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PubMed1976

Afterload reduction therapy with nitroprusside in severe aortic regurgitation: improved cardiac performance and reduced regurgitant volume.

To assess the hemodynamic effects of afterload reduction in severe aortic regurgitation, nitroprusside was infused at cardiac catheterization in 12 patients with aortic regurgitation. Cardiac hemodynamics, angiographic variables and regurgitant volumes were quantified during control periods, and nitroprusside was infused to reduce systemic systolic pressure to 110 to 125 mm Hg. The following were reduced by the drug: systolic arterial pressure (from 154 +/- 6.4 to 115 +/- 2.3 mm Hg, P less than 0.001); left ventricular end-diastolic pressure (from 23 +/- 2.2 to 11 +/- 1.0 mm Hg, P less than 0.001); systemic vascular resistance (from 1,782 +/- 133 to 1,148 +/- 94 dynes sec cm-5, P less than 0.001); left ventricular end-diastolic volume (from 242 +/- 25 to 196 +/- 19 ml, P less than 0.001); aortic regurgitant fraction (from 0.53 +/- 0.05 to 0.44 +/- 0.06, P less than 0.01); and aortic regurgitant minute volume (from 5.5 +/- 0.10 to 4.3 +/- 0.09 liters/min, P less than 0.01). Effective cardiac index increased (from 2.49 +/- 0.19 to 3.10 +/- 0.24 liters/min per m2, P less than 0.01), and left ventricular ejection fraction rose (from 0.55 +/- 0.03 to 0.61 +/- 0.03, P less than 0.005). These data indicate that afterload reduction with nitroprusside in severe aortic regurgitation improves cardiac performance, greatly decreases left ventricular preload and reduces aortic regurgitant volume. Thus, nitroprusside therapy has special value in severe aortic regurgitation that is of particular benefit in critical clinical conditions.

Aged↗
PubMed1981

Comparison of effects of prostaglandin E1 and nitroprusside on pulmonary vascular resistance in children after open-heart surgery.

Prostaglandin E1 (PGE1) is a vasodilator. Because the drug is metabolized by lung, we postulated a selective effect on pulmonary vasculature. Twenty-six patients aged 3 months to 16 year (mean, 6.5 years) were studied after repair of atrial septal defect (5), ventricular septal defect (10), tetralogy of Fallot (3), and other lesions (8). Fourteen patients also received nitroprusside. PGE1 (0.1 to 1.0 micrograms/kg/min) or nitroprusside (0.59 to 8.7 micrograms/kg/min) was infused through a central venous catheter until mean pulmonary or mean systemic arteria pressure decreases at least 10%. Prostaglandin E1 and nitroprusside both decreased mean systemic arterial pressure and systemic vascular resistance (P less than 0.05). Although both drugs caused an average decrease in pulmonary arterial pressure and resistance, nitroprusside produced a more consistent response. Side-effects limited the use of PGE1 in 5 patients. PGE1 is an effective vasodilator and has advantages for some patients, but it does not produce selective vasodilation of pulmonary vessels.

Adolescent↗
PubMed1979

Nitroprusside and epinephrine for treatment of low output in children after open-heart surgery.

We evaluated the acute hemodynamic effects of treatment of the low output state with sodium nitroprusside and epinephrine in 13 children after intracardiac operation. The 13 patients were selected from a consecutive series of 106 children undergoing cardiopulmonary bypass. They had a cardiac index less than 2.0 L/min/m2, even after an increase in left ventricular filling pressure and during infusion of nitroprusside. Although the nitroprusside brought about a significant increase in cardiac output and decrease in systemic vascular resistance, the cardiac index remained critically low (less than 2 L/min/m2). Epinephrine resulted in a further significant increase in the cardiac index, without a significant change in systemic resistance. This study suggests that in selected patients the simultaneous use of both a vasodilator drug (sodium nitroprusside) and a positive inotropic agent (epinephrine) is advantageous in the short-term treatment of the low cardiac output state after intracardiac operation.

Adolescent↗
PubMed1978

Improved myocardial performance in postoperative cardiac surgical patients with sodium nitroprusside.

Myocardial performance in the immediate postoperative period was studied 49 cardiac surgical patients treated with nitroprusside alone. With a thermodilution catheter positioned in the pulmonary artery, cardiac output was calculated and cardiac index, systemic vascular resistance index, and stroke work index were derived before after treatment with nitroprusside. The drug was a administered to all patients because of elevated systemic vascular resistance index. Based on their mean arterial pressure and cardiac index before treatment, the patients fell into two groups. Group I patients (N = 25) had elevated mean arterial pressure and normal cardiac index. Group II patients (N = 24) had normal mean arterial pressure and subnormal cardiac index. Nitroprusside administration resulted in a significant reduction of systemic vascular resistance index in all patients. In Group I the mean arterial pressure was lowered significantly while cardiac index increased only slightly. In Group II there was no change in arterial pressure, but cardiac index improved significantly. The results not only confirm that nitroprusside is effective in managing postoperative hypertension, but also demonstrate that in patients with postoperative left ventricular failure, the drug can improve cardiac output by reducing systemic vascular resistance without significantly lowering arterial blood pressure.

Adult↗
PubMed1996

Nitroprusside decreases the early post-denervation depolarization of diaphragm muscle fibres of the rat.

The application of sodium nitroprusside, which degrades to nitric oxide (NO) in solution, inhibits early post-denervation depolarization of isolated rat diaphragm fibres. The observation that "old' solutions of sodium nitroprusside (that have been allowed to decompose) are without effect and that haemoglobin, oxadiazolo quinoxalinone (ODQ) and methylene blue can antagonize the inhibition normally produced by sodium nitroprusside suggests that the inhibitory effects of sodium nitroprusside on early post-denervation depolarization are mediated by NO and guanylyl cyclase. This is in accord with our recent observations with NO synthase activation and inhibition in the diaphragm.

Animals↗
PubMed2000

Sodium nitroprusside in patients with compromised left ventricular function undergoing coronary bypass: reduction of cardiac proinflammatory substances.

OBJECTIVE: The aim of the present study was to investigate whether the nitric oxide donor sodium nitroprusside can reduce the cardiac inflammatory response during coronary artery bypass grafting in patients with severely compromised left ventricular function. METHODS: Patients (n = 30) were assigned to receive placebo or sodium nitroprusside (0.5 microg. kg(-1). min(-1)) for the first 60 minutes of reperfusion. Interleukin 6, interleukin 8, and tumor necrosis factor alpha levels; platelet adhesion molecule CD41 and CD62 levels; and CD11b on leukocytes were determined in the radial artery and coronary sinus before cardiopulmonary bypass and during reperfusion (1, 5, 10, 35, and 75 minutes). RESULTS: At 1 minute of reperfusion, coronary venous levels of CD41-positive polymorphonuclear leukocytes were 8% lower than arterial levels in the placebo group and 18% higher in the sodium nitroprusside group (P =.021). At 5 minutes of reperfusion, the respective levels were 29% and 1% for interleukin 6 (P =.015), -5% and 20% for CD41-positive monocytes (P =.032), and -2% and 16% for CD11b-positive monocytes (P =.038). At 10 minutes of reperfusion, these levels were -14% and 21% for CD41-positive monocytes (P =.006). At 35 minutes of reperfusion, these levels were -13% and 7% for CD41-positive monocytes (P =.017), -41% and 23% for CD11b-positive monocytes (P =.001), and 7% and 25% for CD62-positive platelets (P =. 041). At 75 minutes of reperfusion, the levels were 15% and -7% for tumor necrosis factor alpha (P =.025) and -10% and 10% for CD62-positive platelets (P =.041). CONCLUSIONS: Transcardiac production of proinflammatory cytokines is reduced in patients undergoing coronary artery bypass grafting treated with the nitric oxide donor sodium nitroprusside. At the same time, less activated leukocytes and platelets are retained in the coronary circulation.

Aged↗
PubMed1999

Intraportal administration of glyceryl trinitrate or nitroprusside exerts more systemic than intrahepatic effects in anaesthetised cirrhotic rats.

BACKGROUND/AIMS: Increased intrahepatic vascular tone can be pharmacologically manipulated in isolated cirrhotic livers. Intrahepatic endothelial dysfunction may lead to a decreased production of the potent endogenous vasodilator nitric oxide in cirrhotic livers. The aims of the study were to determine whether portal pressure can be lowered in vivo by injecting nitric oxide donors glyceryl trinitrate or nitroprusside directly in the portal vein and whether this is related to a decrease in intrahepatic resistance. METHODS: In anaesthetised CCl4 cirrhotic rats, intraportal doses of glyceryl trinitrate 0.5, 1 or 5 microg/kg/ min or nitroprusside 1, 5 or 10 microg/kg/min did not decrease portal pressure but only arterial pressure. Systemic and splanchnic haemodynamics were measured before and during 15 min intraportal infusion of glyceryl trinitrate 10 microg/kg/min or nitroprusside 20 microg/kg/min. RESULTS: Glyceryl trinitrate decreased portal pressure from 14.0+/-1.1 to 11.8+/-1.4 mm Hg, splanchnic perfusion pressure from 102+/-10 to 74+/-5 mm Hg and portal sinusoidal flow from 2.11+/-0.38 to 1.70+/-0.35 ml/min/g liver (all p<0.05). Nitroprusside did not decrease portal pressure significantly but led to a reduction of the splanchnic perfusion pressure (104+/-9 to 66+/-7 mm Hg) and the portal sinusoidal flow (2.39+/-0.50 to 1.77+/-0.31 ml/min/g liver; all p<0.05). Portal sinusoidal resistance was not altered by either drug. CONCLUSIONS: Intraportal infusion of nitric oxide donors decreased arterial pressure more than portal pressure. Portal sinusoidal resistance remained unaffected, but the liver parenchyma became less perfused with high doses. The systemic effects of nitric oxide donating drugs prevailed.

Animals↗
PubMed1983

Comparison of the effects of nitroprusside and nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy: altered left ventricular loading or improved muscle inactivation?

The calcium channel blocking agent, nifedipine, has been shown to improve indexes of left ventricular relaxation, diastolic filling and compliance in patients with hypertrophic cardiomyopathy. The mechanism of action of nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy is unclear and could result from an improvement in myocardial inactivation or from systemic vasodilation and left ventricular unloading. To distinguish between these mechanisms, the effects of nifedipine and the vasodilator nitroprusside on left ventricular diastolic properties were compared in 10 patients with nonobstructive hypertrophic cardiomyopathy using simultaneous micromanometer left ventricular pressure and echocardiographic measurements. Left ventricular peak systolic pressure was comparable during nitroprusside infusion (132 +/- 38 mm Hg) and after nifedipine (132 +/- 32 mm Hg). During nitroprusside infusion, the decrease in left ventricular end-diastolic pressure (22 +/- 11 to 17 +/- 11 mm Hg, p less than 0.05) was associated with a decrease in left ventricular end-diastolic dimension. In contrast, the decrease in left ventricular end-diastolic pressure after nifedipine (22 +/- 11 to 18 +/- 10 mm Hg, p less than 0.05) was associated with no reduction of left ventricular end-diastolic dimensions, suggesting an increase in left ventricular distensibility. Compared with nitroprusside, nifedipine was associated with less prolongation of the left ventricular isovolumic relaxation time and less depression of the peak left ventricular posterior wall thinning rate and peak left ventricular internal dimension filling rate. These data suggest that the effects of the calcium channel blocker, nifedipine, on diastolic mechanics in hypertrophic cardiomyopathy result not only from systemic vasodilation but also from improved cardiac muscle inactivation.

Adolescent↗
PubMed1983

Abnormal neurohumoral response to nitroprusside infusion in congestive heart failure.

Vasodilator drugs produce tachycardia and an increase in circulating plasma norepinephrine in normal subjects. In contrast, heart rate does not change when the same drugs are given to patients with congestive heart failure. To assess if this difference could be related to a different reflex activation of the sympathetic nervous system, the response of plasma norepinephrine to nitroprusside infusion and to head-up tilt was studied in 5 normal subjects and in 46 patients with chronic congestive heart failure. Norepinephrine and heart rate increased significantly during both stimuli in normal subjects but were unchanged during nitroprusside infusion for the entire group of patients with heart failure, with considerable variability in individual responses. In 21 patients (Group I) norepinephrine increased during nitroprusside infusion, while in the remaining 25 (Group II) norepinephrine decreased. The hemodynamic response to nitroprusside was similar in the two groups, thus suggesting that the different changes in plasma norepinephrine could not be explained on the basis of a different hemodynamic response to the drug. Plasma norepinephrine also did not change significantly in Group II during tilt, although the decrease in intracardiac pressure and the increase in peripheral resistance were similar to those in Group I who increased norepinephrine normally by 56%. These data indicate that a subset of patients with severe ventricular dysfunction have an abnormal humoral, reflex sympathetic response to changes in arterial or intracardiac pressure, or both. The higher mortality in Group II suggests that this alteration in the sympathetic response may be a marker of the severity and prognosis of heart failure.

Adult↗
PubMed1989

Vasodilator properties of atrial natriuretic factor: a comparison with nitroglycerin, nitroprusside, and phentolamine during cardiopulmonary bypass.

Thirty-five patients scheduled for coronary artery surgery were studied during hypothermic cardiopulmonary bypass (CPB) to compare the arteriolar and venodilator properties of a bolus dose of atrial natriuretic factor (ANF), 100 micrograms, with those of nitroglycerin, 200 micrograms, sodium nitroprusside, 120 micrograms, phentolamine, 3 mg, and placebo. A decrease observed in mean arterial pressure was used as an indicator of a decrease in systemic vascular resistance (arteriolar dilation), while a decrease in reservoir blood volume of the CPB circuit was considered to indicate an increase in venous capacitance (venodilation). All vasodilators decreased mean arterial pressure, and there was no difference in the maximal decrease of the pressure between the drugs. However, the decrease caused by ANF appeared later than that caused by the other vasodilators and lasted longer than with nitroglycerin and sodium nitroprusside. Nitroglycerin and sodium nitroprusside decreased reservoir blood volume, while ANF and phentolamine had no effect. It is concluded that ANF is an arteriolar dilator with a time profile of its effect differing from those of nitroglycerin, sodium nitroprusside, and phentolamine. ANF seems to have no venodilator activity in patients undergoing hypothermic CPB.

Atrial Natriuretic Factor↗
PubMed1995

A comparison of prostacyclin and sodium nitroprusside for the treatment of heart failure after cardiac surgery.

OBJECTIVE: To study the effects of the two vasodilators, prostacyclin and sodium nitroprusside, on central hemodynamics in heart failure after cardiac surgery. DESIGN: Randomized cross-over study. SETTING: Multi-institutional university hospital. PARTICIPANTS: Ten patients. INCLUSION CRITERIA: cardiac index less than 2.5 L/min/m2; pulmonary capillary wedge pressure greater than 15 mmHg, systemic vascular resistance index greater than 2,500 dynes.s.cm-5/m2, and treatment with inotropic support. Five patients were treated with intra-aortic balloon counterpulsation. INTERVENTIONS: After control measurements, mean arterial pressure was decreased by 10% to 20% with each vasodilator in each patient. MEASUREMENTS AND RESULTS: Sodium nitroprusside induced decreases in mean pulmonary arterial pressure (-21%), pulmonary capillary wedge pressure (-29%), central venous pressure (-17%), and systemic vascular resistance (-25%), and increases in cardiac output (+7%) and stroke volume (+6%) compared with control. Prostacyclin decreased mean pulmonary arterial pressure (-14%), pulmonary capillary wedge pressure (-19%), central venous pressure (-7%), and systemic (-40%) and pulmonary (-25%) vascular resistances, whereas cardiac output (+25%) and stroke volume (+22%) increased compared with control. Prostacyclin, compared with sodium nitroprusside, induced a more pronounced increase in cardiac output and stroke volume, associated with less pronounced decreases in cardiac filling pressures and more profound decreases in systemic and pulmonary vascular resistances. CONCLUSION: Prostacyclin appears to be a useful agent, superior to sodium nitroprusside, in the treatment of postoperative heart failure in patients with normal or mildly elevated cardiac filling pressures, where vasodilator treatment is indicated.

Aged↗
PubMed2003

Mechanistic studies on the interaction of reduced cobalamin (vitamin B12r) with nitroprusside.

The electron-transfer reaction between reduced cobalamin (Cbl(II)) and sodium pentacyanonitrosylferrate(II) (sodium nitroprusside, NP), as well as the subsequent processes following the electron-transfer step, were investigated by spectroscopic (UV-vis, (1)H NMR, EPR), electrochemical (CV, DPV) and kinetic (stopped-flow) techniques. In an effort to clarify the complex reaction pattern observed at physiological pH, systematic spectroscopic and kinetic studies were undertaken as a function of pH (1.8-9) and NP concentration (0.0001 - 0.09 M). The kinetics of the electron-transfer reaction was studied under pseudo-first-order conditions with respect to NP. The reaction occurs in two parallel paths of different order, viz. pseudo-first and pseudo-second order with respect to the NP concentration, respectively. The contribution of each path depends on pH and the [NP]/[Cbl(II)] ratio. At low pH and total NP concentration (pH < 3, [NP]/[Cbl(II)] approximately 1), the cyano-bridged successor complex [Cbl(III)-(mu-NC)-Fe(I)(CN)(3)(NO(+))](-) (1(s)()) is the final reaction product formed in an inner-sphere electron transfer reaction that is coupled to the release of cyanide from coordinated nitroprusside. At higher pH, subsequent reactions were observed which involve the attack of cyanide released in the electron transfer step on the initially formed cyano-bridged species, and lead to the formation of Cbl(III)CN and [Fe(I)(CN)(4)(NO(+))](2)(-). The strong dependence of the rate and mechanism of the subsequent reactions on pH is attributed to the large variation in the effective nucleophilicity of the cyanide ligand in the studied pH range. An alternative electron-transfer pathway observed in the presence of excess NP involves the reaction of the precursor complex [Cbl(II)-(mu-NC)-Fe(II)(CN)(4)(NO(+))](2)(-) (1(p)()) with NP to give [Cbl(III)-(mu-NC)-Fe(II)(CN)(4)(NO(+))](-) (2) and reduced nitroprusside, [Fe(CN)(5)NO](3)(-), as the initial reaction products. Analysis of the kinetic data allowed elucidation of the rate constants for the inner- and outer-sphere electron-transfer pathways. The main factors which influence the kinetics and thermodynamics of the observed electron-transfer steps are discussed on the basis of the spectroscopic, kinetic and electrochemical results. A general picture of the reaction pathways that occur on a short (s) and long (min to h) time scale as a function of pH and relative reactant concentrations is derived from the experimental data. In addition, the release of NO resulting from the one-electron reduction of NP by Cbl(II) was monitored with the use of a sensitive NO electrode. The results obtained in the present study are discussed in reference to the possible influence of cobalamin on the pharmacological action of nitroprusside.

Electrochemistry↗
PubMed1987

Atrial natriuretic factor and sodium nitroprusside increase cyclic GMP in cultured rat lung fibroblasts by activating different forms of guanylate cyclase.

We used cultured rat lung fibroblasts to evaluate the role of particulate and soluble guanylate cyclase in the atrial natriuretic factor (ANF)-induced stimulation of cyclic GMP. ANF receptors were identified by binding of 125I-ANF to confluent cells at 37 degrees C. Specific ANF binding was rapid and saturable with increasing concentrations of ANF. The equilibrium dissociation constant (KD) was 0.66 +/- 0.077 nM and the Bmax. was 216 +/- 33 fmol bound/10(6) cells, which corresponds to 130,000 +/- 20,000 sites/cell. The molecular characteristics of ANF binding sites were examined by affinity cross-linking of 125I-ANF to intact cells with disuccinimidyl suberate. ANF specifically labelled two sites with molecular sizes of 66 and 130 kDa, which we have identified in other cultured cells. ANF and sodium nitroprusside produced a time- and concentration-dependent increase in intracellular cyclic GMP. An increase in cyclic GMP by ANF was detected at 1 nM, and at 100 nM an approx. 100-fold increase in cyclic GMP was observed. Nitroprusside stimulated cyclic GMP at 10 nM and at 1 mM a 500-600-fold increase in cyclic GMP occurred. The simultaneous addition of 100 nM-ANF and 10 microM-nitroprusside to cells resulted in cyclic GMP levels that were additive. ANF increased the activity of particulate guanylate cyclase by about 10-fold, but had no effect on soluble guanylate cyclase. In contrast, nitroprusside did not alter the activity of particulate guanylate cyclase, but increased the activity of soluble guanylate cyclase by 17-fold. These results demonstrate that rat lung fibroblasts contain ANF receptors and suggest that the ANF-induced stimulation of cyclic GMP is mediated entirely by particulate guanylate cyclase.

Animals↗
PubMed1998

Effect of sodium nitroprusside and L-arginine methyl ester on rat hearts stored at 4 degrees C for 24 h.

1. This study examined the effects of altering nitric oxide levels with sodium nitroprusside or L-arginine in rat hearts stored hypothermically.2. Hearts were microperfused at 4 degrees C for 24 h with a modified Krebs-Henseleit buffer (KHB) that contained either sodium nitroprusside, L-arginine, L-arginine methyl ester or dexamethasone.3. After hypothermic storage, hearts were rewarmed to 37 degrees C with KHB alone or KHB containing sodium nitroprusside or L-arginine. Cardiac function was then assessed in either Langendorff mode or working heart mode.4. Compared with values from fresh unstored hearts, hypothermic stored hearts showed a significant decrease in coronary flow and left ventricular developed pressure when the stored hearts were perfused in Langendorff mode. These hearts also produced less aortic flow and cardiac output when perfused in the working mode.5. Hearts hypothermically microperfused with buffer containing either L-arginine or sodium nitroprusside and then reperfused in the Langendorff mode with untreated KHB buffer had the highest left ventricular developed pressure and coronary flow values. Aortic flow and cardiac output were also higher in these hearts.6. In all groups of stored hearts, the concentrations of both ATP and creatine phosphate were significantly low, when compared with values from freshly isolated hearts. Addition of dexamethasone to the buffer either during storage or during reperfusion had no beneficial effect on high-energy phosphate loss or cardiac performance of stored hearts.7. This study showed that the addition of nitric oxide donors to storage buffer significantly improves cardiac function on normothermic reperfusion. The improved functional recovery is unrelated to the high-energy phosphate content of these hearts.

Adenosine Triphosphate↗
PubMed2007

Urocortin 1 modulates the neurohumoral response to acute nitroprusside-induced hypotension in sheep.

In addition to haemodynamic actions, Ucn1 (urocortin 1) has been reported to affect a number of hormonal systems; however, it remains unclear whether Ucn1 modulates circulating hormones under physiological conditions. Accordingly, in the present study, we have examined the effects of Ucn1 on haemodynamics, hormones and renal indices in normal conscious sheep subjected to a nitroprusside-induced hypotensive stimulus designed to alter hormonal levels within the physiological range. Ucn1 administration did not alter the haemodynamic response to nitroprusside-induced hypotension. However, compared with the rise observed on the control day, plasma ANP (atrial natriuretic peptide; P=0.043), BNP (brain natriuretic peptide; P=0.038) and endothelin-1 (P=0.011) levels were reduced following Ucn1 administration. Associated with this significant reduction in natriuretic peptides, the increase in urinary sodium output associated with rising pressures post-nitroprusside was abolished following Ucn1 administration (P=0.048). Ucn1 had no significant effect on the response of hormones of the renin-angiotensin-aldosterone system or the hypothalamo-pituitary-adrenal axis. In conclusion, Ucn1, administered at physiologically relevant levels during nitroprusside-induced hypotension, attenuates the secretion/release of endothelin-1 and the cardiac natriuretic peptides ANP and BNP. Suppression of ANP and BNP probably led to an attenuated natriuretic response to recovery from acute hypotension. The threshold for the action of Ucn1 on the natriuretic peptides and endothelin-1 appears to be below that of other actions of Ucn1.

Aldosterone↗
PubMedDate not supplied

Effect of sodium nitroprusside on mouse sperm migration in vitro.

In the present study the effect of sodium nitroprusside, a nitric oxide releaser, on mouse sperm motion behavior was examined. The number of sperm migrating in experimental plate to medium containing sodium nitroprusside in concentration 50 nM was significantly higher than the number migrating to control. This effect was observed after 3 and 5 h of incubation, and it was not time dependent. The presence of sodium nitroprusside in higher concentrations did not cause any visible changes or decrease the migration of sperm. These effects were interpreted as chemokinesis but not chemotaxis of sperm induced by influence of sodium nitroprusside on sperm metabolism and motility.

Animals↗
PubMed1977

Intracranial pressure changes in neurosurgical patients during hypotension induced with sodium nitroprusside or trimetaphan.

Intracranial pressure has been measured in 45 patients undergoing neurosurgery during the induction of deliberate hypotension using either sodium nitroprusside or trimetaphan. A statistically significant increase in intracranial pressure (ICP) occurred during the early stages of the infusion of nitroprusside in normocapnic patients. A non-significant increase in ICP was obtained in hypocapnic patients. The mean ICP increased from 6.3 mm Hg to 11.7 mm Hg when the arterial pressure was reduced slightly, but the response in individual patients varied widely (range -1.6 mm Hg to +20.9 mm Hg). When the arterial pressure (BP) had decreased to 70% of the value existing before infusion of nitroprusside, mean ICP returned to control values and thereafter decreased with further reductions in BP. In patients rendered hypotensive with trimetaphan, there was no change in mean ICP but two patients showed moderate increases (+9.3 mm Hg and +5.7 mm Hg). The mechanism of the increase in ICP with nitroprusside is thought to be expansion of the intracranial blood volume as a result of cerebral vasodilatation. Trimetaphan does not usually produce ICP changes except when intracranial compression is severe, for in these circumstances a small change in intracranial blood volume consequent upon autoregulation may trigger an increase in ICP.

Blood Pressure↗
PubMed1979

Metabolic effects of induced hypotension with trimetaphan and sodium nitroprusside.

In two groups of patients undergoing induced hypotension with sodium nitroprusside or trimetaphan blood concentrations of lactate, pyruvate and standard bicarbonate did not differ significantly between the groups. In the nine patients who received trimetaphan there was a progressive, but statistically non-significant, decrease in mean lactate. Nitroprusside (15 patients) was associated with a small increase in mean lactate, but at low dosage there was a small decrease. No relationship to dose rate of nitroprusside was found with these short-term infusions. It is concluded that sodium nitroprusside can be used safely for induced hypotension at doses less than 1.5 mg kg-1 and that simple blood-gas analysis is adequate for the assessment of toxic effects when greater doses are given.

Adolescent↗