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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There has been no description of the hemodynamic dose-response relationship between halothane and sodium nitroprusside (SNP), although these drugs are used together frequently for induction of deliberate hypotension. Utilizing aortic root cannulation and thermister-tipped pulmonary artery catheterization, this relationship was studied in 6 beagles receiving a standard 100 microgram/kg infusion of SNP solution administered at 3 different infusion rates (5, 10, and 20 microgram/kg/min) while anesthetized with 3 different concentrations of halothane (0.5, 1, and 2%). Sodium nitroprusside infusion resulted in dose-related reductions in mean arterial pressure, systemic vascular resistance, and left ventricular stroke work. Increasing concentrations of halothane significantly potentiated the hypotensive effects of SNP. Cardiac output increase as the SNP infusion rate increased, whereas increasing the halothane concentration resulted in a reduction of cardiac output at each SNP infusion rate studied. Pulmonary artery wedge pressure was significantly reduced by SNP infusion at all 3 halothane concentrations, whereas mean pulmonary artery pressure was unchanged. Arterial pH fell in response to each SNP infusion, from 7.46 at the beginning of the study to 7.32 at the end (p less than 0.001). Sodium nitroprusside predictably induced hypotension during halothane anesthesia at the cost of a dose-related metabolic acidosis. Increasing the depth of halothane anesthesia afforded a greater percentage reduction in arterial pressure at each SNP infusion rate studied. Metabolic acidosis, however, developed no more rapidly at 2% halothane than it did at 0.5 or 1%.
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PMID:Increasing halothane concentrations reduce nitroprusside dose requirement. 3 Mar 40

The severity of mitral regurgitation is, in part, determined by aortic impedance to left ventricular outflow. Sodium nitroprusside acutely decreases regurgitant flow, but the importance of its dual vasodilating effects, the lowering of peripheral vascular resistance and increasing of venous capacitance, is unclear. We studied the hemodynamic response to intravenous hydralazine, which selectively acts on the arteriolar resistance bed, in 10 patients with severe mitral regurgitation. Hydralazine produced a 50% increase in forward stroke volume (22 +/- 2 to 33 +/- 3 ml/m2, P less than 0.001) and a 33% reduction in regurgitant stroke volume (40 +/- 6 to 27 +/- 6 ml/m2, P less than 0.001), with a resultant fall in pulmonary capillary wedge v wave and mean pressures. Unlike nitroprusside, it did not alter left ventricular end-diastolic volume or pressure. Oral hydralazine maintained this hemodynamic improvement for at least 48 hours and, in three patients, provided more sustained clinical improvement. We conclude that hydralazine, by virtue of its selective lowering of aortic impedance, reduces the amount of mitral regurgitation and thus may be a useful mode of interim or chronic therapy in selected patients.
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PMID:Beneficial effects of hydralazine in severe mitral regurgitation. 66 75

The influence of controlled hypotension (mean arterial pressure 60 mmHg) induced by sodium nitroprusside and trimethaphan on systemic circulation and myocardial oxygen consumption was studied in 7 anaesthetized closed chest dogs. The hypotensive effect of both drugs was primarily mediated by a reduction in total peripheral resistance. No change in cardiac output was observed. Stroke volume decreased in the presence of tachycardia. Left ventricular max dp/dt remained unaffected during sodium nitroprusside hypotension and was reduced by trimethaphan. Max dp/dt, load data and heart rate indicated that trimetaphan possesses negative inotropic properties. Sodium nitroprusside induced a hyperperfusion of the heart with a marked decrease in myocardial arteriovenous difference in oxygen. Myocardial oxygen consumption remained unchanged. Trimethaphan, on the other hand, induced only small increments in coronary blood flow and a rise in the arteriovenous difference in oxygen of the heart. This resulted in a higher myocardial oxygen consumption (+16%). Cardiac efficiency was lessened by trimethaphan and remained unaffected in the presence of sodium nitroprusside. As sodium nitroprusside neither affects myocardial oxygen consumption nor alters myocardial contractility, we conclude that sodium nitroprusside has advantages over trimethaphan in the management of controlled hypotension and in the therapy of hypertensive crisis and cardiogenic shock.
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PMID:[The effects of sodiumnitroprusside and trimethaphan induced hypotension on haemodynamics and myocardial oxygen consumption (author's transl)]. 125 27

The aims of this randomized study were (1) to determine if isoflurane is effective in controlling blood pressure during thoracic aortic cross-clamping, and (2) to compare its effects on hemodynamics and oxygen transport to those of sodium nitroprusside. Sodium nitroprusside (SNP group, n = 10) or isoflurane (ISO group, n = 10) was started 2 minutes before cross-clamping and was adjusted to maintain systolic arterial pressure as near as possible to preinduction values. The duration of thoracic aortic cross-clamping was 26 +/- 4 minutes in the SNP group and 30 +/- 4 minutes in the ISO group. Administration of isoflurance and sodium nitroprusside was stopped 2 minutes before unclamping. The same anesthetic technique using fentanyl, 6 micrograms/kg, flunitrazepam, 0.02 mg/kg, pancuronium, 0.1 mg/kg, and 50% N2O was used for all patients. At the time of clamping, either isoflurance (maximal expired concentration, 2.5% +/- 0.3%) or sodium nitroprusside (cumulative dose, 11.1 +/- 1.0 mg) was effective in maintaining the systolic blood pressure below 160 mm Hg, whereas the pulmonary capillary wedge pressure did not change. However, only SNP was able to bring the arterial pressure above the cross-clamp back to postinduction levels. During clamping, stroke index values were similar in both groups, but cardiac index increased only in patients receiving SNP. In both groups, at clamping and unclamping, PvO2 was higher than postinduction values, indicating that throughout the study the oxygen needs of the perfused area were adequately met. There was no evidence of acute left ventricular decompensation because pulmonary capillary wedge pressures did not abruptly increase, nor did pulmonary edema occur.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of isoflurane with sodium nitroprusside for controlling hypertension during thoracic aortic cross-clamping. 213 64

Adenosine receptor stimulation, such as by adenosine monophosphate (AMP), elicits systemic vasodilation that may be useful to control cardiac afterload during treatment of acute low-output cardiac failure. This study compared the hemodynamic effects of graded doses of sodium nitroprusside (SNP) with those of AMP when infused alone or in combination with the positive inotropic agent dopamine (DA) in anesthetized dogs. Both SNP (2-25 micrograms.kg-1.min-1) and AMP (200-2500 micrograms.kg-1.min-1) were effective vasodilators and reduced systemic vascular resistance and arterial pressure in a dose-dependent manner. Heart rate and cardiac index were increased by both agents. When compared at dosages that caused similar decreases in arterial pressure, cardiac index was increased more by AMP than by SNP. Also, AMP-induced vasodilation was associated with less tachyphylaxis. Sodium nitroprusside and AMP, at the dosages used, did not depress atrioventricular nodal conduction or antagonize DA-induced increases in renal blood flow. At equivalent decreases in mean arterial pressure, the increase from baseline in cardiac and stroke indices observed with AMP alone was further increased by the concomitant administration of DA. These results suggest that AMP and DA-AMP may offer significant advantages over SNP or DA-SNP in situations where elevation of cardiac output and reduction in afterload are required.
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PMID:Comparison of hemodynamic changes induced by adenosine monophosphate and sodium nitroprusside alone and during dopamine infusion in the anesthetized dog. 229 5

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.
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PMID:Differential hemodynamic and sympathoadrenal effects of sodium nitroprusside and hydralazine in hypertensive subjects. 242 68

We investigated the potential value of vasodilating therapy in critically ill patients with inappropriately low cardiac output during acute illness. In seven patients with low flow state during septic or postoperative state, sodium nitroprusside (20-100 micrograms/min) was compared with nicergoline (NIC) (0.5 to 2.5 mg/min), a new selective alpha 1-blocking agent with negative chronotropic action. Sodium nitroprusside (NP) decreased arterial pressure (from 90 +/- 5 to 68 +/- 5 mm Hg, p less than 0.01) and pulmonary artery balloon-occluded pressure from 20.3 +/- 3.1 to 15.4 +/- 2.8 mm Hg, p less than 0.01) and increased heart rate (from 110 +/- 11 to 120 +/- 13 beats/min, p less than 0.05) but failed to increase stroke volume (from 24.7 +/- 4.8 to 23.4 +/- 4.4 ml, NS). During NIC administration, a comparable decrease in systemic vascular resistance was associated with a significant increase in stroke volume (from 21.6 +/- 3.3 to 25.6 +/- 3.2 ml/m2, p less than 0.01) and cardiac output (CO) (from 2.4 +/- 0.3 to 2.7 +/- 0.3 L/min/m2, p less than 0.025), whereas the decrease in arterial pressure was less significant (from 91 +/- 8 to 84 +/- 7 mm Hg, p less than 0.05). Because NIC has no positive inotropic action, the most likely mechanism is that a baroreceptor-mediated increase in heart rate with NP was prevented by the negative chronotropic action of NIC. Both drugs adversely affected arterial blood oxygenation. By its unique property to decrease heart rate, NIC could represent a valuable vasodilating agent, especially in acute conditions.
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PMID:Afterload reduction in the critically ill: nicergoline versus sodium nitroprusside. 243 35

Hypertension is common following coronary artery bypass surgery. The safety of labetalol, a recently released combined alpha-1 and beta-adrenergic blocking agent for treatment of hypertension in this clinical situation is controversial. The authors compared the hemodynamic effects of labetalol with those of sodium nitroprusside (SNP) in 91 patients with good left ventricular function and equally severe coronary artery disease and in whom coronary artery bypass surgery had been just completed. They were anesthetized using fentanyl, diazepam, and enflurane. If hypertension developed postoperatively, patients were randomized to receive labetalol, 2 mg/min to a maximum of 300 mg (20 patients) or sodium nitroprusside in 0.5 micrograms.kg-1.min-1 increments by infusion (20 patients) to return blood pressure to normal. Compared with control values, labetalol brought about significant (P less than 0.05) reductions in heart rate, and cardiac index. No change was noted in stroke volume or systemic vascular resistance, but slight increases were found in central venous pressure and pulmonary capillary wedge pressure. Sodium nitroprusside treatment caused significant increases in heart rate and cardiac index while reducing diastolic blood pressure, central venous pressure, and pulmonary capillary wedge pressure. Stroke volume remained unchanged. Following the study period, blood pressure was controlled in all patients with SNP. Total doses of SNP in the 16 h following the study period were significantly less in the labetalol group (46.6 +/- 11.7 mg) versus (116.1 +/- 10.3 mg) in the SNP group (P less than 0.05). In this clinical circumstance, labetalol can be safe and effective for controlling hypertension, but its mechanism of achieving this effect varies from that for sodium nitroprusside.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intravenous labetalol versus sodium nitroprusside for treatment of hypertension postcoronary bypass surgery. 268 94

To determine the hemodynamic effects of a hypotensive dose of atrial natriuretic factor (ANF), a synthetic peptide containing 26 amino acids of endogenous rat ANF (Arg-Arg-Ser-Ser-Cys-Phe-Gly-Gly-Arg-Ile-Asp-Arg-Ile-Gly-Ala-Gln-Ser-Gly -Leu-Gly-Cys-Asn-Ser-Phe-Arg-Tyr-COOH) was studied in two groups of barbiturate anesthetized rats. In the first experiment, a 20-minute infusion of a hypotensive dose, 95 pmole/min i.v., of the synthetic ANF decreased mean arterial pressure (MAP) by 40 +/- 3 mm Hg from a baseline of 128 +/- 5 mm Hg, and cardiac output (CO) (microsphere method) by 7.8 +/- 1.8 ml/min/100 gm from a baseline of 23.5 +/- 1.3 ml/min/100 gm. Synthetic ANF did not significantly affect the total peripheral resistance (TPR) measured at the end of the 20-minute infusion. Sodium nitroprusside (SNP), infused at an equihypotensive dose of 20 micrograms/kg/min i.v., produced the same hemodynamic profile in seven other animals; in contrast, 0.3 mg/kg i.v. of hydralazine (n = 7) lowered MAP by 56 +/- 6 mm Hg and reduced TPR index by 3.0 +/- 0.6 mm Hg/ml/min/100 gm, but did not change CO. Other than an increase in coronary blood during SNF infusion, there were no significant changes in the distribution of cardiac output. Infusion of the saline vehicle had no significant effects on any of these parameters. The results of the second experiment in anesthetized rats confirmed that hypotensive doses of 40 and 100 pmole/kg/min i.v. lowered CO (dye dilution method) from a baseline of 33 +/- 6 to a minimum of 24 +/- 2 ml/min/100 gm (p less than 0.05) without affecting TPR. In addition, synthetic ANF did not significantly affect heart rate (HR) but it slightly reduced cardiac contractility (dp/dt50). These results suggest that the hypotensive dose of synthetic ANF reduced cardiac output, partially by diminishing stroke volume, and perhaps contractility.
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PMID:Cardiac and hemodynamic responses to synthetic atrial natriuretic factor in rats. 294 28

The influence of the piston-cassette pump fill stroke on the pharmacodynamic response to sodium nitroprusside was evaluated prospectively in 10 adult patients in the surgical intensive-care unit. Simultaneous analog recordings of blood pressure and fill stroke were made over three complete pump fill cycles in each patient. Sodium nitroprusside flow rates and concentrations were recorded throughout the data-collection period. Analysis was based on the maximum pressure obtained during the two-minute baseline period before a fill stroke (Pmax baseline), the pressure at the initiation of the fill stroke (P initial), and the maximum pressure obtained during the two-minute period after the fill stroke (Pmax postfill). The maximum systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean blood pressure (MBP) during the baseline and post-fill-stroke periods were significantly different. The mean (+/- S.D.) variability in pressure between the time periods Pmax baseline and Pmax postfill was 3.9 +/- 5.8 mm Hg for SBP (range, -8 to +16), 3.5 +/- 5.7 mm Hg for DBP (range, -7 to +13), and 3.6 +/- 5.6 mm Hg for MBP (range, -7 to +14). The likelihood of a pharmacodynamic change was inconsistent both between and within patients. Within patients the difference between cycles for the variability between time periods ranged from a minimum of 2 mm Hg to a maximum of 16 mm Hg for SBP, 2 mm Hg to 17 mm Hg for DBP, and 1 mm Hg to 17 mm Hg for MBP. The variability within the baseline period (Pmax baseline - P initial) in SBP was significantly greater than the variability between the time periods, while the differences for DBP and MBP were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of infusion pump fill-stroke flow interruption on response to sodium nitroprusside in surgical patients. 335 17


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