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 145 records · Page 8Linked to original sources
PubMed1976

Sodium nitroprusside: pharmacology, toxicology and therapeutics.

Sodium nitroprusside is a potent, effective, and readily reversible direct vasodilating agent. It is broken down by hemoglobin into cyanide, which is in part detoxified by liver and kidney to thiocyanate. Some cyanide, especially in nitroprusside- "resistant" individuals who need large amounts of the drug, appears to remain free to cause cyanide poisoning. Patients requiring inordinate amounts probably should not continue to receive the drug, although maximum dosage limits for long-term therapy are not established. Blood thiocyanate levels do not indicate the extent to which free cyanide is limiting oxygen utilization in essential tissue, nor do blood cyanide levels. Metabolic acidosis, elevated lactate levels, elevated lactate/pyruvate ratios, and elevated mixed venous blood oxygen content are at present the best indications of the presence of cyanide poisoning during nitroprusside administration. Nitroprusside appears useful for induction of hypotension during surgery, and for treatment of hypertensive emergencies from all causes, although continuance for more than a few days is probably unwise. The reductions of cardiac afterload and ventricular filling pressure by nitroprusside appear useful in treatment of severe myocardial failure or infarction, but studies of myocardial cyanide toxicity are needed before complete acceptance of this therapy is warranted. Initial dose rates between 0.5 and 1.5 mug/kg/min are recommended only as starting points for very careful titration. Total projected intra-operative dosage should be calculated as quickly as possible and should not exceed 3-3.5 mg/kg. It is hoped that future studies will reveal the maximum dose of nitroprusside that can safely be metabolized in a 24-hour period, and may indicate that cofactors of rhodanase such as thiosulfate, or cobalamins such as hydroxocobalamin, can be administered with nitroprusside to prevent cyanide poisoning.

Anesthesia, General↗
PubMed1998

[Treatment of the hypertensive response during coronary surgery: comparison of high-dose propofol to propofol with nitroprusside].

OBJECTIVE: To determine the efficacy of high doses of propofol for controlling hypertension during coronary surgery and to compared cardiovascular stability with propofol to that observed under lower doses of propofol with nitroprusside. PATIENTS AND METHODS: Forty patients were studied prospectively. The patients had good ventricular function and were scheduled for coronary surgery, randomized to two groups. Group P (n = 20) received 0.3 mg/kg propofol plus a 10 mg/kg/h perfusion. Hypertensive responses were treated with boluses of 0.3 mg/kg of propofol and progressive increases in the perfusion dose of 2.5 mg/kg/h at intervals of 2 minutes (maximum 15 mg/kg/h). If hypertension persisted it was treated with nitroprusside. Group N (n = 20) received propofol in perfusion at a dose of 8 mg/kg/h and hypertension was controlled directly with nitroprusside. During extracorporeal circulation, the propofol dose was reduced to 3 mg/kg/h in both groups and was adjusted in response to changes in arterial pressure, with nitroprusside added as needed. We recorded the number of patients becoming hypertensive during sternotomy and mediastinal dissection, the maximum doses of propofol and nitroprusside and the time taken to achieve control of hypertension. Arterial pressure and heart rate were recorded at intervals of one minute throughout the operation. RESULTS: Eight patients in group P and eleven in group N suffered hypertension (NS). Increasing the dose of propofol in group P controlled arterial hypertension in one patient. We found no significant differences between groups in amount of nitroprusside needed or time taken to bring episodes under control. Differences between the two groups in rates of intraoperative hypertension (65% in group P and 85% in group N) and hypotension (75% in group P and 55% in group N) and in duration of episodes were not statistically significant. CONCLUSIONS: Using high doses of propofol rather than moderate doses in combination with nitroprusside in coronary surgery does not improve control of either hypertension or hemodynamic stability.

Aged↗
PubMed1977

Sodium nitroprusside-induced hypothermia in mice.

The hypothermic response following sublethal doses (1.25, 2.5, and 5 mg/kg) of sodium nitroprusside was investigated in mice. The magnitude and duration of rectal temperature depression were shown to be dose related. Oral administration of nitroprusside (5 mg/kg) failed to alter rectal temperature significantly; subcutaneous, intraperitoneal, intravenous, and intracerebral injections at the same dosage level caused respective drops of 3.61, 3.65, 6.44, and 3.48 degrees. The degree of rectal temperature depression following nitroprusside (5 mg/kg ip) was dependent upon the ambient temperature. The time course of the effect of nitroprusside (5 mg/kg ip) on tail temperature was noted. A transient rise in tail temperature, which coincided with the onset of rectal temperature depression, was attributed to the vasodilatory effect of the drug. Tail temperature depression occurred at the peak and throughout the remainder of the rectal temperature response, suggesting that nitroprusside may decrease heat production. Body temperature depression via intracerebral administration, as well as pronounced sedation following nitroprusside injection, suggests a central component to the thermolytic response.

Administration, Oral↗
PubMed1994

The effect of intracoronary nitroprusside on cyclic GMP and regional mechanics is altered in a canine model of left ventricular hypertrophy.

Nitroprusside can produce negative inotropy by activating cGMP. We hypothesized that in left ventricular hypertrophy produced by aortic valve plication (LVH), control of myocardial work and metabolism by cGMP production would be altered in response to nitroprusside. In anesthetized open chest preparations using 9 LVH and 12 control dogs, nitroprusside (4 micrograms/kg/min) was infused into the left anterior descending coronary artery. The circumflex (CFX) region served as an internal control. Segment force (miniature gauge) and length (sonomicrometer) were measured in both regions. Segment work was calculated as the integrated products of local force and segment shortening. Regional myocardial O2 consumption was calculated from blood flow measurements (radioactive microspheres) and regional O2 saturations (microspectrophotometry). Radioimmunoassay was used to determine regional cGMP levels. In control dogs, nitroprusside significantly reduced force in the treated region (from 10.3 +/- 0.8 to 7.9 +/- 0.9 g) and segment work (from 1889 +/- 296 to 1254 +/- 252 g.mm/min). In the LVH group, regional work, force, and shortening did not change. In the CFX regions of both groups, regional myocardial mechanics, as well as regional myocardial O2 consumption, were not altered during nitroprusside infusion. Cyclic GMP levels were elevated to a much greater extent in the LVH animals (from 3.26 +/- 0.60 to 15.23 +/- 4.65 pmole/g) than in the control animals (from 2.16 +/- 0.60 to 2.89 +/- 0.56 pmole/g). Thus, in contrast to control myocardium, significant increases in cGMP production during nitroprusside infusion failed to produce negative inotropy in LVH. These findings suggest an uncoupling between the second messenger and systems controlling muscle contraction.

Animals↗
PubMed1983

The effects of glyceryl trinitrate, isosorbide dinitrate and sodium nitroprusside on haemodynamics, coronary blood flow and myocardial oxygen consumption - an experimental study.

The influences of glyceryl trinitrate, isosorbide dinitrate and sodium nitroprusside intravenously on haemodynamics, coronary circulation and myocardial oxygen consumption were investigated in closed chest dogs (n = 8). In an attempt to simulate heart failure the dogs received blood transfusion (15 ml/kg) in the presence of halothane-induced myocardial depression. All three nitrates reduced the loads for the left ventricle. With isosorbide dinitrate and sodium nitroprusside the preload and pulmonary pressure decreased to a greater extent than with glyceryl trinitrate. The haemodynamic results suggest that sodium nitroprusside is the favourable nitrate in left ventricular failure because it produces a balanced reduction in the ratio of pre- and afterload. Four micrograms/kg X min sodium nitroprusside induced marked coronary dilatation; glyceryl trinitrate had only a slight coronary vasodilating effect. With isosorbide dinitrate the myocardial blood flow remained well adapted to oxygen demand, the coronary vascular resistance did not change. Sodium nitroprusside produced a significant change of the transmural myocardial blood distribution-expressed as the epi/endocardial blood flow ratio. The ratio was increased by sodium nitroprusside, much more than by glyceryl trinitrate or isosorbide dinitrate.

Animals↗
PubMed2001

Remifentanil and controlled hypotension; comparison with nitroprusside or esmolol during tympanoplasty.

PURPOSE: To determine whether remifentanil, combined with propofol, could induce controlled hypotension, reduce middle ear blood flow (MEBF) measured by laser-Doppler flowmetry, provide a "dry" operative field, and could be compared with nitroprusside or esmolol combined with alfentanil and propofol. METHODS: Thirty patients undergoing tympanoplasty and anesthetized with 2.5 mg x kg(-1) propofol iv followed by a constant infusion of 120 microg x kg(-1) x min(-1), were randomly assigned in three groups to receive either 1 microg x kg(-1) remifentanil iv followed by a continuous infusion of 0.25 to 0.50 microg x kg(-1) x min(-1), or nitroprusside iv, or esmolol iv combined for the latter two groups with alfentanil iv. RESULTS: Controlled hypotension was achieved at the target pressure of 80 mmHg within 107 +/- 16, 69 +/- 4.4, 53.3 +/- 4.4 sec for remifentanil, nitroprusside and esmolol respectively. MEBF decreased by 24 +/- 0.3, 22 +/- 3.3, 37 +/- 3% and preceded the decrease in SABP, within 30 +/- 6.1, 11.2 +/- 3.1, 15 +/- 2.8 sec for remifentanil, nitroprusside and esmolol respectively. Remifentanil, and nitroprusside decreased MEBF autoregulation less than esmolol (0.36 +/- 0.1, 0.19 +/- 0.2, -0.5 +/- 0.2). Controlled hypotension was sustained in all three groups throughout surgery, and the surgical field rating decreased in a range of 80% in all three groups. Nitroprusside decreased pH and increased PaCO2. There were no postoperative complications in any of the groups. CONCLUSIONS: Remifentanil combined with propofol enabled controlled hypotension, reduced middle ear blood flow and provided good surgical conditions for tympanoplasty with no need for additional use of a potent hypotensive agent.

Adjuvants, Anesthesia↗
PubMed1979

Differences in hemodynamic effects of nitroprusside and prazosin in severe chronic congestive heart failure: evidence for a direct negative chronotropic effect of prazosin.

To compare the hemodynamic effects of prazosin and nitroprusside in patients with severe congestive heart failure, nine patients with heart failure refractory to conventional therapy received oral prazosin and intravenous nitroprusside administered so as to produce a similar decrease in left ventricular filling pressure in each patient. By this comparison, both drugs produced similar decreases in mean right atrial pressure, mean pulmonary arterial pressure and systemic and pulmonary vascular resistance. However, with nitroprusside, cardiac index increased more (+0.97 versus +0.73 liters/min per m2, P less than 0.01) and mean arterial pressure decreased less (-13.7 versus -18.3 mm Hg, P less than 0.05) than with prazosin. Both drugs produced similar changes in stroke volume index (+11.7 cc/beat per m2 with nitroprusside and +12.5 with prazosin) and stroke work index (+8.1 g-m/m2 with nitroprusside and +6.6 with prazosin). Therefore, the differences in the hemodynamic responses observed with the two agents were due to the significantly greater decrease in heart rate with prazosin (-8 beats/min) than with nitroprusside (-2 beats/min, P less than 0.05). These clinical data support experimental evidence suggesting that there is a significant negative chronotropic action of prazosin independent of its peripheral vascular effects.

Administration, Oral↗
PubMed1987

Comparison of esmolol and nitroprusside for acute post-cardiac surgical hypertension.

Because acute systemic hypertension early after cardiac surgery has been linked to catecholamine elevation, an open-label, randomized, crossover study was performed to compare the efficacy of esmolol, a new ultra-short-acting intravenous beta-blocking agent, to nitroprusside, the standard therapy. Controlled drug infusions to maximal dosage (esmolol, 300 micrograms/kg/min, and nitroprusside, 10 micrograms/kg/min) were titrated to achieve at least a 15% reduction in systolic pressure. The blood pressure (BP) endpoint was achieved with esmolol (within 29 +/- 14 minutes) in 18 of 20 patients (90%), compared with 19 of 20 (95%) with nitroprusside infusion (within 21 +/- 15 minutes, difference not significant [NS]). Systolic BP decreased from 170 +/- 13 to 136 +/- 12 mm Hg (mean +/- standard deviation) with esmolol and from 170 +/- 13 to 141 +/- 13 mm Hg with nitroprusside infusion (both p less than 0.05). Diastolic BP was reduced from 71 +/- 12 to 64 +/- 11 mm Hg with esmolol and from 71 +/- 12 to 52 +/- 13 mm Hg with nitroprusside infusion (both p less than 0.05). Esmolol infusion resulted in decreased heart rate, cardiac index and stroke volume index and increased right atrial pressure (all p less than 0.05), whereas nitroprusside infusion resulted in increased heart rate and cardiac index and decreased right atrial pressure, pulmonary arterial wedge pressure and systemic vascular resistance (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1983

Comparison of intravenous nitroglycerin and sodium nitroprusside in acute myocardial infarction.

Initial studies from our institution demonstrated beneficial anti-ischemic effects of short-term infusion of intravenous nitroglycerin in patients with acute myocardial infarction. At lower doses, nitroglycerin was shown to be principally a venodilator; at higher doses, a mixed venous and arterial dilating effect was demonstrated. The acute hemodynamic effects of nitroglycerin varied in the presence or absence of left ventricular failure; patients with the most severe degree of left ventricular dysfunction had the most beneficial hemodynamic effect. Similar differential effects have been demonstrated for nitroprusside in other studies. A comparison of the arterial vasodilating potency of nitroglycerin and nitroprusside in patients in whom acute hypertension develops following coronary artery bypass surgery revealed that equal lowering of arterial pressure and systemic vascular resistance could be demonstrated in 85 percent of the patients with comparable infusion rates. Review of previous clinical and laboratory studies in animals, in which the effects of nitroglycerin and nitroprusside were compared, in most cases revealed opposite effects on intercoronary collateral flow and, thereby, opposite effects on the severity of regional ischemia. Our recently completed randomized placebo-controlled clinical trial employing a 48-hour infusion of nitroglycerin demonstrated a higher incidence of significant improvement in abnormalities noted on scintigraphy when nitroglycerin treatment was initiated within 10 hours of the onset of symptoms. Beneficial effects of early nitroglycerin treatment have also been demonstrated in previous clinical trials. In similar studies, which utilized nitroprusside infusions in patients with acute myocardial infarction, some investigators found an increase in short-term mortality with early nitroprusside treatment whereas others found benefit. The uniformly favorable results of the clinical trials that utilized intravenous nitroglycerin, although not necessarily supporting its routine use in all patients, would support a preference for nitroglycerin over nitroprusside for the treatment of congestive heart failure and/or acute hypertension complicating acute myocardial infarction.

Aged↗
PubMed1981

Fetal toxicity of nitroprusside in the pregnant ewe.

Sodium nitroprusside, a direct-acting vasodilator, has been used to treat the hypertension associated with preeclampsia and eclampsia. Fatal cyanide intoxication has been reported during infusion of nitroprusside. We have investigated placental transfer and fetal toxicity of nitroprusside in the acute pregnant ewe model. A maternal intravenous infusion of nitroprusside solution was maintained at a rate sufficient to decrease mean maternal arterial pressure by 20% for 1 hour. Maternal and fetal levels of nitroprusside were in equilibrium at the 20 minute sample. Five of the eight animals exhibited tachyphylaxis to nitroprusside, and their fetuses died in utero with lethal levels of cyanide. No significant changes were observed in uterine blood flow.

Animals↗
PubMed1986

The involvement of catalytic site thiol groups in the activation of soluble guanylate cyclase by sodium nitroprusside.

Sodium nitroprusside, a potent activator of soluble guanylate cyclase, potentiated mixed disulfide formation between cystine, a potent inhibitor of the cyclase, and enzyme purified from rat lung. Incubation of soluble guanylate cyclase with nitroprusside and [35S]cystine resulted in a twofold increase in protein-bound radioactivity compared to incubations in the absence of nitroprusside. Purified enzyme preincubated with nitroprusside and then gel filtered (activated enzyme) was activated 10- to 20-fold compared to guanylate cyclase preincubated in the absence of nitroprusside and similarly processed (nonactivated enzyme). This activation was completely reversed by subsequent incubation at 37 degrees C (activation-reversed enzyme). Incorporation of [35S]cystine into guanylate cyclase was increased twofold with activated enzyme, while no difference was observed with activation-reversed enzyme, compared to nonactivated enzyme. Cystine decreased the activity of nonactivated and activation-reversed enzyme about 40% while it completely inhibited activated guanylate cyclase. Mg+2- or Mn+2-GTP inhibited the incorporation of [35S]cystine into nonactivated or activated guanylate cyclase. Also, diamide, a potent thiol oxidant that converts juxtaposed sulfhydryls to disulfides, completely blocked incorporation of [35S]cystine into nonactivated or activated guanylate cyclase. These data indicate that activation of soluble guanylate cyclase by nitroprusside results in an increased availability of protein sulfhydryl groups for mixed disulfide formation with cystine. Protection against mixed disulfide formation with diamide or substrate suggests that these groups exist as two or more juxtaposed sulfhydryl groups at the active site or a site on the enzyme that regulates catalytic activity. Differential inhibition by mixed disulfide formation of nonactivated and activated enzyme suggests a mechanism for amplification of the on-off signal for soluble guanylate cyclase within cells.

Animals↗
PubMed1995

Effect of nitroprusside on regional cerebral cyclic GMP, blood flow and O2 consumption in rat.

This investigation was conducted to test whether topical nitroprusside (NP), a cytosolic guanylate cyclase activator, would increase the level of cyclic GMP and alter O2 consumption or blood flow in the cerebral cortex of rats. Male Long-Evans rats were used in a control (n = 9), low dose NP (n = 13, 10(-3) M) or high dose NP (n = 12, 10(-2) M) group. Nitroprusside or saline was topically applied to the right side of the cerebral cortex and the left side was used as a control. The cyclic GMP level was determined in five rats in each group using a radioimmunoassay. In the other rats in each group, regional cerebral blood flow was measured by [14C]iodoantipyrine and regional arterial and venous O2 saturations were determined microspectrophotometrically. Nitroprusside significantly increased the cyclic GMP level from 21.4 +/- 12.0 pmol/g (contralateral cortex) to 52.2 +/- 36.7 pmol/g (NP treated cortex) in low dose nitroprusside group and from 19.9 +/- 22.6 pmol/g (contralateral cortex) to 58.5 +/- 15.1 pmol/g (NP treated cortex) in high dose nitroprusside group. High dose nitroprusside significantly increased cerebral blood flow from 80 +/- 11 ml.min-1.100 g (contralateral cortex) to 114 +/- 11 ml.min-1.100 g (NP treated cortex). However, there was no significant difference in O2 extraction and O2 consumption between the NP treated cortex and contralateral cortex in either the low or the high dose NP groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effects of sodium nitroprusside on cytosolic calcium level in vascular smooth muscle.

The inhibitory effect of sodium nitroprusside on the cytosolic Ca2+ level ([Ca2+]cyt), measured simultaneously with contraction by means of a fluorescence dye, fura-2, and on the 45Ca2+ uptake was tested in the isolated rat aortic smooth muscle. Norepinephrine increased muscle tension, 45Ca2+ uptake and [Ca2+]cyt. In a Ca2+-deficient solution, norepinephrine transiently increased muscle tension and [Ca2+]cyt. Sodium nitroprusside inhibited all changes induced by norepinephrine although the inhibition of [Ca2+]cyt was less than that of muscle contraction. Sodium nitroprusside also inhibited the high K+-induced contraction at concentrations higher than those needed to inhibit norepinephrine-induced contraction. Inhibition of the high K+induced contraction was accompanied by a small decrease in [Ca2+]cyt and a smaller decrease in 45Ca2+ uptake. Methylene blue antagonized, and M&B 22,948 potentiated the inhibitory effect of sodium nitroprusside. These results suggest that sodium nitroprusside has multiple sites of action. At relatively low concentrations, sodium nitroprusside could inhibit the Ca2+ influx and Ca2+ release. At relatively high concentrations, this inhibitor could also augment Ca2+ sequestration and decrease the sensitivity of contractile elements to Ca2+.

Animals↗
PubMed1986

Requirement for bivalent cations in the actions of insulin and sodium nitroprusside on metabolism in rat adipocytes.

The requirement for Ca2+ and Mg2+ in the actions of insulin and sodium nitroprusside on rat adipocyte metabolism was investigated: sodium nitroprusside, but not insulin, increased cGMP levels in cells incubated in the absence of Ca2+ and/or Mg2+; sodium nitroprusside and insulin are unable to increase the incorporation of [14C]glucose into triglycerides and [14C]leucine into proteins in the absence of Ca2+ and Mg2+; sodium nitroprusside and insulin showed antilipolytic actions in Ca2+- and Mg2+-free medium. We conclude that in the absence of Ca2+ and Mg2+, sodium nitroprusside and insulin have very similar regulatory properties on triglyceride, protein synthesis and adrenaline-stimulated lipolysis, but not on cGMP levels in rat adipocytes. This could provide evidence that omission of bivalent cations was inhibitory at more than one site, or that sodium nitroprusside mimics insulin's actions by another mechanism that does not involve cGMP.

Adipose Tissue↗
PubMed1981

Sodium nitroprusside inhibition of parathyroid hormone release is not mediated through cyclic GMP.

Sodium nitroprusside effected a rapid, dose-dependent increase in intracellular cGMP accumulation in freshly dispersed bovine parathyroid cells. The effect was half-maximal between 10(-4) and 3 X 10(-4)M, maximal at 3 X 10(-3)M nitroprusside and could be amplified (approximately 50%) by the addition of methylisobutylxanthine (4 X 10(-4)M). The dose-response characteristics were similar to those previously described for the inhibition of cAMP accumulation and PTH release by this agent. Neither dibutyryl cGMP (10(-3)M) nor 8'-bromo-cGMP (10(-3)M) mimicked the inhibitory effect of nitroprusside on cAMP accumulation or PTH release. Dose-dependent stimulation of guanylate cyclase was found in a particulate preparation of parathyroid cells; activity was maximal at 10(-4)M nitroprusside while higher concentrations appeared to inhibit the enzyme. Nitroprusside significantly reduced both (-)isoproterenol and guanine nucleotide-stimulated adenylate cyclase activity in the particulate preparation with maximum inhibition between 10(-3)-10(-2)M. cGMP concentrations as high as 10(-4)M did not affect agonist-stimulated cAMP synthesis. Thus, although the kinetic and dose-response characteristics of the nitroprusside effect on cGMP suggest a linkage to its previously described effects on cAMP and PTH secretion, no direct evidence was found to indicate a causal relationship between the two. Rather it would appear that the effects on the adenylate and guanylate cyclase enzymes occur in parallel, possibly the result of some common primary perturbation of cellular physiology.

Adenylyl Cyclases↗
PubMed1992

Use of nitroprusside to increase tissue temperature during local hyperthermia in normal and tumor-bearing dogs.

The present study investigates the effects of nitroprusside, a potent vasodilating agent, on tissue temperature during local hyperthermia in five normal and five tumor-bearing dogs. Caudal thigh muscles were heated in normal dogs and muscle temperatures were recorded during hyperthermia. Tumor-bearing dogs received two hyperthermia treatments during a course of radiation therapy. Temperatures were recorded in tumor and surrounding normal tissues. Mean arterial pressure was decreased by approximately 40-45% during nitroprusside infusion and was associated with a compensatory increase in heart rate and increases in tissue temperature. In normal dogs, muscle temperatures increased an average of 1.7 degrees C with nitroprusside administration. When nitroprusside was administered at the beginning of local hyperthermia to induce step-down heating, approximately 48% of the measured positions in caudal thigh muscle achieved a temperature greater than or equal to 43 degrees C, sufficient to induce step-down heating, during the hyperthermia episode. In tumor-bearing dogs, there was a significant increase in tumor and normal tissue temperatures during nitroprusside administration. Estimated T90 and T50 descriptors increased by 0.9 degrees C and 1.6 degrees C, respectively, for tumor tissue and by 0.4 degrees C and 1.2 degrees C, respectively, for normal tissue. Despite the increase in normal tissue temperatures no toxicity was observed in these dogs. Nitroprusside may be a useful agent for manipulation of tumor temperatures during the entire hyperthermia treatment or for a short time period at the initiation of treatment to induce step-down heating.

Animals↗
PubMed1990

Effects of nitroprusside on transmitral flow velocity patterns in extreme heart failure: a combined hemodynamic and Doppler echocardiographic study of varying loading conditions.

To explore the mechanisms of change of left ventricular diastolic filling associated with preload and afterload reduction, the influence of nitroprusside on the transmitral flow velocity pattern, pulmonary capillary wedge pressure and left ventricular pressure interaction was studied in 11 patients with end-stage heart failure. Pulsed Doppler echocardiographic recordings of mitral inflow were obtained with simultaneous high fidelity left ventricular and phase-corrected pulmonary capillary wedge pressure recordings before and during levels of nitroprusside infusion. With nitroprusside, left ventricular systolic and end-diastolic pressures decreased by 14% and 41% (p less than 0.05, p less than 0.05), respectively, and cardiac output increased by 67% (p less than 0.05). The pulmonary capillary wedge-left ventricular crossover pressure decreased by 41% (p less than 0.05), but the time constant of isovolumetric left ventricular pressure decrease T was insignificantly changed. Isovolumetric relaxation time and acceleration and deceleration times of the early diastolic filling wave were significantly prolonged with nitroprusside infusion (p less than 0.05, p less than 0.05 and p less than 0.05, respectively). Peak early diastolic filling velocity was maintained (65 +/- 11 to 62 +/- 13 cm/s, p = NS) in spite of the decreased absolute crossover pressure. Changes in peak early diastolic filling velocity correlated weakly with changes in the crossover pressure (r = 0.48, p less than 0.05) and correlated better with the crossover to left ventricular minimal pressure difference (r = 0.78, p less than 0.05). Peak early diastolic filling velocity appears to be most affected by the early diastolic pulmonary capillary wedge to left ventricular pressure difference rather than the absolute pulmonary capillary wedge pressure. The lack of peak flow velocity change during nitroprusside infusion could be explained by either the associated decrease in left ventricular minimal pressure or downward shift of left ventricular diastolic pressure by the same amount as the decrease in pulmonary capillary wedge pressure. This may reflect a reduction of external constraint to ventricular distensibility produced by a reduction in filling volume in patients with a markedly dilated ventricle. Thus, a prolonged early diastolic filling period and preserved peak early diastolic filling velocity in spite of decreased left ventricular filling pressure and constant relaxation rate are associated with the beneficial effects of nitroprusside on left ventricular function in patients with severe congestive heart failure.

Blood Flow Velocity↗
PubMed1991

Comparison of nicardipine and sodium nitroprusside in the treatment of paroxysmal hypertension following aortocoronary bypass surgery.

In an open, randomized, multicenter trial, intravenous nicardipine was compared with sodium nitroprusside in 74 patients with hypertension (mean arterial pressure [MAP] greater than or equal to 100 mm Hg) following coronary artery bypass surgery. Nicardipine was administered as a 2.5- to 12.5-mg bolus followed by a 2 to 4 mg/h infusion, and nitroprusside as a 0.5 to 6.0 micrograms/kg/min infusion. The aim was to reduce MAP to less than 90 mm Hg within 50 minutes and maintain it stable at 85 +/- 5 mm Hg. Nicardipine was effective in 35 of 38 patients (92%), and nitroprusside in 29 of 36 (81%) (NS). The decrease in MAP was not statistically different, but time until reaching the therapeutic end-point was shorter with nicardipine (P less than 0.01). Significant differences follow: increase in heart rate and decreases in mean pulmonary artery, right atrial, and pulmonary capillary wedge pressures were more marked with nitroprusside (P less than 0.01 and P less than 0.05, respectively), whereas elevation of cardiac index and depression of systemic vascular resistance were more marked with nicardipine (P less than 0.01 and P less than 0.05, respectively). Postreduction MAP was more stable with nicardipine, 51% +/- 24% of readings falling within the range 85 +/- 5 mm Hg versus 41% +/- 18% on nitroprusside (P = 0.058). Dose adjustment during the following 24 hours was less frequent with nicardipine, 1.1 +/- 1.6 versus 2.7 +/- 2.6 (P less than 0.01). Transfused blood volume was lower with nicardipine (924 +/- 644 mL) than nitroprusside (1,306 +/- 901 mL) (P = 0.08), despite similar postoperative blood losses.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗