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PubMedDate not supplied

Differential hemodynamic and sympathoadrenal effects of sodium nitroprusside and hydralazine in hypertensive subjects.

The hemodynamic and sympathoadrenal effects of serial incremental doses of a mixed veno-arteriolar dilator (intravenous sodium nitroprusside 0.0125-0.50 micrograms/kg/min) and a pure arteriolar dilator (bolus injections of hydralazine, 0.05-0.3 mg/kg) were compared in 18 subjects with uncomplicated essential hypertension. Blood pressure was reduced to the same extent over approximately the same time with both drugs. Sodium nitroprusside produced significant reduction in cardiac output (9%) and stroke volume (16%) despite an 11% increase in heart rate. Total peripheral resistance did not change. In contrast, hydralazine produced a significant (39%) reduction in peripheral resistance with a compensatory increase in heart rate (19%), stroke volume (20%), and cardiac output (42%). The catecholamine responses to the drugs differed both quantitatively and qualitatively. Administration of both drugs was associated with gradual increases in plasma norepinephrine, but the levels were consistently 40% higher with sodium nitroprusside for the same fall in blood pressure. No consistent change in plasma epinephrine was found with sodium nitroprusside, whereas with hydralazine, the concentration increased gradually after the blood pressure had been reduced by 9 mm Hg. This threshold was independent of the starting blood pressure. These differences in catecholamine response could reflect different patterns of regional sympathetic activation by the low pressure mechanoreceptors (sodium nitroprusside) and by the arterial baroreceptors (hydralazine). Neither drug has an ideal hemodynamic profile, particularly in subjects with cardiac disease, but a balanced combination of the two may produce a favorable hemodynamic profile and optimal hypotensive effect, minimizing the need for large doses of sympathetic inhibitors.

Adult↗
PubMed1994

Nitroprusside infusion improves arterial baroreflex control of heart rate in dogs with chronic congestive heart failure.

To determine if nitroprusside improves arterial baroreflex responsiveness in chronic congestive heart failure (CHF), we administered nitroprusside to 11 conscious dogs with pacing-induced CHF. Baroreflex sensitivity was determined by plotting the R-R interval against systolic aortic pressure after a bolus injection of phenylephrine (PE). At baseline, dogs with CHF had higher heart rate (HR), increased left atrial blood pressure (BP), and reduced left ventricular (LV) dP/dt as compared with 10 sham-operated normal animals. Baroreflex sensitivity index was significantly lower in CHF dogs, (8.3 +/- 1.3 ms/mm Hg) than normal dogs (25.1 +/- 1.2 ms/mm Hg, p < 0.001). Intravenous (i.v.) administration of nitroprusside (1 microgram/kg/min) to CHF dogs decreased left atrial BP (23 +/- 1-17 +/- 1 mm Hg) and HR (131 +/- 4-115 +/- 4 beats/min), but had no significant effect on either cardiac output (CO) or systolic aortic BP. This resulted in a 58% increase in baroreflex sensitivity index to 13.1 +/- 1.3 ms/mm Hg (p < 0.001); and the change correlated significantly with magnitude of decrease in left atrial BP (r = 0.884, p < 0.001) but not with the increase in R-R interval (r = 0.390, p > 0.10). In contrast, administration of nitroprusside sufficient to decrease left atrial BP (9.0 +/- 1.4-6.4 +/- 1.2 mm Hg) did not alter baroreflex sensitivity (26.4 +/- 3.4-26.4 +/- 3.9 ms/mm Hg) in 5 normal dogs. The results suggest that nitroprusside infusion increases arterial baroreflex sensitivity only in dogs with CHF and that this effect is probably functionally linked to the reductions of cardiac filling pressure.

Animals↗
PubMed1998

Saterinone, dobutamine, and sodium nitroprusside: comparison of cardiovascular profiles in patients with congestive heart failure.

The acute hemodynamic effects of the phosphodiesterase (PDE) III inhibitor saterinone were compared with dobutamine and sodium nitroprusside in 12 patients with idiopathic congestive cardiomyopathy (NYHA III). Hemodynamic measurements were obtained with a Swan-Ganz thermodilution catheter. At the peak of its dose-response curve, saterinone induced an increase in cardiac index (+102%), stroke volume (+97%), and heart rate (+6%), paralleled by a decrease in pulmonary capillary wedge pressure (-46%), right atrial pressure (-51%), pulmonary arterial pressure (systolic -32%, diastolic -45%, mean -38%), systemic blood pressure (systolic -3%, diastolic -13%, mean -9%), systemic vascular resistance (-54%), and pulmonary vascular resistance (-58%). Dobutamine had similar effects on cardiac index (+106%) and stroke volume (+87%) but lacked vasodilatory characteristics. In contrast to dobutamine, both nitroprusside and saterinone demonstrated more pronounced vasodilatory effects. Nitroprusside was less effective on cardiac index (+66%) and stroke volume (+56%) than was saterinone. The double product was markedly increased by dobutamine (+28%), did not change with saterinone treatment (+2%), and decreased with nitroprusside (-10%). This indicates that according to double product, only the application of dobutamine caused a relevant increase in myocardial oxygen consumption. Saterinone was demonstrated to be a safe and potent drug on short-term application; it combines the vasodilating properties of sodium nitroprusside with the positive inotropic effects of dobutamine without major changes in myocardial oxygen consumption.

Adult↗
PubMed2001

Nitroprusside and ECS-induced retrograde amnesia.

Previous research found that the administration of verapamil and felodipine immediately before electroconvulsive shocks (ECS) attenuated ECS-induced retrograde amnesia. This study examined whether sodium nitroprusside, an antihypertensive drug that does not affect calcium channels, has a similar action. Adult male Sprague-Dawley rats received nitroprusside (0.5 mg/kg ip) or saline 3 minutes before each of three once-daily true or sham ECS. Retention of pre-ECS learning was studied 1 day after ECS using a passive avoidance task. Nitroprusside was associated with increased seizure duration in ECS-treated rats, and with enhanced recall in both true and sham ECS groups. The latter finding suggests that nitroprusside nonspecifically improves cognitive functions, and does not support the hypothesis that ECS-induced cognitive impairment is a result of blood-brain barrier breach. Nitric oxide mechanisms may underlie the benefits purveyed by nitroprusside.

Amnesia, Retrograde↗
PubMed1982

Nitroprusside-hypotension: cerebral blood flow and cerebral oxygen consumption in neurosurgical patients.

The effects of nitroprusside-induced hypotension on cerebral blood flow and cerebral oxygen consumption were investigated in nine patients scheduled for cerebral arterial aneurysm surgery. Anesthesia was maintained with nitrous oxide/oxygen and fentanyl; muscle relaxation was achieved with pancuronium; PaCO2 was maintained at 4.79-5.32 kPa. Mean arterial pressure was reduced to 50 mmHg by nitroprusside infusion after opening of the dura. Measurements were recorded and blood samples were taken 15 min before induction of hypotension, during stable hypotension and 15 min after termination of nitroprusside infusion. Measurements included: cerebral blood flow, using the argon-washin technique, cardiac output (thermodilution), mean arterial pressure and heart rate. Cerebral blood flow averaged 56 +/- 6 min . 100 g before hypotension. Nitroprusside produced hypotension but did not significantly alter cerebral blood flow (61 +/- 7 ml/min . 100 g). Cerebral blood flow remained virtually at preinfusion values upon cessation of infusion (53 +/- 6 ml/min . 100 g). Cerebral oxygen uptake averaged 3 +/- 0.2 ml/min . 100 g before hypotension and did not change significantly during hypotension (3.3 +/- 0.3 ml/min . 100 g) and after termination of hypotension (2.7 +/- -0.3 ml/min . 100 g). In two patients nitroprusside produced a 17 and 20% increase, respectively, in cerebral blood flow with no change in cerebral oxygen consumption, together with a marked increase in cardiac output and heart rate.

Adolescent↗
PubMedDate not supplied

Effect of verapamil and sodium nitroprusside on the potassium contracture of smooth muscle strips from the reticular groove of adult cattle.

The effects of verapamil and sodium nitroprusside on smooth muscle strips from the floor of the reticular groove of adult cattle were studied. The mechanical activity of the muscle strips was recorded isometrically. Depolarization was induced with cumulative KCl concentrations (8.8-42.4 mmol/l) in Tyrode solution. This response was extracellular Ca2+ dependent. Verapamil and sodium nitroprusside caused a concentration dependent reduction of the KCl-induced contraction of the reticular groove muscle preparations; their IC50 were 3.9 x 10(-6) mol/l and 1.4 x 10(-4) mol/l, respectively. Pre-incubation with both antagonists (30 min) before KCl addition showed that sodium nitroprusside (10(-6) mol/l) did not affect, but verapamil (10(-6) mol/l) inhibited the KCl response of the muscle preparations. CaCl2 caused a concentration dependent (0.25-7 mmol/l) contraction of the KCl-depolarized muscle strips. Pre-incubation with verapamil (10(-6) mol/l) and sodium nitroprusside (10(-6) mol/l) before CaCl2 addition inhibited the response for about 80% and 20% respectively. These results indicate that action of verapamil may be related to voltage-dependent channel blockade. However, the nitroprusside action could not be completely attributed to these channels.

Animals↗
PubMed1992

Inhibition by sodium nitroprusside or PGE1 of tyrosine phosphorylation induced in platelets by thrombin or ADP.

Upon platelet activation, numerous proteins are known to be tyrosine phosphorylated. To investigate the mechanisms of the regulation of tyrosine phosphorylation and its physiological significance, the effects on tyrosine phosphorylation of agents that elevate the platelet level of the cyclic nucleotides cAMP and cGMP were examined in aspirin-treated gel-filtered platelets by Western blotting with a specific antiphosphotyrosine antibody. The effects of these agents on other aspects of platelet activation, i.e., aggregation, secretion, and elevation of the concentration of cytosolic ionized calcium ([Ca2+]i), were also examined in parallel experiments. Tyrosine phosphorylation in platelets activated by alpha-thrombin (1 nM) was inhibited by prostaglandin (PG) E1 (2 microM) or by sodium nitroprusside (100 microM). Elevation of [Ca2+]i, aggregation, and serotonin secretion was also strongly inhibited. On the other hand, a higher concentration of alpha-thrombin (10 nM) induced tyrosine phosphorylation of the same proteins, elevation of [Ca2+]i, platelet aggregation, and serotonin secretion, irrespective of pretreatment of platelets by either PGE1 or sodium nitroprusside. Inhibition by sodium nitroprusside of tyrosine phosphorylation induced by alpha-thrombin (1 nM) was accompanied by an increased concentration of cGMP. 8-BrcGMP (2 mM) also inhibited tyrosine phosphorylation and aggregation, although less than sodium nitroprusside. ADP (20 microM) induced platelet shape change and tyrosine phosphorylation of only a few proteins; these effects were also inhibited by either PGE1 or sodium nitroprusside. Thus tyrosine phosphorylation in platelets can be inhibited by elevation of either cAMP or cGMP, an effect that is overcome by a high concentration of thrombin, resulting in granule secretion and aggregation. Some of the proteins that are tyrosine phosphorylated may be important in the regulation of platelet functions.

Adenosine Diphosphate↗
PubMed1983

Regional venous return: nitroprusside effect in normal and chronically congested dogs.

The venous circulation is a key determinant of cardiac loading conditions. Although it may be altered by chronic congestive heart failure and vasodilating drugs, the mechanisms of these alterations have not been thoroughly studied, and their exact nature is unclear. We used venous return curves characterized by the pressure at zero flow (PZF) and resistance to venous return (RVR) to study the effect of nitroprusside and chronic congestion on regional venous return from the splanchnic and superior vena cava (systemic) venous beds in dogs. Chronic venous congestion was induced by prior creation of tricuspid insufficiency and pulmonic stenosis (TIPS). Nitroprusside lowered splanchnic PZF but not systemic PZF in both normal and TIPS animals. In normal animals systemic RVR increased during nitroprusside infusion but was unchanged in the congested animals. Resting values of PZF and RVR were different in the splanchnic and systemic venous beds in both normal and TIPS animals. We conclude that 1) nitroprusside works to selectively lower PZF in the splanchnic venous bed, 2) the regionally specific site of action of nitroprusside is not altered by TIPS, and 3) the independent behavior of the venous parameters of the two beds represents an important mechanism for the control of cardiac output.

Animals↗
PubMed1984

Diminished arterial smooth muscle response to sodium nitroprusside during Na-K pump inhibition.

Helical strips of rabbit coronary and femoral arteries were used to determine whether Na-K pump inhibition would diminish relaxation in response to sodium nitroprusside. Ouabain (10(-5) M) decreased relaxation by 10(-7) M sodium nitroprusside from 87.0 +/- 5.4 to 65.2 +/- 9.1% in coronary, and from 62.0 +/- 6.9 to 32.8 +/- 3.3% in femoral artery strips. A low Na solution and a K-free solution also decreased relaxation by sodium nitroprusside. Relaxation in response to K+, an index of Na-K pump activity in arterial smooth muscle, was enhanced in the presence of sodium nitroprusside. These results may reflect an interaction between sodium nitroprusside and the sarcolemmal Na-K pump of arterial smooth muscle.

Animals↗
PubMed1978

Effect of nitroprusside on regional myocardial blood flow in coronary artery disease. Results in 25 patients and comparison with nitroglycerin.

The effect of nitroprusside on regional myocardial specific blood flow (RMBF) was evaluated in 25 patients with the xenon-133 washout technique. Six patients were normal (group 1), six patients had coronary artery disease without collateral vessels (group 2), and thirteen patients had coronary artery disease with collateral vessels (group 3). In group 1, RMBF was unchanged following nitroprusside. RMBF decreased significantly in both group 2 and group 3, including seven patients in group 3 with high-grade collateral vessels. The results were compared to the effect of nitroglycerin in 31 patients previously studied using the same technique. Mean arterial pressure and pressure-rate product were comparably reduced by both drugs. In contrast to the findings with nitroprusside, after sublingual nitroglycerin RMBF decreased markedly in normals and increased in patients with coronary artery disease and high-grade collaterals. The data suggest that nitroprusside may primarily affect resistance vessels within the coronary circulation, as opposed to the effect of nitroglycerin on conductance vessels. Thus, nitroprusside could result in redistribution of blood flow away from ischemic areas and potentially increase ischemic injury in some patients with coronary artery disease.

Blood Pressure↗
PubMed1979

Effects of nitroprusside and dopamine on pulmonary arterial vasculature in children after cardiac surgery.

The hemodynamic effects of nitroprusside and dopamine were studied in 28 children early after intracardiac repair. Children were placed in six groups, five according to their anatomic lesion and one made up of those who had postoperative pulmonary artery hypertension, to evaluate the possible differences in response of the pulmonary arterial vasculature to the drugs. Seven children had repair of an atrial septal defect; six, repair of tetralogy of Fallot; four, repair of ventricular septal defect; five, surgery for pulmonary stenosis; one, closure of a left ventricular to right atrial tunnel; and five, postoperative pulmonary artery hypertension. Dopamine was infused at 8 microgram/kg/min, and nitroprusside at 3 microgram/kg/min. With dopamine, the heart rate increased an average of 10% and the cardiac index 11%; both increases were statistically significant. Changes in systemic and pulmonary vascular resistance, however, were not. With nitroprusside, the heart rate increased an average of 9% and the cardiac index 5%, while there was a significant decrease in both systemic (-20%) and pulmonary (-27%) vascular resistance. With the combination of dopamine and nitroprusside, both the cardiac index (+13%) and heart rate (+20%) increased significantly while systemic vascular resistance fell an average of 23% from control, and the pulmonary vascular resistance decreased 21%. Drug response among all five anatomic subgroups tended to be similar. We conclude that an afterload-reducing agent, such as nitroprusside and an inotropic drug such as dopamine, may have potential clinical advantages when used together in children providing heart rate does not become excessive.

Adolescent↗
PubMed1987

Diastolic function in patients with severe heart failure: comparison of the effects of enoximone and nitroprusside.

To assess whether the phosphodiesterase inhibitor enoximone has a specific, direct effect on left ventricular diastolic function distinct from its inotropic and vasodilator actions, we compared the effects of enoximone and the pure vasodilator nitroprusside in 11 patients with severe heart failure. Mean (+/- SEM) left ventricular ejection fraction was 0.20 +/- 0.03. Simultaneous left ventricular pressure and radionuclide angiographic volume were obtained at baseline, during infusion of nitroprusside, and after intravenous administration of enoximone. Left ventricular end-diastolic pressure (LVEDP) and volume (LVEDV) decreased with both agents (p less than .01 vs control); LVEDP was lower for nitroprusside than for enoximone (p less than .01) despite a similar LVEDV. Nitroprusside decreased the time constant of exponential left ventricular pressure decay, TL (measured by the logarithmic method), from 84 +/- 10 to 65 +/- 8 msec (p less than .01) but had no significant effect on TD (measured by the derivative method), maximum negative dP/dt, or the peak rate of early diastolic filling. Enoximone shortened TL from 86 +/- 12 to 61 +/- 9 msec (p less than .01) and increased maximum negative dP/dt from 897 +/- 101 to 1135 +/- 134 mm Hg/sec (p less than .01) but did not affect TD or the peak filling rate. The left ventricular diastolic pressure-volume relation was shifted downward in only three of 11 patients on nitroprusside and three of 11 patients on enoximone, and these shifts were attenuated by adjusting for simultaneous changes in right atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Diastole↗
PubMed1988

Comparative effects of nitroprusside and pinacidil on myocardial blood flow and infarct size in awake dogs with acute myocardial infarction.

The effect of nitroprusside in limiting myocardial infarct was compared with that of pinacidil, a new antihypertensive agent with potent coronary vasodilator properties, in instrumented awake dogs subjected to 4 hr of left anterior descending coronary artery occlusion and 20 hr of reperfusion. Dogs were randomly assigned to receive intravenous normal saline, nitroprusside, or pinacidil beginning 40 min after the onset of coronary artery occlusion and continuing throughout the occlusion and the first hour of reperfusion. Nitroprusside and pinacidil were titrated to decrease mean aortic pressure by 25 mm Hg; normal saline had no effect on mean aortic pressure. Other systemic hemodynamic variables were not significantly altered by normal saline or nitroprusside, and myocardial blood flow did not change during normal saline infusion in normal and ischemic myocardium. In contrast, nitroprusside increased the blood flow and the endocardial/epicardial flow ratio in ischemic myocardium. This increase in ischemic myocardial blood flow was accompanied by a significant reduction in infarct size (40 +/- 3% of region at risk vs 58 +/- 4% in the normal saline group; p less than .05). Pinacidil increased heart rate, cardiac output, and the peak rate of rise of left ventricular pressure. Furthermore, despite causing a threefold to fourfold increase in normal myocardial blood flow, pinacidil had no effect on either blood flow to ischemic myocardium or infarct size (57 +/- 5%). The data indicate that the marked coronary vasodilator effect of pinacidil does not cause an increase in ischemic blood flow or a reduction in infarct size.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Intravenous fenoldopam versus sodium nitroprusside in patients with severe hypertension.

In an open-label study, we compared the efficacy and safety of intravenous infusion of fenoldopam mesylate with that of sodium nitroprusside in patients with severe hypertension or in hypertensive crisis. Both antihypertensive medications were infused at a maximal dose increment of 0.2 microgram/kg/min (fenoldopam) and 1 microgram/kg/min (nitroprusside), with a maximal infusion rate of 1.5 micrograms/kg/min fenoldopam mesylate or 8 micrograms/kg/min sodium nitroprusside. Once the desired reduction in diastolic blood pressure was achieved (less than 110 mm Hg if initial diastolic blood pressure was 120-149 mm Hg, or by at least 40 mm Hg if initial diastolic blood pressure was 150-190 mm Hg), the maximal infusion rate used was maintained for at least 1 hour, and then, the infusion was slowed gradually over 2 hours. After the infusion treatment, patients remained in the hospital for 2 days of follow-up. Both antihypertensive agents successfully controlled the blood pressure in all the patients by the end of the maintenance periods. Between the baseline and the end of the maintenance period, analysis of variance showed that the changes in the variables induced by fenoldopam mesylate did not differ significantly from those induced by sodium nitroprusside. The incidence of side effects listed were similar in both groups of patients. The detection of toxic levels of thiocyanate in two patients treated with nitroprusside, however, shows that fenoldopam might be preferable for the control of a hypertensive crisis or severe hypertension in patients with decreased renal function.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMedDate not supplied

Nitroprusside-induced vascular relaxation in DOCA hypertensive rats.

Vascular responsiveness to nitroprusside and to norepinephrine was examined in two different preparations from DOCA hypertensive and normotensive control Sprague-Dawley rats. The blood-perfused renal vasculatures of DOCA hypertensive rats were significantly more sensitive than those of normotensive controls to the vasodilator action of low doses of nitroprusside. At high doses, responses in DOCA hypertensive and normotensive rats were similar. Since basal "structural" vascular resistances were greater in the hypertensive rats, It is possible that further vasodilation with nitroprusside was impeded more in DOCA-treated than in control rats. Nitroprusside produced a greater degree of vascular smooth muscle relaxation in tail artery strips from DOCA hypertensive rats than in those from normotensive controls. The current study is the first characterization of the effects of a vasodilator in mineralocorticoid hypertension. The two preparations gave divergent results with respect to vascular sensitivity to norepinephrine. When compared with control rats, the DOCA hypertensive rats showed a greater sensitivity to norepinephrine in tail arteries but a lesser renal vascular reactivity. It is evident that one must take a number of variables into consideration when characterizing changes in vascular responses that occur in a given model of hypertension: 1) the region of the vasculature (renal vs caudal artery);2) the level of the arterial tree (conduit vs resistance vessels);3) the technique employed for measurement of vascular changes (smooth muscle contraction vs vascular resistance changes);4) the initial vasoconstrictor tone of the preparation; and 5) the agonist used (nitroprusside vs norepinephrine).

Animals↗
PubMed1989

Comparison of relaxation induced by glyceryl trinitrate, isosorbide dinitrate, and sodium nitroprusside in bovine airways.

Nitrates are generally regarded as bronchial smooth muscle relaxants. However, reports about the clinical efficacy of the nitrates in the treatment of asthma are conflicting. In the present study, the relaxant effects of glyceryl trinitrate, isosorbide dinitrate, sodium nitroprusside, and isoproterenol were measured and compared in vitro in airway preparations isolated from variously sized airways in bovine lung. Strips of trachealis from cervical and thoracic ends of the trachea and rings of intrapulmonary bronchi of various diameters (14 to 1 mm outer diameters) were mounted for recording of isometric tension. Submaximal tone was induced using 10(-6) M carbachol, and responses to cumulatively increasing concentrations of glyceryl trinitrate, isosorbide dinitrate, sodium nitroprusside, or isoproterenol were measured. Isoproterenol (10(-8) to 10(-4) M) was equiactive as a relaxant in all preparations. Glyceryl trinitrate (10(-7) to 10(-5) M) relaxed trachealis, but was progressively and significantly less effective as a relaxant as the diameters of the bronchial rings decreased. Although less potent than isoproterenol, sodium nitroprusside (10(-6) to 10(-4) M) was effective in relaxing all the airway preparations. Similar to glyceryl trinitrate, sodium nitroprusside was less effective in small than in large airways. However, the relationship between relaxant responses to sodium nitroprusside and airway size was not as marked as for glyceryl trinitrate. Isosorbide dinitrate at concentrations as great as 10(-5) M did not relax carbachol-induced tone in any of the bronchial rings and only induced a small amount of relaxation in trachealis at 10(-5) M.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

Aortic input impedance during nitroprusside infusion. A reconsideration of afterload reduction and beneficial action.

Beneficial effects of nitroprusside infusion in heart failure are purportedly a result of decreased afterload through "impedance" reduction. To study the effect of nitroprusside on vascular factors that determine the total load opposing left ventricular ejection, the total aortic input impedance spectrum was examined in 12 patients with heart failure (cardiac index <2.0 liters/min per m(2) and left ventricular end diastolic pressure >20 mm Hg). This input impedance spectrum expresses both mean flow (resistance) and pulsatile flow (compliance and wave reflections) components of vascular load. Aortic root blood flow velocity and pressure were recorded continuously with a catheter-tip electromagnetic velocity probe in addition to left ventricular pressure. Small doses of nitroprusside (9-19 mug/min) altered the total aortic input impedance spectrum as significant (P < 0.05) reductions in both mean and pulsatile components were observed within 60-90 s. With these acute changes in vascular load, left ventricular end diastolic pressure declined (44%) and stroke volume increased (20%, both P < 0.05). Larger nitroprusside doses (20-38 mug/min) caused additional alteration in the aortic input impedance spectrum with further reduction in left ventricular end diastolic pressure and increase in stroke volume but no additional changes in the impedance spectrum or stroke volume occurred with 39-77 mug/min. Improved ventricular function persisted when aortic pressure was restored to control values with simultaneous phenylephrine infusion in three patients. These data indicate that nitroprusside acutely alters both the mean and pulsatile components of vascular load to effect improvement in ventricular function in patients with heart failure. The evidence presented suggests that it may be possible to reduce vascular load and improve ventricular function independent of aortic pressure reduction.

Adult↗
PubMed1981

Treatment of acute low pressure pulmonary edema in dogs: relative effects of hydrostatic and oncotic pressure, nitroprusside, and positive end-expiratory pressure.

Severe pulmonary edema sometimes develops despite normal pulmonary capillary wedge pressure (Ppw). The equation describing net transvascular flux of lung liquid predicts decreased edema when hydrostatic pressure is reduced or when colloid osmotic pressure is increased in the pulmonary vessels. We tested these predictions in a model of pulmonary capillary leak produced in 35 dogs by intravenous oleic acid. 1 h later, the dogs were divided into five equal groups and treated for 4 h in different ways: (a) not treated, to serve as the control group (Ppw = 11.1 mm Hg); (b) given albumin to increase colloid osmotic pressure by 5 mm Hg (Ppw = 10.6 mm Hg); (c) ventilated with 10 cm H(2)O positive end-expiratory pressure (Peep) (transmural Ppw = 10.4 mm Hg); (d) phlebotomized to reduce Ppw to 6 mm Hg; (e) infused with nitroprusside, which also reduced Ppw to 6 mm Hg. Phlebotomy and nitroprusside reduced the edema in excised lungs by 50% (P< 0.001), but Peep and albumin did not affect the edema. Pulmonary shunt decreased on Peep and increased on nitroprusside, and lung compliance was not different among the treatment groups, demonstrating that these variables are poor indicators of changes in edema. Cardiac output decreased during the treatment period in all but the nitroprusside group, where Ppw decreased and cardiac output did not. We conclude that canine oleic acid pulmonary edema is reduced by small reductions in hydrostatic pressure, but not by increased colloid osmotic pressure, because the vascular permeability to liquid and protein is increased. These results suggest that low pressure pulmonary edema may be reduced by seeking the lowest Ppw consistent with adequate cardiac output enhanced by vasoactive agents like nitroprusside. Further, colloid infusions and Peep are not helpful in reducing edema, so they may be used in the lowest amount that provides adequate circulating volume and arterial O(2) saturation on nontoxic inspired O(2). Until these therapeutic principles receive adequate clinical trial, they provide a rationale for carefully monitored cardiovascular manipulation in treating patients with pulmonary capillary leak.

Albumins↗