI hydrolysis. Taken together, these results suggest that the parent molecule itself, nitroprusside, contributes primarily in inhibiting EAA-induced PI hydrolysis. Inhibition of EAA-induced PI hydrolysis may in part mediate the mechanisms of nitroprusside toxicity in primary cultures of differentiating cerebellar granule neurons.

Animals↗
PubMed1997

Neurotrophin protection against toxicity induced by low potassium and nitroprusside in cultured cerebellar granule neurons.

Long-term survival of cultured rat cerebellar granule neurons requires depolarizing concentrations of potassium (high potassium; 25 mM KCl). A high-potassium culturing condition has been reported to increase the intracellular calcium concentration ([Ca2+]i) and the expression of brain-derived neurotrophic factor (BDNF), which in turn induces the expression of neurotrophin-3 (NT-3) in these neurons. We therefore examined the neurotrophic effect of these two neurotrophins in low-potassium (5 mM) cultures and their neuroprotective capabilities against sodium nitroprusside-induced neurotoxicity in both low- and high-potassium cultures. Neuronal survival and neurotrophic effects were monitored by [3H]ouabain binding and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays. In low-potassium cultures, the neurotrophic effect of BDNF approached that found in high-potassium cultures but was much more robust than that of NT-3. In contrast, undifferentiated neurons cultured in high-potassium medium were much less responsive to BDNF and not responsive at all to NT-3. Induction of nitroprusside neurotoxicity occurred more readily in low- than in high-potassium cultures. BDNF, NT-3, and a high potassium concentration, alone or in combination, were unable to protect neurons treated with nitroprusside at 50 or 100 microM. However, the neurotoxicity of a lower dose of nitroprusside (10 microM) was reversed by the combined actions of these two neurotrophins in low-potassium cultures and by BDNF alone in high-potassium cultures. Because nitroprusside neurotoxicity is less robust in high-potassium cultures, high-potassium-induced BDNF expression and subsequent NT-3 expression may participate in its neuroprotection and neurotrophism in these cultures. Also, we found that toxic doses of nitroprusside antagonized KCl- and NMDA-induced rises in [Ca2+]i, suggesting that this effect is related to nitroprusside-induced neurotoxicity.

Animals↗
PubMed2005

Comparison of phenoxybenzamine to sodium nitroprusside in infants undergoing surgery.

OBJECTIVES: The purpose of this study was to compare the effects of a direct-acting arterial dilator, sodium nitroprusside, to an alpha-adrenergic receptor blocker, phenoxybenzamine, in infants with congenital heart defects undergoing cardiac repairs on cardiopulmonary bypass. DESIGN: A prospective, multicenter, observational study. SETTING: Tertiary care center. PARTICIPANTS: Sixty infants scheduled for elective congenital cardiac surgery repair requiring cardiopulmonary bypass. INTERVENTIONS: Patients received either sodium nitroprusside 2 to 5 microg/kg/min infusion intraoperatively and in the intensive care unit (n=30 patients) or received phenoxybenzamine 1 mg/kg slowly intravenously at the onset of cardiopulmonary bypass (n=30 patients). MEASUREMENT AND MAIN RESULTS: Despite similar mean arterial pressures during cardiopulmonary bypass in both groups, infants who received phenoxybenzamine had a significantly higher flow compared with those who received sodium nitroprusside (180+/-4.8 v 73+/-5.12 mL/kg/min, p<0.0001). Base deficit was significantly larger in the sodium nitroprusside group compared with the phenoxybenzamine group intraoperatively and postoperatively (3.4+/-0.5 v 1.3+/-0.5 mEq/L, p<0.05). The core-to-peripheral temperature gradient was significantly larger in the sodium nitroprusside group compared with the phenoxybenzamine group intra- and postoperatively at all points studied. In the intensive care unit, the left atrial pressure was significantly higher in the sodium nitroprusside group compared with the phenoxybenzamine group (9+/-0.4 v 7+/-0.4 mmHg, p<or=0.0005). CONCLUSION: The use of phenoxybenzamine can maintain organ perfusion on cardiopulmonary bypass and improve peripheral circulation as shown by less base deficit and smaller temperature gradients intraoperatively and in the intensive care unit better than nitroprusside.

Cardiopulmonary Bypass↗
PubMed1997

Drug-induced vasodilation: the effects of sodium nitroprusside, hydralazine, and cromakalin on the rabbit carotid artery: in vitro and in vivo study.

Extreme arterial and venous constructions are common problems in microvascular surgery, often leading to tissue injury and flap failure. The ideal pharmacologic tool to counteract ischemia should exert its action both locally and distally in the microcirculation of the flap. In this study, the vascular properties of sodium nitroprusside, hydralazine, and cromakalin were evaluated and compared in in vitro and in vivo models in the rabbit carotid artery. In the in vitro study, 20 rings from the rabbit carotid artery were bathed in Krebs-Ringers solution, stretched progressively to an optimal tension of 3.7 to 4.2 gm, and their isometric contractile activity was measured. The specimens were precontracted with norepinephrine (1 microM) and a dose-response curve was established by adding cumulatively either sodium nitroprusside (n = 7), cromokalin (n = 7), or hydralazine (n = 7) at increasing concentrations. In the in vivo study, microvascular anastomoses were performed bilaterally in the rabbit carotid artery in 19 animals using 9-0 nylon suture and standard microsurgical techniques. In each animal, one side was treated with heparinized sodium chloride, and served as control. The other side was treated blindly with the topical application of 1 ml of either sodium nitroprusside (10 mg/ml, n = 5), hydralazine (20 mg/ml, n = 5), or cromakalin (25 mg/ml, n = 4), during and after the anastomoses. Blood-flow changes in the vessels were continuously monitored with the transonic Doppler applied to both carotid arteries for 60 min after the procedure. Sodium nitroprusside and cromakalin elicited a concentration-dependent relaxation of norepinephrine-precontracted carotid artery rings in vitro. Sodium nitroprusside was significantly more effective than cromakalin in inducing relaxation. Hydralazine elicited a biphasic response, with low concentrations (1.5 x 10(-5) to 1.5 x 10(-3) M) potentiating the norepinephrine-induced contraction, and high concentrations relieving this contraction. Microsurgical anastomosis in the rabbit carotid artery-produced a significant decrease of blood flow through the vessel as measured by the transonic Doppler for 30 min. Topical application of heparinized saline did not significantly change the blood flow after the microvascular anastomosis. Topical application of sodium nitroprusside and cromakalin significantly increased the blood flow in the vessel after the anastomosis; however, the topical hydralazine did not significantly alter blood flow, but demonstrated a trend toward increased flow values. The data support the conclusion that sodium nitroprusside and cromakalin could be used to relieve vascular constriction. It is suggested that further studies on the clinical use of these drugs in microsurgery is warranted.

Animals↗
PubMed1993

The effect of intrathecal sodium nitroprusside on severe chronic vasospasm.

The efficacy of sodium nitroprusside in resolving cerebral vasospasm was evaluated with multicisternal injections. Twelve animals received fresh, unheparinized arterial blood via three injections (15 ml total) into the cisterna magna. Selective vertebral arteriography was performed on Day 0, and blood injections were performed on the second and third days after the first injection. On the seventh day selective arteriography was performed to evaluate the diameter of the basilar artery. In the sodium nitroprusside group, intrathecal injections of the drug were started on Day 4 and continued for two days (25 micrograms/kg/day). The diameter of the basilar artery was reduced 72.98 +/- 11.07% in control experiments. For the animals treated with intrathecal sodium nitroprusside, the mean diameter of the basilar artery was reduced 29.25 +/- 4.54%. The effect of intrathecal sodium nitroprusside on intracranial pressure (ICP), blood pressure (BP) and electrocardiogram (ECG) was also evaluated in 14 animals. There were no prominent changes in ICP, BP, or ECG when sodium nitroprusside was given intrathecally, but BP decreased and ICP and heart rate increased with intravenous doses of sodium nitroprusside. These results support the hypothesis that sodium nitroprusside administered intrathecally is an effective treatment for cerebral vasospasm.

Animals↗
PubMed1989

Additive effects of enoximone and nitroprusside in unstable chronic heart failure.

In the present study, the safety and efficacy of the combined administration of intravenous nitroprusside and oral enoximone, an experimental compound with phosphodiesterase inhibitory properties, were evaluated. Ten patients with unstable chronic heart failure maintained on digitalis and diuretics were selected to receive enoximone because of their poor response to intravenous nitroprusside. For a mean peak dose of 115 micrograms min-1 nitroprusside, cardiac index increased from 1.8 +/- 0.4 to 2.0 +/- 0.4 l min-1 m-2, while pulmonary artery diastolic pressure and mean right atrial pressure decreased from 29 +/- 6 to 24 +/- 5 and from 15 +/- 6 to 11 +/- 3 mmHg respectively; mean arterial pressure and heart rate were unchanged. The addition of 1.6 mg kg-1 oral enoximone t.i.d. to nitroprusside resulted in a substantial improvement of cardiac function: cardiac index increased further to 2.8 +/- 0.5 l min-1 m-2 (P less than 0.001), pulmonary artery diastolic pressure and right atrial pressure decreased to 18 +/- 5 and 7 +/- 3 mmHg (P less than 0.01), respectively, while mean arterial pressure rose from 90 +/- 11 mmHg to 95 +/- 0 mmHg (P less than 0.05); heart rate was unchanged. The salutary haemodynamic response to combined nitroprusside-enoximone therapy persisted for more than 32 h, and cardiac performance remained improved on enoximone for a further 8 h despite the discontinuation of nitroprusside. No serious side-effects or changes in the arrhythmia profile were observed. The addition of oral enoximone to nitroprusside has beneficial haemodynamic effects in unstable chronic heart failure.

Aged↗
PubMed1999

The effects of clonidine on sensitivity to phenylephrine and nitroprusside in patients with essential hypertension recovering from surgery.

UNLABELLED: Clonidine reduces postoperative circulatory instability in patients with essential hypertension. It also increases the sensitivity to vasopressors before and during anesthesia. We investigated blood pressure responses to phenylephrine and nitroprusside pre- vs postoperatively and the effect of clonidine on these responses in patients with essential hypertension. Twenty patients received clonidine 6 microg/kg orally 120 min before anesthesia and 3 microg/kg IV over the final hour of surgery or an identical placebo. During increasing bolus doses of phenylephrine and nitroprusside (30-300 microg), the maximal systolic pressure responses were recorded at baseline on the day before surgery, before the induction of anesthesia, and 1 and 3 h postoperatively. Sensitivity to phenylephrine and nitroprusside was interpolated from linear regression of the data. There was no difference between preoperative and postoperative sensitivity to phenylephrine or nitroprusside in either group. Clonidine increased sensitivity to phenylephrine versus placebo before and after surgery (response to dose of 1.5 microg/kg: 42+/-14 vs 27+/-8 mm Hg preinduction, 37+/-10 vs 26+/-8 mm Hg 3 h postoperatively; both P < 0.01), but not to nitroprusside (38+/-6 vs 37+/-10 mm Hg preinduction and 40+/-6 vs 39+/-8 mm Hg postoperatively). Clonidine increases the sensitivity to phenylephrine but not nitroprusside at baseline and postoperatively in hypertensive patients. IMPLICATIONS: Clonidine increases the sensitivity to bolus injections of the vasoconstrictor phenylephrine, but not the vasodilator sodium nitroprusside, before and after surgery in patients with preexisting hypertension. The doses of vasopressors should be reduced accordingly in hypertensive patients receiving perioperative clonidine.

Aged↗
PubMed1977

A comparison of the cardiovascular effects of sodium nitroprusside and trimethaphan.

In dogs anesthetized with pentobarbital-chloralose, cardiac output and blood flows of four regional vascular beds (superior mesenteric, left renal, left circumflex coronary and left femoral) were continuously monitered with electromagnetic flowmeters. Arterial blood pressure and heart rate were also measured. Hypotension was induced with intravenous infusions of sodium nitroprusside and trimethaphan for 5-16 min to produce comparable reductions of mean arterial pressure (32 mm Hg or 26 per cent with nitroprusside and 37 mm Hg or 31 per cent with trimethaphan). Cardiac output also decreased, but to a lesser extent (11.5 per cent with nitroprusside and 12.5 per cent with trimethaphan). Thus, total peripheral resistance was consistently decreased. Nitroprusside caused slight tachycardia, while trimethaphan produced bradycardia. Both drugs decreased mesenteric blood flow and increased mesenteric vascular resistance. Renal blood flow was maintained or increased with nitroprusside; thus, renal vascular resistance decreased; with trimethaphan, renal blood flow decreased and renal vascular resistance did not change. Both nitroprusside and trimethaphan reduced coronary blood flow; the reduction was more pronounced with the latter. Nitroprusside affected femoral blood flow minimally, with a slight reduction of femoral vascular resistance. In contrast, trimethaphan increased femoral blood flow and markedly decreased femoral vascular resistance. Redistribution of cardiac output favoring the dilated skin and muscle vascular beds appears to be an important undesirable effect of trimethaphan.

Animals↗
PubMed1977

Cyanide release from sodium nitroprusside in the dog.

Thirty-nine dogs (including eight from a previous study) were given during a one-hour infusion either low (less than 1.0 mg/kg) or high doses (greater than 1.0 mg/kg) of sodium nitroprusside in the presence or absence of circulating methemoglobin. In animals given low doses, the metabolic effects were relatively mild and consistent with those accounted for by a reduction in arterial pressure to 40 torr. In animals given high doses (with the same arterial pressure), metabolic alterations were significantly magnified and oxygen extraction was decreased. Animals pretreated with methemoglobin and given high doses of nitroprusside (again at the same arterial pressure) showed no toxic effect of nitroprusside. In separate studies, blood and tissue levels of cyanide were measured in dogs given high doses of nitroprusside (2.5-3.5 mg/kg) in the presence or absence of methemoglobin. In dogs given methemoglobin, 60 per cent of the administered cyanide (as nitroprusside) was recovered in the blood (as cyanmethemoglobin) after a one-hour infusion. Thereafter, blood cyanide levels declined over three hours to 25 per cent of peak levels, presumably by conversion to thiocyanate, since tissue levels of cyanide were negligible. In dogs not given methemoglobin, blood cyanide levels qualitatively followed a similar pattern but quantitatively were a fourth to a third those of pretreated dogs, and tissue levels of cyanide became elevated. It is concluded that in the dog nitroprusside, acutely administered, causes cyanide toxicity at doses exceeding 1.0-1.5 mg/kg, that the release of cyanide from nitroprusside in blood is rapid and in large quantities, that detoxification (presumably by conversion of cyanide to thiocyanate) is likewise fairly rapid but insufficient to prevent toxicity, and that protection is provided by methemoglobin.

Animals↗
PubMed1977

Pulmonary shunt and cardiovascular responses to CPAP during nitroprusside-induced hypotension.

The effects of continuous positive airway pressure (CPAP) on cardiovascular dynamics and pulmonary shunt (QS/QT) were investigated in 12 dogs before and during sodium nitroprusside infusion that decreased mean arterial blood pressure 40-50 per cent. Before nitroprusside infusion, 5 cm H2O CPAP significantly, P less than .05, decreased arterial blood pressure, but did not significantly alter heart rate, cardiac output, systemic vascular resistance, or QS/QT. Ten cm H2O CPAP before nitroprusside infusion produced a further decrease in arterial blood pressure and significantly increased heart rate and decreased cardiac output and QS/QT. Nitroprusside caused significant decreases in arterial blood pressure and systemic vascular resistance and increases in heart rate, but did not change cardiac output or QS/QT. Five cm H2O CPAP during nitroprusside did not further alter any of the above-mentioned variables. However, 10 cm H2O CPAP decreased arterial blood pressure, cardiac output, and QS/QT. These data indicate that nitroprusside infusion rates that decrease mean arterial blood pressure by 40-50 per cent do not change cardiac output or QS/QT. During nitroprusside infusion low levels of CPAP do not markedly alter cardiovascular dynamics, but high levels of CPAP (10 cm H2O), while decreasing QS/QT, produce marked decreases in arterial blood pressure and cardiac output.

Animals↗
PubMed1981

Effect of sodium nitroprusside on cardiovascular function and pulmonary shunt in canine oleic acid pulmonary edema.

The authors investigated the acute effects of nitroprusside on intrapulmonary shunt (Qs/Qt), cardiac output, and left ventricular function in dogs with normal lungs, and again after they developed oleic acid pulmonary edema. Before oleic acid, nitroprusside reduced pulmonary capillary wedge pressure (PCWP) and stroke volume, and there were no changes in Qs/Qt. Ninety minutes after oleic acid, PCWP, Qs/Qt, and systemic vascular resistance increased and stroke volume decreased. Then nitroprusside increased cardiac output by 35 per cent and increased Qs/Qt from 12 to 18 per cent. After oleic acid, stroke volume increased on nitroprusside from 18 to 23 ml (P less than 0.05) despite reduced preload, as PCWP decreased from 10.4 to 4.4 torr on nitroprusside (P less than 0.05). Increased stroke volume may be explained by the reduction in resistive afterload, as nitroprusside reduced systemic vascular resistance from 60 to 34 torr . l-1 . min. To the extent that canine oleic acid pulmonary edema represents low pressure edema in patients, nitroprusside is a potential treatment to reduce PCWP, pulmonary microvascular pressure, and pulmonary edema while maintaining cardiac output.

Animals↗
PubMed1985

Effectiveness of sodium nitroprusside as a function of total peripheral resistance in the anesthetized dog.

To determine the influence of background vasomotor tone on the effectiveness of sodium nitroprusside in decreasing total peripheral resistance, experiments were performed on 12 open-chest dogs under halothane anesthesia. In the first experiment, the vasomotor condition of six dogs was changed by altering the background infusion rate of phenylephrine (0,40, and 0 microgram/min). Increasing background phenylephrine infusion from 0 to 40 micrograms/min significantly enhanced the effectiveness of nitroprusside in decreasing total peripheral resistance. In contrast, the effectiveness of nitroprusside in decreasing arterial pressure was not altered significantly. In a second experiment on six other dogs, phenylephrine was infused continuously at 40 micrograms/min, and the vasomotor condition was changed by the infusion of phentolamine (0, 60-100, 0 microgram/min). Phentolamine significantly diminished the effectiveness of nitroprusside in decreasing peripheral resistance. In contrast, the effectiveness of nitroprusside in decreasing arterial pressure was not altered significantly. Stepwise linear regression analysis indicated that the background peripheral resistance was the hemodynamic variable that could account partially for the changes in nitroprusside effectiveness. Increasing background total peripheral resistance significantly enhanced the effectiveness of nitroprusside in decreasing total peripheral resistance.

Anesthesia, Inhalation↗
PubMed1999

Microcirculatory basis for nonuniform flow delivery with intravenous nitroprusside.

BACKGROUND: The purpose of this study was to determine the effects of systemic infusions of nitroglycerin and sodium nitroprusside on flow distribution and wall shear stress in the microcirculation. METHODS: With university approval, the cremaster muscle of 28 anesthetized (70 mg/kg pentobarbital given intraperitoneally) hamsters (Harlan Sprague Dawley: Syrian; weight, 121+/-11 g [mean +/- SDD) was observed using in vivo fluorescence microscopy. Arteriolar diameter, erythrocyte flux, and velocity were measured for a feed arteriole and its sequential branches. Observations were made during control (mean arterial pressure, 88+/-4 mm Hg) and after 30 min of intravenous delivery of sodium nitroprusside or nitroglycerin, titrated to decrease mean arterial pressure by 20 mm Hg. RESULTS: Sodium nitroprusside significantly dilated select upstream portions of the network (23+/-2.6 to 29+/-2.6 microm); no arterioles were dilated with nitroglycerin. Erythrocyte flux into the feed (i.e., inflow into the arteriolar network) and into the sequential branches (i.e., distribution within the network) were evaluated. With nitroglycerin, inflow decreased significantly from 1,560+/-335 to 855+/-171 cells/s, and flux into the branches decreased evenly. With sodium nitroprusside, inflow increased significantly to 2,600+/-918 cells/s, yet cells were "stolen" from upstream branches (a decrease from 425+/-67 to 309+/-87 cells/s in the first branch). Excess flow passed into a downstream "thorough-fare channel," significantly increasing flux from 347+/-111 to 761+/-246 cells/s. Wall shear stress decreased uniformly with nitroglycerin infusion, with a decrease in the feed from 8.8+/-2.5 to 6+/-1.7 dyn/cm2. With sodium nitroprusside, variable changes occurred that were location specific within the network. For instance, at the inflow point to the network, wall shear stress changed from 8.3+/-2.5 to 4.2+/-3.3 dyn/cm2. CONCLUSIONS: Nitroglycerin infusion promoted homogeneity of flow. Sodium nitroprusside significantly increased the heterogeneity of flow within this arteriolar network; an anatomic location for steal induced by sodium nitroprusside is identified.

Animals↗
PubMed2002

Direct comparison of the effects of nebulized nitroprusside versus inhaled nitric oxide on pulmonary and systemic hemodynamics during hypoxia-induced pulmonary hypertension in piglets.

OBJECTIVE: To test the hypothesis that nebulized nitroprusside and inhaled nitric oxide would not differ in producing selective pulmonary vasodilation during hypoxia-induced pulmonary hypertension in piglets. SETTING: University laboratory. SUBJECTS: Five piglets. INTERVENTIONS: Piglets (n = 5) were anesthetized and instrumented to monitor systemic arterial pressure, pulmonary artery pressure, and cardiac output continuously. Hypoxia was induced (DeltaFio2 from 0.5 to 0.08), and either nebulized nitroprusside (5 mg/mL at 4 L/min flow; total dose 25 mg) or inhaled nitric oxide (20 ppm) was introduced into the ventilator circuit for 15 mins. Normoxia was then restored, and a repeat cycle of hypoxia followed by the alternate vasodilator treatment was initiated. MEASUREMENTS AND MAIN RESULTS: Hypoxia significantly reduced Pao2 (from 206 to 30 torr) and elevated pulmonary artery pressure (from 18 to 33 torr) while not significantly affecting systemic arterial pressure or cardiac output. During hypoxia, inhaled nitric oxide reduced pulmonary artery pressure from 33 to 21 torr (p <.01), whereas systemic arterial pressure and cardiac output were unchanged. During hypoxia, nebulized nitroprusside also reduced pulmonary artery pressure from 33 to 23 mm Hg (p <.01; p = nonsignificant vs. inhaled nitric oxide), whereas systemic arterial pressure and cardiac output again remained constant. The time course of the reduction in pulmonary artery pressure during inhaled nitric oxide was roughly ten-fold more rapid (<5 secs) than during nebulized nitroprusside ( approximately 1 min). Neither inhaled nitric oxide nor nebulized nitroprusside altered pH, Pao2, or Paco2. CONCLUSION: Both inhaled nitric oxide and nebulized nitroprusside produced prompt, significant, selective reduction of pulmonary artery pressure and pulmonary vascular resistance in piglets with hypoxia-induced pulmonary hypertension, without apparent effects on systemic hemodynamics or pulmonary gas exchange. The equivalence of the two effects in this animal model suggests that cautious extrapolation of the use of nebulized nitroprusside as a convenient bridge to inhaled nitric oxide in selected clinical contexts for human infants may be warranted.

Analysis of Variance↗
PubMedDate not supplied

Impact of captopril on hemodynamic and hormonal effects of nitroprusside.

The impact of oral captopril, 2 mg . kg-1, on the dose and on the hemodynamic and hormonal effects of nitroprusside was studied in seven patients (Group II). A comparable group (Group I, n = 7) received nitroprusside alone. In both groups, nitroprusside produced comparable decreases in mean arterial pressure, systemic vascular resistance, and right atrial pressure; cardiac output increased because of a significant change in heart rate. Although plasma renin activity increased significantly (compared with control values) in both groups, it was greater (p = 0.01) through the operative period in patients pretreated with captopril. Plasma aldosterone concentration increased in Group I (p = 0.01) but decreased in Group II (p = 0.01). Plasma catecholamine concentrations increased (p = 0.01) with nitroprusside alone but were unchanged in captopril-treated patients. Plasma converting enzyme activity was markedly inhibited (p = 0.001) by captopril. Following cessation of nitroprusside infusion in Group I, rebound hypertension occurred in conjunction with a significant (p = 0.01) increase in systemic vascular resistance; it was associated with elevated plasma renin activity, catecholamines, and aldosterone concentrations. In contrast, captopril-treated patients showed no rebound hemodynamic changes. Nitroprusside dose was less (p = 0.01) with captopril pretreatment (2.1 +/- 0.3 vs. 4.8 +/- 0.9 microgram . kg-1 . min-1). Thus, captopril is a useful adjunct to nitroprusside-induced hypotension.

Adult↗
PubMed2000

Nitroprusside in resuscitation of major torso trauma.

OBJECTIVE: Patients with thoracic aortic injury (TAI) usually have sustained other major trauma, and may require aggressive shock resuscitation. In the 24 hours after aortic repair and during resuscitation, our cardiothoracic surgeons request intravenous nitroprusside to maintain mean arterial pressure (MAP) less than 90 mm Hg to minimize bleeding at the repair. We compared the resuscitation response of patients who sustained major torso trauma (MTT) and TAI with that of patients who had MTT with no TAI to determine whether nitroprusside can effectively control MAP during resuscitation and whether use of nitroprusside, because of its peripheral vasodilatory effects, is associated with a favorable resuscitation response. METHODS: During the 9-month study period, 11 patients who sustained TAI and 38 patients who sustained MTT with no TAI met multiple organ failure risk/shock criteria and were resuscitated by a standardized protocol emphasizing volume loading and hemoglobin replacement to maintain systemic oxygen delivery index (DO2I) > or = 600 mL O2/min-m2 for the first 24 intensive care unit hours. For TAI patients, postoperative management included intravenous nitroprusside infusion titrated by the bedside nurse to maintain mean arterial pressure (MAP) less than 90 mm Hg during the same 24 hours. Data were obtained prospectively during resuscitation. Retrospectively, the resuscitation response of TAI and non-TAI patients was compared. RESULTS: For the TAI group, nitroprusside effectively controlled MAP (range, 77-87 mm Hg); for the non-TAI group, mean MAP exceeded 95 mm Hg within 5 hours. During the first 8 hours, MAP, pulmonary capillary wedge pressure, and systemic vascular resistance index were less, and DO2I was greater for the TAI than for the non-TAI group. The resuscitation goal of DO2I > or = 600 mL O2/ min-m2 was attained at 4 hours for the TAI group, and was attained at 12 hours for the non-TAI group. No revisions of aortic repairs were required during or as a result of resuscitation. CONCLUSION: During aggressive shock resuscitation, control of MAP using nitroprusside is feasible and is associated with a favorable resuscitation response. Nitroprusside may be a useful adjunct during shock resuscitation of MTT as a vasoactive agent that promotes peripheral tissue perfusion.

Adult↗
PubMed1995

Topical nitroprusside may reduce histamine-induced plasma exudation in human nasal airways.

Mucosal exudation of nonsieved bulk plasma is a key feature of airway defense and inflammation. We have previously observed in guinea pig tracheobronchial airways that endogenous nitric oxide (NO) of the mucosa may tonically suppress the permeability of the subepithelial microcirculation, and that topical administration of the NO donor nitroprusside may reduce plasma exudation responses. The present study examines whether nitroprusside affects histamine-induced mucosal exudation of plasma in the human nasal airway. In a dose-finding tolerability experiment, using changes in nasal patency as response, placebo and nitroprusside (1.2 and 3.6 mg per nasal cavity) were applied on the mucosal surface with a nasal-spray device. Nasal peak expiratory flow (PEF) rates were measured before the application and thereafter every third minute for 15 min. Nitroprusside produced a dose-dependent decrease in nasal PEF rates compared to placebo. Placebo or nitroprusside (7.2 mg) was then given to the right nasal cavity, followed 3 min later by challenge with saline or histamine (600 micrograms). The drug and the challenge were both applied with a nasal-spray device. With a nasal pool-device, the same large part of the nasal mucosal surface was lavaged before and after the treatment/challenge. The lavage fluid levels of alpha 2-macroglobulin were measured as an index of mucosal exudation of bulk plasma. The histamine-induced lavage fluid level of alpha 2-macroglobulin was significantly higher after treatment with placebo than with nitroprusside. The present data indicate that nitroprusside may have antiexudative effects in human airways. Hence, unlike other microvascular permeability active agents, this pharmacologic principle may be active in both guinea pig and human airways.

Administration, Topical↗