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Renal and hemodynamic effects of intravenous fenoldopam versus nitroprusside in severe hypertension.

The renal and hemodynamic effects of intravenously administered fenoldopam mesylate, a novel dopamine-1 receptor agonist, were compared with those of sodium nitroprusside in 28 patients (18 male; 26 black, two white; average age, 49 +/- 3 years) with an average blood pressure of 219/137 mm Hg, most of whom presented with acute target organ damage. Fenoldopam and nitroprusside lowered blood pressure safely to an average pressure of 176/105 mm Hg; highly significant dose-response relations were found for the 13 patients receiving fenoldopam and the 15 receiving nitroprusside. Volume and sodium, potassium, and creatinine concentrations were measured in freely voided urine specimens both before and during intravenous therapy. In the fenoldopam-treated patients, there were significant increases in urinary flow (92 +/- 21 to 168 +/- 37 ml/hr, p less than 0.003), sodium excretion (227 +/- 73 to 335 +/- 90 mu eq/min, p less than 0.001), and creatinine clearance (70 +/- 11 to 93 +/- 13 ml/hr, p less than 0.003). In the nitroprusside-treated group, however, all these parameters decreased, but not significantly. For direct comparison of the two agents, the increments in urinary flow rate (+76 +/- 20 vs. -16 +/- 15 ml/hr, fenoldopam vs. nitroprusside), sodium excretion (+109 +/- 28 vs. -39 +/- 28 mu eq/min), and creatinine clearance (+23 +/- 6 vs. -11 +/- 7 ml/min) were significantly greater (p less than 0.001 for each) in the fenoldopam-treated group. Significant differences were also obtained when these parameters were calculated as percentage increase over baseline. Fenoldopam and nitroprusside are effective therapies for severe, accelerated, or malignant hypertension, but fenoldopam had additional salutary renal effects in these patients.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Acute effects of nitric oxide on left ventricular relaxation and diastolic distensibility in humans. Assessment by bicoronary sodium nitroprusside infusion.

BACKGROUND: In isolated mammalian cardiomyocytes, papillary muscle preparations, and ejecting hearts, nitric oxide (NO) or other cyclic GMP-elevating interventions increase diastolic cell length and reduce peak contractile performance by hastening onset of myocardial relaxation. In the present study, the effect of NO on left ventricular (LV) relaxation and diastolic distensibility was investigated in humans. METHODS AND RESULTS: The NO donor substance sodium nitroprusside was infused during cardiac catheterization in the global coronary bed of the LV of patients (n = 13) investigated for chest pain who were without evidence of obstructive coronary artery or other cardiac disease. Sodium nitroprusside was infused intracoronarily at a dosage (< or = 4 micrograms/min) that was previously shown to be devoid of systemic effects when infused into the brachial artery to investigate the reactivity of the forearm vascular bed. The effect of this global intracoronary infusion of the NO donor sodium nitroprusside was assessed by sequential LV angiograms and tip-micromanometer pressure recordings. During global intracoronary nitroprusside infusion, there was a decrease in heart rate from 78 +/- 11 to 76 +/- 12 beats per minute (P < .05), in LV peak systolic pressure from 161 +/- 18 to 146 +/- 18 mm Hg (P < .001), and in time to onset of LV relaxation (interval from Q wave on the ECG to LV dP/dtmin) from 432 +/- 36 to 419 +/- 36 milliseconds (P < .01). In 7 patients in whom adequate sequential LV angiograms could be obtained, LV end-diastolic volume increased from 158 +/- 34 to 165 +/- 40 mL (P < .05), whereas LV end-diastolic pressure fell from 18 +/- 5 to 12 +/- 3 mm Hg (P < .02), and in 5 of these 7 patients, a downward shift of the diastolic LV pressure-volume relation was observed. In 5 patients, a right atrial infusion of sodium nitroprusside was performed either before (n = 2) or after the global intracoronary infusion. The decrease in LV peak systolic pressure observed during right atrial infusion was significantly smaller (P < .01) than during global intracoronary infusion. CONCLUSIONS: The present study reveals reduced LV pressure development, an LV relaxation-hastening effect, and improved LV diastolic distensibility during global intracoronary infusion of the NO donor substance sodium nitroprusside. These effects appeared to be unrelated to systemic vasodilation or to pericardial constraint and could be explained by a direct myocardial effect of NO, probably through activation of guanylyl cyclase to increase cyclic GMP or through modification of other cellular proteins.

Cardiac Catheterization↗

Effect of sodium-potassium pump inhibitors and membrane-depolarizing agents on sodium nitroprusside-induced relaxation and cyclic guanosine monophosphate accumulation in rat aorta.

The purpose of this study was to investigate the relationship between sodium nitroprusside-induced relaxation, inhibition of the sodium-potassium pump, and cyclic guanosine monophosphate. Exposure of rat thoracic aorta to ouabain, or potassium- or magnesium-free Krebs-Ringer bicarbonate solution, procedures which presumably inhibit the sodium-potassium pump, or to potassium chloride or tetraethylammonium, membrane-depolarizing agents, inhibited relaxation to nitroprusside. These conditions had little or no effect on the elevated cyclic guanosine monophosphate levels at a concentration of nitroprusside (0.1 microM) that relaxed norepinephrine contracted tissues by 80%. However, at a maximum relaxant concentration of nitroprusside (1.0 microM), these conditions decreased the elevation of cyclic guanosine monophosphate. The inhibition of elevated cyclic guanosine monophosphate levels was independent of the endothelium, extracellular calcium, and the cyclic guanosine monophosphate phosphodiesterase inhibitor, M&B 22,948. The inhibitory effects of ouabain and of potassium- and magnesium-free solution on the increased levels of cyclic guanosine monophosphate caused by 1.0 microM nitroprusside were abolished when tissues were incubated without norepinephrine, or with norepinephrine in the presence of the alpha-adrenergic blocker, phentolamine. In contrast, a beta-adrenergic blocker, propranolol, had no effect on the ouabain-induced inhibition of elevated cyclic guanosine monophosphate levels, with norepinephrine present. These results are consistent with the hypothesis that membrane events regulate cyclic guanosine monophosphate synthesis. At nitroprusside concentrations greater than 0.1 microM, the formation of cyclic guanosine monophosphate appears to be coupled to the status of the smooth muscle cell membrane and integrity of the sodium-potassium pump.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Influence of nitroprusside on cerebral pressure autoregulation.

The authors studied 10 cats to assess the question of abolition of cerebral autoregulation attendant on the use of nitroprusside for hypotensive anesthesia. After the establishment of stable base line parameters, a continuous infusion of sodium nitroprusside was begun in a dose sufficient to maintain a mean systemic arterial pressure of 65 mm Hg. Infusion was continued for incremental periods of 30 seconds to 10 minutes, increasing the time of infusion by 30 seconds after each subsequent trial. At 10 seconds after the cessation of nitroprusside administration, intravenous dopamine was infused to raise the systemic arterial pressure to a mean of 100 mm Hg, and the subsequent response in intracranial pressure was recorded in each instance. In no animal was a loss of cerebral autoregulation noted when the nitroprusside infusion was maintained for 3 minute or less. When the infusion was maintained for 4 minutes or longer, cerebral autoregulation was lost in each animal, and the length of time to return of cerebral autoregulation correlated with the duration of nitroprusside infusion. Sodium nitroprusside disturbs the integrity of cerebral pressure autoregulation, and the onset and extent of this disturbance is a dose-dependent phenomenon.

Animals↗

Vasodilator therapy during coronary artery surgery. Comparison of nitroglycerin and nitroprusside.

Intraoperative hypertension is a common problem in patients undergoing myocardial revascularization. Twenty patients who developed acute hypertension after sternotomy were studied. Ten patients received three doses of intravenous nitroglycerin (32, 64, and 96 mcg. per minute), and 10 patients received nitroprusside, (20, 40, and 60 mcg. per minute). All patients were anesthetized with morphine, diazepam, nitrous oxide, oxygen, and pancuronium bromide. Five patients in each group also received enflurane. The study compared the effects of nitroglycerin and nitroprusside on systemic hemodynamics, myocardial oxygen supply/demand relationships, and ischemic changes on the electrocardiogram. Both drugs decreased preload and afterload in a dose-related manner. Heart rate increased significantly only with the largest dose of each drug. Myocardial oxygen demand was decreased significantly by both drugs, while the coronary perfusion pressure was decreased more by nitroprusside. Both nitroglycerin and nitroprusside improved left ventricular performance. Nitroglycerin improved ST-segment depression in eight of 10 patients; while nitroprusside improved the ST segments in six patients, and worsened the ST segments in three patients. None of the nitroglycerin group had worsening of the electrocardiographic ST segments. These findings demonstrate that both drugs can control intraoperative hypertension and can decrease myocardial oxygen demand. Nitroglycerin was shown to improve ischemic changes on the electrocardiogram more often than nitroprusside.

Adult↗

Sodium nitroprusside-induced cyanide intoxication and prevention with sodium thiosulfate prophylaxis.

Sodium nitroprusside is an antihypertensive agent used frequently in the critical care setting. Recently, the Food and Drug Administration (FDA) published a report that led to a labeling change emphasizing the pharmacokinetics of nitroprusside with metabolism to highly toxic cyanide. Although evidence validates that cyanogenesis occurs with nitroprusside administration, prevention and treatment of cyanide poisoning is rarely instituted in clinical practice. Simultaneous infusion of thiosulfate with nitroprusside provides the sulfur donor necessary to prevent cyanide accumulation. Cyanide combines with thiosulfate to form the less toxic sodium thiocyanate, which is then excreted. A 10:1 ratio of nitroprusside to thiosulfate in the infusion eliminates the possibility of cyanide intoxication without altering the efficacy of nitroprusside.

Antidotes↗

Postoperative hypertension: a comparison of diltiazem, nifedipine, and nitroprusside.

In previous studies, the treatment of postoperative hypertension with sodium nitroprusside induced ischemic metabolism without a decrease in coronary sinus blood flow. In contrast, the calcium antagonists diltiazem and nifedipine reduce blood pressure and may improve myocardial metabolism. A prospective randomized trial was performed in 62 patients, in whom hypertension developed (mean arterial pressure greater than 95 mm Hg) after coronary bypass procedures, to compare diltiazem (n = 22), nifedipine (n = 20), and nitroprusside (n = 20). All three agents reduced blood pressure equally (p less than 0.0001, by analysis of variance). Heart rate decreased with diltiazem (p = 0.006) but increased with nifedipine and nitroprusside (p less than 0.05). Left ventricular diastolic function (the relation between left atrial pressure and left ventricular end-diastolic volume) was not changed with the three drugs. Systolic function (the relation between systolic blood pressure and left ventricular end-systolic volume) was depressed with diltiazem (p = 0.05 by analysis of covariance) and nifedipine (p = 0.05) but not with nitroprusside. Myocardial performance (the relation between left ventricular stroke work index and end-diastolic volume) was depressed most by diltiazem (p = 0.001 by analysis of covariance), and to a lesser extent with nifedipine (p = 0.03), but not with nitroprusside. Myocardial lactate flux in response to the stress of atrial pacing decreased with nitroprusside but not with diltiazem or nifedipine (p = 0.03 by analysis of variance). Diltiazem and nifedipine are effective agents for treating postoperative hypertension after coronary artery bypass operations.

Clinical Trials as Topic↗

Comparison of intraoperative nitroprusside unloading in mitral and aortic regurgitation.

To compare the hemodynamic effect of vasodilator therapy on different regurgitant lesions, we infused sodium nitroprusside intraooperatively in 12 patients with mitral regurgitation and 15 with aortic regurgitation. During the critical period preceding establishment of cardiopulmonary bypass, both groups had developed intense vasoconstriction and cardiac decompensation. All demonstrated improved cardiac function with vasodilator therapy; however, the degree of improvement with nitroprusside differed in the two groups. Stroke volume increased 10 ml. per beat per meter squared in those patients with aortic regurgitation and only 6 ml. per beat per meter squared in those with mitral regurgitation (p less than 0.05). The percent increase in stoke volume induced by nitroprusside was inversely correlated to the preoperative left ventricular ejection fraction (r = 0.44, p less than 0.02). Patients with aortic regurgitation had lower preoperative left ventricular ejection fractions than those with mitral regurgitation (0.53 versus 0.63, p less than 0.02). Therefore, we conclude that patients with aortic regurgitation derived greater intraoperative hemodynamic benefit from unloading with nitroprusside, because they came to surgery with greater impairment of left ventricular contractility. Although nitroprusside improved cardiac function in both groups, only the patients with aortic regurgitation achieved normal pulmonary artery pressure (17 torr) and pulmonary vascular resistance (2.1 units) as a result of unloading. Those with mitral regurgitation continued to have pulmonary hypertension (28 torr) and increased pulmonary vascular resistance (3.9 units) despite vasodilator therapy. Thus the data suggest that patients with mitral regurgitation derived less hemodynamic benefit from intraoperative nitroprusside therapy because they were also limited by right ventricular dysfunction and a less responsive pulmonary vasculature.

Adult↗

Properties of purified soluble guanylate cyclase activated by nitric oxide and sodium nitroprusside.

Highly purified rat lung soluble guanylate cyclase was activated with nitric oxide or sodium nitroprusside and the degree of activation varied with incubation conditions. With Mg2+ as the action cofactor, about 2- to 8-fold activation was observed with nitric oxide or sodium nitroprusside alone. Markedly enhanced activation (20-40 fold) was observed when 1 muM hemin added to the enzyme prior to exposure to the activating agent. The activation with hemin and sodium nitroprusside was prevented in a dose-dependent manner by sodium cyanide. The level activation was also increased by the addition of 1 mM dithiothreitol, but unlike hemin which had no effect on basal enzyme activity, dithiothreitol led to a considerable increase in basal activity. Activated guanylate cyclase decayed to basal activity within one hour at 2 degrees C and the enzyme could be reactivated upon re-exposure to nitroprusside or nitric oxide. Under basal conditions, Michaelis-Menten kinetics were observed, with a Km for GTP of 140 muM with Mg2+ cofactor. Following activation with nitroprusside or nitric oxide, curvilinear Eadie-Hofstee transformations of kinetic data were observed, with Km's of 22 MuM and 100 MuM for Mg-GTP. When optimal activation (15-40 fold) was induced by the addition of hemin and nitroprusside, multiple Km's were also seen with Mg-GTP and the high affinity form was predominant (22 MuM). Similar curvilinear Eadie-Hofstee transformations were observed with Mn2+ as the cation cofactor. These data suggest that multiple GTP catalytic sites are present in activated guanylate cyclase, or alternatively, multiple populations of enzyme exist.

Animals↗

Effects of acetylcholine and nitroprusside on cGMP-dependent protein kinase in the perfused rat heart.

The effects of acetylcholine and sodium nitroprusside on the activity of cGMP-dependent protein kinase were studied in the perfused rat heart. Acetylcholine produced a dose-dependent increase in cGMP levels and cGMP-dependent protein kinase activity, and reduced the force of contraction. Both acetylcholine and sodium nitroprusside produced rapid increases in cardiac cGMP, with nitroprusside being the more potent agent. Only acetylcholine, however, raised the activity ratio of the cGMP-dependent protein kinase and decreased the force of contraction. Whereas acetylcholine and nitroprusside were slightly additive in their effects on total cGMP levels, the increase in the activity ratio of the cGMP-dependent protein kinase and the decrease in the force of contraction produced by acetylcholine were unchanged by nitroprusside. The results suggest that the cGMP produced by acetylcholine, but not nitroprusside, was coupled to protein kinase activation in this tissue.

Acetylcholine↗

[The use of sodium nitroprusside (Nipruton) in ischemia-related acute heart insufficiency].

By controlled vasodilation with nitroprusside sodium we succeed in improving the negative haemodynamic effects of the pumping insufficiency in myocardial ischamia. Increased filling pressures decrease, volumes of output increase in clearly decreased oxygen consumption of the myocardium. The influence on the time volume of the heart depends on the height and reaction of the filling pressure on nitroprusside sodium. In normal LVEDP the time volume of the heart decreases by nitroprusside sodium. The local function of the heart may clearly be improved under nitroprusside sodium in ischaemia. Altogether the hitherto got results in man are not homogeneously interpreted. Problems result from in form of therapy necessary frequent controls of the filling pressures and volumes of output as well as from the possible decrease of the time volume of the heart and the critical reduction of the perfusion pressure. According to own results of experiments on animals the sequelae of ischaemia may be reduced under the infusion of nitroprusside sodium. The restricted regional function of the heart is particularly improved. An obligatory judgment concerning the temporarily restricted use of nitroprusside sodium in the pumping insufficiency conditioned by ischaemia is not yet possible. A complicating effect have the individually different dose-effect-relations as well as not foreseeable haemodynamic results as a sequel of the basic disease in the complicated myocardiac infarction which is to be regarded as indication.

Animals↗

The haemodynamic effects of sodium nitroprusside following cardiopulmonary bypass: a clinical study.

Measurements of cardiac index were made in 18 patients (14 male and 4 female) preoperatively and thereafter during a 12-hour period immediately following coronary artery bypass grafting for stable angina pectoris. Patients with evidence of impaired left ventricular function were not included in the study. Individuals were allocated randomly to one of two groups. The first group received sodium nitroprusside as a constant, variable dose infusion during the post bypass study period (nitroprusside group). The second group received no nitroprusside (control group). The operative and postoperative management of these patients was otherwise identical. Following bypass, both groups showed a gradual drop in cardiac index with an associated increase in peripheral vascular resistance. In the control group, the mean cardiac index fell below the mean preoperative value. In the nitroprusside group, however, the mean cardiac index always remained above the mean preoperative level for the group, the differences between the groups being statistically highly significant at 1 1/2 hours postoperatively (p less than .005) and still significant at 3 hours postoperatively (p less than .05). The subsequent rise in cardiac index over the next 9 hours was more rapid in the nitroprusside treated patients and left ventricular function was better as demonstrated by a consistently higher mean cardiac index for any given left ventricular filling pressure. It is concluded that nitroprusside increases cardiac output and improves left ventricular function in the early postoperative period following cardiopulmonary bypass.

Blood Pressure↗

Treatment of postoperative hypertension after coronary artery bypass surgery. Double-blind comparison of intravenous isradipine and sodium nitroprusside.

BACKGROUND: Hypertension commonly occurs after cardiac surgery and requires therapy to prevent the potentially deleterious effects. METHODS AND RESULTS: After coronary artery bypass graft surgery (CABG), 177 patients with elevated blood pressure > or = 90 mm Hg during the initial 6-hour postsurgical period were selected for this random blinded, parallel study to receive intravenous infusions of either isradipine (n = 90) or sodium nitroprusside (n = 87). Isradipine produced a statistically significant decrease in mean arterial pressure (MAP, delta-23 mmHg) during a 90-minute treatment period. Target MAP (< or = 85 mmHg or a decrease of 10 mmHg, if baseline MAP was between 90 and 95 mmHg) was achieved in 94% of patients 30 minutes after initiation of isradipine infusion (total mean dose, 411 micrograms); target MAP was achieved in 75% of nitroprusside-treated patients (total mean dose, 1708 micrograms). The mean time to control MAP was 18 minutes for isradipine compared with 24 minutes for nitroprusside. Global smoothness in MAP control was graded on a scale of 0 (not controlled) to 5 (excellent). Approximately 76% of isradipine-treated patients received a rating of > or = 3 (mean score, 3.5); 40% of the sodium nitroprusside-treated patients achieved a score of > or = 3 (mean score, 2.0). Both isradipine and nitroprusside produced statistically significant reductions in systolic and diastolic blood pressures, a decrease in systemic vascular resistance, and increases in heart rate, cardiac index, and stroke volume index. Isradipine produced no significant decreases in pulmonary artery occlusion wedge pressure compared with nitroprusside. CONCLUSIONS: Intravenous isradipine was effective and well tolerated in patients with hypertension after CABG and offers an additional therapeutic option to treat patients after cardiac surgery.

Coronary Artery Bypass↗

Pulmonary vasodilation after heart transplantation. A comparison among prostacyclin, sodium nitroprusside, and nitroglycerin on right ventricular function and pulmonary selectivity.

The aim of this study was to compare the effects of prostacyclin on central hemodynamics and right ventricular function to the more widely used vasodilators, sodium nitroprusside and nitroglycerin, and to investigate whether prostacyclin is more selective to the pulmonary vascular bed compared to sodium nitroprusside and nitroglycerin in patients after heart transplantation. Hemodynamic measurements were made after the operation in the intensive care unit with a pulmonary artery fast-response ejection fraction/volumetric thermodilution catheter. The aim was to maintain mean arterial pressure around 70 mm Hg with each drug. After a 10-minute infusion of each drug at a stable infusion rate, central hemodynamic variables and right ventricular end-diastolic volume, end-systolic volume, and ejection fraction were measured or derived in triplicate. The average infusion rates of sodium nitroprusside, nitroglycerin, and prostacyclin were 3.3 +/- 1.7 micrograms/kg/min, 6.6 +/- 1.8 micrograms/kg/min, and 12.4 +/- 1.7 ng/kg/min, respectively. Cardiac output, stroke volume, right ventricular end-diastolic volume, and central filling pressures were highest for prostacyclin compared to both nitroglycerin and sodium nitroprusside. Pulmonary vascular resistance was lower for prostacyclin compared to nitroglycerin but was comparable to that of sodium nitroprusside. Systemic vascular resistance was lowest for prostacyclin compared to both sodium nitroprusside and nitroglycerin. The pulmonary vascular resistance/systemic vascular resistance ratio used as an index of pulmonary selectivity did not differ between the vasodilators. The right ventricular ejection fraction did not differ among the three drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Nitroprusside selectively reduces ventricular preload in the stage 21 chick embryo.

OBJECTIVE: Embryonic cardiovascular function is dynamically regulated at the tissue level. Nitric oxide (NO) regulates vascular tone and influences cardiovascular function in neonatal and mature circulations. However, the role of NO in regulating embryonic cardiovascular function is undefined. We hypothesized that NO released from nitroprusside alters embryonic vascular tone with secondary effects on ventricular function. METHODS: We measured ventricular pressure and calculated ventricular volume from area using ellipsoid geometry for 180 s after suffusion of 0.0, 0.1, 1.0, or 2.5 micrograms of nitroprusside in 10 microliters of KHB buffer, or after acute venous hemorrhage in stage 21 chick embryos (n > or = 8 per group). We plotted pressure-volume loops and analyzed standard parameters of cardiovascular function by ANOVA, regression analysis, and ANCOVA. RESULTS: Following nitroprusside, heart rate was unchanged, end-diastolic volume (EDV), stroke volume (SV), and end-systolic pressure decreased (P < 0.05 at 180 s). For 1.0 microgram of nitroprusside, EDV decreased by 27 +/- 6%, SV decreased by 36 +/- 6%, and end-systolic pressure decreased by 28 +/- 3%. The EDV vs. SV relationship was unchanged with the exception of the 2.5 micrograms nitroprusside dose. Arterial elastance was unchanged with the exception of the 2.5 micrograms nitroprusside dose. The EDV vs. SV relationship and arterial elastance during preload reduction suggest that ventricular afterload did not decrease following NO. CONCLUSIONS: In contrast to the mature circulation, NO reduced preload without decreasing ventricular afterload. Thus, vasoactive agents may have unique roles in the regulation of cardiovascular structure and function during embryogenesis.

Animals↗

Effect of sodium nitroprusside on cerebral haemodynamics during cross-clamping of the descending thoracic aorta in pigs.

OBJECTIVE: To assess the effect of sodium nitroprusside on cerebral haemodynamics during cross-clamping of the descending thoracic aorta in pigs. DESIGN: Non-randomised controlled animal study. SETTING: University hospital, Norway. MATERIAL: 17 Pigs. INTERVENTIONS: Cross-clamping of the descending thoracic aorta for 30 minutes. In 8 pigs sodium nitroprusside was given to prevent proximal hypertension (sodium nitroprusside group); 9 pigs were given no sodium nitroprusside (control group). MAIN OUTCOME MEASURES: Intracerebral pressure, sagittal sinus pressure, cerebral flux, and internal carotid artery blood flow. RESULTS: Intracerebral pressure, sagittal sinus pressure, and cerebral flux increased in both groups during cross-clamping of the descending thoracic aorta. There were no differences between the groups in these variables despite significantly lower mean proximal aortic pressure in the sodium nitroprusside group. CONCLUSIONS: Sodium nitroprusside did not affect intracerebral pressure, sagittal sinus pressure, or cerebral flux during cross-clamping of the descending thoracic aorta. Increased cerebral blood flow rather than venous congestion is the most likely cause of increased intracranial pressure during cross-clamping of the descending thoracic aorta.

Animals↗

Comparison of intravenous nifedipine and sodium nitroprusside for treatment of acute hypertension after cardiac surgery.

BACKGROUND: The present study was designed to compare the hemodynamic effects of nifedipine and sodium nitroprusside, intravenously administered to control acute systemic hypertension in the immediate postoperative period after open heart surgery. METHODS: The study was carried out on 16 patients who developed acute systemic hypertension, defined as mean systemic arterial pressure (MAP) values above 90 mmHg, within the first hour after ICU admission, which followed cardiac surgery for valvular and coronary disease. After control measurements during the hypertensive status, each patient was treated by alternating infusions of sodium nitroprusside and nifedipine in order to obtain MAP values of about 80 mmHg with each administration. All patients had preoperative left ventricular ejection fraction above 45%. RESULTS: Nifedipine produced a superior and significant increase in cardiac index (CI) (+28%) and stroke volume index (SVI) (+30%), and a greater decrease in systemic vascular resistance index (SVRI) (-39%), when compared with sodium nitroprusside [CI (+5%), SVI (no change), SVRI (-27%)]. On the contrary the right and left ventricular filling pressures were reduced significantly by sodium nitroprusside [pulmonary capillary wedge pressure (-30%), central venous pressure (-20%)], while nifedipine induced small and not significant changes in the preload values. No ECG changes suggesting ischemic myocardial events were observed in any patient. CONCLUSIONS: On the basis of these results it has been concluded that nifedipine affects primarily the arteriolar resistance vessels without significant changes in venous tone, which is on the contrary markedly reduced by sodium nitroprusside. The better improvement in cardiac index and stroke volume index obtained with the administration of nifedipine, makes this drug a good alternative to sodium nitroprusside for treatment of acute hypertension after cardiac surgery in patients with a good preoperative left ventricular function.

Acute Disease↗

Venodilator effects of adenosine triphosphate and sodium nitroprusside; comparisons during controlled hypotension.

Adenosine triphosphate as well as sodium nitroprusside has been used for hypotensive anesthesia. The purpose of this study was to examine the possibility that two hypotensive drugs may exert different effects on venous capacitance during controlled hypotension. In rats anesthetized with ketamine, mean arterial pressure was lowered to 50 mmHg by intravenous infusion of adenosine triphosphate or sodium nitroprusside. Venous capacitance was assessed before and during induced hypotension by measuring the mean circulatory filling pressure (MCFP). MCFP was measured after briefly arresting the circulation by inflating an indwelling balloon in the right atrium. MCFP was lower during adenosine triphosphate-induced as well as sodium nitroprusside-induced hypotension as compared with the respective value at control (P < 0.01 for adenosine triphosphate and sodium nitroprusside). However, the decrease in MCFP by adenosine triphosphate (0.8 +/- 0.1 mmHg) was less (P < 0.01) than that by sodium nitroprusside (2.3 +/- 0.3 mmHg). These results suggest that at a comparable level of arterial hypotension venodilator effect of adenosine triphosphate was less than that of sodium nitroprusside. Less venodilatation during adenosine triphosphate-induced hypotension may contribute to the maintenance of cardiac output during hypotensive anesthesia.

Journal Article↗