Nitroprusside In Patients Research Articles

Clevidipine as a therapeutic and cost-effective alternative to sodium nitroprusside in patients with acute aortic syndromes.

Sodium nitroprusside is the preferred agent for the treatment of high blood pressure during acute aortic syndrome if blood pressure remains elevated after heart rate control with beta-blockers. The increasing cost of sodium nitroprusside in the USA led us to assess the efficacy and safety of intravenous clevidipine, a calcium channel blocker with quick onset of action, short half-life and significantly lower costs than sodium nitroprusside, in patients presenting with acute aortic syndrome. We performed a retrospective chart review of consecutive patients admitted to the Cleveland Clinic Cardiac Intensive Care Unit from 2013-2016 with a diagnosis of acute aortic syndrome. Patients who received intravenous sodium nitroprusside were compared with those receiving intravenous clevidipine. The primary outcome was a significant difference in blood pressure at one, three and six hours. Secondary outcomes included time to achieving blood pressure target and in hospital mortality with rates of hypotension and bradycardia as safety endpoints. A total of 85 patients with suspected acute aortic pathology received clevidipine and 50 received sodium nitroprusside. Clinical and demographic characteristics were similar in both groups, except for a higher incidence of abdominal aortic aneurysm in the clevidipine group and for a trend towards higher use of labetalol in the clevidipine group. There were no significant differences in blood pressure or heart rate at one, three and six hours after starting either infusion. The rates of hypotension, bradycardia and in-hospital mortality did not differ. Time to achieve blood pressure control were also similar between groups. Intravenous clevidipine appears to be a safe and effective alternative to sodium nitroprusside for the management of high blood pressure during acute aortic dissection. In the USA, clevidipine could represent a cost effective therapy providing similar outcomes than sodium nitroprusside.

Hemodynamic Response to Nitroprusside in Patients With Low-Gradient Severe Aortic Stenosis and Preserved Ejection Fraction

BackgroundLow-gradient severe aortic stenosis (LGSAS) with preserved ejection fraction (EF) is incompletely understood. The influence of arterial afterload and diastolic dysfunction on the hemodynamic presentation of LGSAS remains unknown. ObjectivesThe authors sought to determine the acute hemodynamic response to sodium nitroprusside in LGSAS with preserved EF. MethodsSymptomatic patients with LGSAS and preserved EF underwent cardiac catheterization with comparison of hemodynamic measurements before and after nitroprusside. ResultsForty-one subjects (25 with low flow [LF], stroke volume index [SVI] ≤35 ml/m2, 16 with normal flow [NF]) were included. At baseline, LF patients had lower total arterial compliance (0.36 ± 0.12 ml/m2/mm Hg vs. 0.48 ± 0.16 ml/m2/mm Hg; p = 0.01) and greater effective arterial elastance (2.77 ± 0.84 mm Hg · m2/ml vs. 1.89 ± 0.82 mm Hg · m2/ml; p = 0.002). In all patients, nitroprusside reduced elastance, left ventricular filling pressures, and pulmonary artery pressures and improved compliance (p < 0.05). Aortic valve area increased to ≥1.0 cm2 in 6 LF (24%) and 4 NF (25%) subjects. Change in SVI with nitroprusside varied inversely to baseline SVI and demonstrated improvement in LF only (3 ± 6 ml/m2; p = 0.02). ConclusionsNitroprusside reduces afterload and left ventricular filling pressures in patients with LGSAS and preserved EF, enabling reclassification to moderate stenosis in 25% of patients. An inverse relationship between baseline SVI and change in SVI with afterload reduction was observed, suggesting that heightened sensitivity to afterload is a significant contributor to LF-LGSAS pathophysiology. These data highlight the utility of afterload reduction in the diagnostic assessment of LGSAS.

Sodium Nitroprusside in Patients With Mixed Pulmonary Hypertension and Left Heart Disease: Hemodynamic Predictors of Response and Prognostic Implications

BackgroundMixed pulmonary hypertension (PH) in heart failure (HF) is defined by transpulmonary gradient ≥ 12 and/or pulmonary vascular resistance (PVR) ≥ 240 dyne/s/cm−5, but diastolic pressure gradient (DPG) ≥ 7 mmHg has been proposed more recently. We evaluated the acute hemodynamic response to sodium nitroprusside (SNP) specifically in relation to the proposed DPG criterion ≥7 mmHg and the prognostic significance of response to SNP in patients with mixed PH and advanced HF. MethodsNinety-eight consecutive patients with advanced HF and mixed PH underwent cardiac catheterization and acute SNP infusion. Baseline hemodynamic parameters included transpulmonary gradient, PVR, DPG, and pulmonary capacitance (PCap). Hemodynamic response to SNP was defined as a reduction in PVR of at least 20%. The composite endpoint was death/heart transplantation/mechanical circulatory support. ResultsSixty of the 98 patients were SNP responders. SNP resulted in significant reductions in filling pressures and PVR and increase in stroke volume and PCap. DPG (not baseline PVR) was significantly associated with hemodynamic response to SNP on logistic regression analysis. The sensitivity and specificity of a DPG ≥7 mmHg to identify nonresponders to SNP were 74% and 97%, respectively. At median follow-up of 218 (148–324) days, 13 and 19 patients of the SNP responders and nonresponders, respectively, met the composite endpoint (P = .021 by log-rank test). Hemodynamic response to SNP and PCap were independently associated with the composite outcome of survival free from transplantation/mechanical circulatory support. ConclusionBaseline DPG ≥ 7 mmHg is associated with poor PVR response to SNP. PVR response to SNP and PCap are associated with a more favorable prognosis in patients with advanced HF and mixed PH.

ASSA14-08-01 The effect of Herbesser on no-reflow and in the role of in patients with acute coronary syndrome undergoing PCI

<h3>Objective</h3> To evaluate the clinical value of Herbesser on the no-reflow in patients with acute coronary syndrome (ACS) under going percutaneous coronary intervention (PCI) Methods: January 2008–May 2014 in our hospital and underwent coronary angiography and drug-eluting stents (DES) implantation in more than 3,000 cases of ACS patients without intraoperative blood 60 cases, male 45 cases , 15 females, aged 35–75 years, mean age (56 ± 20) years old, were randomly divided into A, B groups (30 cases). A group of patients given intracoronary Herbesser 100–200 ug; Group B intraoperative given nitroprusside from coronary 100–200 ug, coronary blood flow was observed after administration of the recovery, cardiovascular events was observed after 30d incidence (the primary endpoint of cardiovascular death, revascularisation, target organs, malignant arrhythmia). The difference between the two groups was not statistically gender, age, severity of disease, complications, etc.: results. A group of intraoperative blood recovery TIMI3 grade 29 cases, TIMI2 flow grade one case, 30d after one case of malignant arrhythmias, angina two cases, no deaths, and target organ revascularisation; B group intraoperative blood recovery TIMI3 level 28 example, TIMI2 flow grade 2 cases, 1 case of malignant arrhythmias 30d, angina three cases, two blood flow is restored and the incidence of cardiovascular events was no statistical difference (p &gt; 0.05). <h3>Conclusion</h3> Herbesser and sodium nitroprusside in patients with acute coronary syndrome (ACS) interventional treatment can reduce the no flow phenomenon, so no blood flow is restored to the level TIMI2–3 blood flow, reduce the incidence of cardiovascular events.

Impact of a novel mutation in the 5′-flanking region of natriuretic peptide precursor B gene on the antihypertensive effects of sodium nitroprusside in patients with hypertension

Our aim was to identify the possible mutations of the natriuretic peptide precursor B (NPPB) gene in a family with hereditary hypertension, and determine whether the mutations are associated with the antihypertensive effect of sodium nitroprusside. The subjects included one family with hereditary hypertension, 36 cases of sporadic hypertension and 120 healthy controls. The 5'-flanking sequence of NPPB was amplified with PCR, and the presence of mutations was analyzed by direct sequencing. Patients with hypertension were treated with sodium nitroprusside and blood pressure data and serum B-type natriuretic peptide (BNP) levels were measured. A novel complex mutation in 5'-flanking sequence of the NPPB gene was detected in three patients (II 2, III 2, and III 5) of the hypertension family, which included c.-1195_ -1176 insert 5'-CCTTCTTTCTTTCTTTCTTT-3', c.-1208 T>A, c.-1214 T>C, and c.-1216 T>A. Patients with this mutation were less sensitive to sodium nitroprusside treatment. Sporadic hypertension patients (without NPPB gene mutation) and patients with the c.-1181 T>A point mutation were sensitive to sodium nitroprusside treatment. BNP levels of patients with the complex mutation were significantly lower than that of sporadic hypertension patients and c.-1181 T>A mutation patients before and during the early stage of sodium nitroprusside treatment. The complex mutation of the NPPB gene might be an etiological factor of hereditary malignant hypertension, and it is associated with low sensitivity to the antihypertensive effect of sodium nitroprusside.

Effects of Vasodilation in Heart Failure With Preserved or Reduced Ejection Fraction: Implications of Distinct Pathophysiologies on Response to Therapy

The purpose of this study was to compare hemodynamic responses to vasodilator therapy in patients with heart failure (HF) and preserved ejection fraction (HFpEF) versus HF and reduced ejection fraction (HFrEF). There is no proven therapy for HFpEF. In the absence of data, medicines with established benefit in HFrEF such as vasodilators are frequently prescribed for HFpEF. We compared baseline hemodynamics and acute responses to vasodilation with intravenous sodium nitroprusside in patients with HFrEF (n = 174) and HFpEF (n = 83), determined invasively by cardiac catheterization. Baseline blood pressure, stroke volume, and cardiac output were greater in HFpEF than HFrEF, while pulmonary artery mean and pulmonary wedge pressures were similar. Left ventricular filling pressures were reduced to a similar extent in each group with nitroprusside, but the drop in systemic arterial pressure was 2.6-fold greater in HFpEF (p < 0.0001), and improvements in stroke volume and cardiac output were each ∼60% lower in HFpEF compared to HFrEF (p < 0.0001). Despite similarly elevated filling pressures, HFpEF patients were fourfold more likely than HFrEF to experience a reduction in stroke volume with nitroprusside (p < 0.0001), suggesting greater vulnerability to preload reduction. Pulmonary artery systolic pressure dropped more in HFpEF than in HFrEF despite similar reduction in pulmonary mean pressure and resistance, suggesting higher right ventricular systolic elastance in HFpEF. As compared to patients with HFrEF, patients with HFpEF experience greater blood pressure reduction, less enhancement in cardiac output, and greater likelihood of stroke volume drop with vasodilators. These findings emphasize fundamental differences in the 2 HF phenotypes and suggest that more pathophysiologically targeted therapies are needed for HFpEF.

Hydralazine and Isosorbide Dinitrate in Heart Failure

Until the 1970s, treatment options for heart failure were limited to digitalis and diuretics.1 Although effective for symptoms, there was no evidence of mortality benefit with this combination, and it was an inadequate option for many patients with advanced symptoms. The search for more effective options led to strategies that modulated hemodynamics.1 Numerous physiological studies showed the dependence of ventricular function on vascular resistance, and drugs that reduced systemic vascular resistance improved cardiac performance.2,–,5 A pivotal study by Franciosa et al6 showed that sodium nitroprusside in patients with heart failure in the setting of acute myocardial infarction reduced left ventricular filling pressures from 22.7±2.0 to 11.3±1.6 mm Hg and led to a modest increase in cardiac output. A subsequent study revealed more striking improvements in patients with refractory heart failure, in whom nitroprusside reduced systemic vascular resistance by 50%, increased cardiac output by 56%, and reduced left ventricular filling pressure by 47%.7 These hemodynamic benefits with nitroprusside led to studies with oral agents, including hydralazine, isosorbide dinitrate (ISDN), prazosin, phentolamine, and minoxidil. Although these drugs did affect hemodynamics, none was as effective as nitroprusside individually.8,–,12 In 1977, Massie et al13 studied the combination of 2 oral agents, hydralazine and ISDN (H-ISDN) in class III to IV heart failure patients, proposing that simultaneously reducing preload with ISDN and afterload with hydralazine would result in a better response than with either drug individually. They found that H-ISDN reduced left ventricular filling pressure by 36%, increased cardiac index by 58%, and reduced systemic vascular resistance by 34%. Later, Pierpont et al14 compared H-ISDN with nitroprusside and showed that the 2 therapies had similar effects on wedge pressure reduction and cardiac index increase. Considering these hemodynamic benefits with …

The Use of Nitroprusside in the Treatment of Acute Myocardial Infarction

In 15 patients with acute myocardial infarction, intravenous infusion of the potent vasodilator, nitroprusside, produced an average 50% fall in the elevated left ventricular filling pressure and a modest reduction in arterial pressure (average, 15.5%) without a change in heart rate. Careful dose adjustment in several patients resulted in a significant fall in left ventricular filling pressure with little or no change in arterial pressure. Cardiac output consistently rose during nitroprusside infusion in patients with clinical signs of left ventricular failure or shock and low control cardiac output, whereas output changed little on those patients with normal cardiac index. A fall in pressure time per minute as well as the fall in left ventricular filling pressure indicated a reduction in myocardial oxygen consumption during the vasodilator infusion. Drug infusion was usually accompanied by subjective improvement, including relief of dyspnea and of chest pain, and reduction in ventricular irritability. These data suggest, that vasodilator therapy, by reducing left ventricular afterload, can improve left ventricular performance in patients with acute myocardial infarction. Such treatment may be a rational approach to the management of patients with heart failure, pulmonary edema, or early shock. 1 Commentary Until the publication of this manuscript, little attention was given to the reduction of the peripheral vascular resistance as a method of improving left ventricular function in patients with acute myocardial infarction. The concern about using vasodilators were either that reducing blood pressure will decrease coronary blood flow or because physicians were concerned that a decrease in blood pressure was associated with clinical deterioration. However, Dr Cohn and his colleagues hypothesized that increases in blood pressure in a failing ventricle is harmful and therefore a control decrease in blood pressure may be expected to decrease left ventricular filling pressure. This is the reason why they used nitroprusside in infusion rates between 30 lg ⁄min and 150 lg ⁄min to control blood pressure in these patients and demonstrated a striking fall in left ventricular filling pressure with very little decrease in blood pressure. They also caution that if patients are hypotensive, one should be careful. In this manuscript, the authors put forth a possible mechanism for why nitroprusside may be beneficial to these patients in decreasing left ventricular afterload more than left ventricular preload. In addition, they suggested that compared with inotropic agents, using nitroprusside in patients with acute myocardial infarction reduced left ventricular oxygen consumption. Finally, the authors conclude that nitroprusside may be beneficial in patients with acute pulmonary edema and those with heart failure or early shock. The next historical vignette will discuss the use of nitroprusside in the treatment of refractory heart failure.

Periodontal Infection Is Associated With Endothelial Dysfunction in Healthy Subjects and Hypertensive Patients

The purpose of this study was to evaluate endothelial function in patients with periodontitis. We evaluated forearm blood flow responses to acetylcholine and sodium nitroprusside in patients with periodontitis who had no other cardiovascular risk factors (32 men; 25+/-3 years of age), in a normal control group (20 men; 26+/-3 years of age), and in hypertensive patients with periodontitis (28 men and 10 women; 56+/-12 years of age) and without periodontitis (control group; 18 men and 6 women; 54+/-13 years of age). Forearm blood flow was measured using strain-gauge plethysmography. Circulating levels of C-reactive protein and interleukin-6 were significantly higher in the periodontitis group than in the control group. Both in healthy and hypertensive subjects, forearm blood flow responses to acetylcholine were significantly smaller in the periodontitis group than in the control group. Sodium nitroprusside-stimulated vasodilation was similar in the 2 groups. Periodontal therapy reduced serum concentrations of C-reactive protein and interleukin-6 and augmented acetylcholine-induced vasodilation in periodontitis patients with and without hypertension. After administration of N(G)-monomethyl-L-arginine, an NO synthase inhibitor, forearm blood flow response to acetylcholine was similar before and after treatment. These findings suggest that periodontitis is associated with endothelial dysfunction in subjects without cardiovascular risk factors, as well as hypertensive patients, through a decrease in NO bioavailability and that systemic inflammation may be, at least in part, a cause of endothelial dysfunction, leading to cardiovascular diseases.

A Comparison of Fenoldopam With Dopamine and Sodium Nitroprusside in Patients Undergoing Cross-Clamping of the Abdominal Aorta

Survey of Anesthesiology: August 2007 - Volume 51 - Issue 4 - p 171-172 doi: 10.1097/01.sa.0000267060.66573.74

Haemodynamic effects of intravenous quinaprilat in comparison to sodium nitroprusside in patients with chronic heart failure

We compared the haemodynamic effects of intravenous boluses of the ACE inhibitor quinaprilat with an intravenous infusion of sodium nitroprusside in 23 patients with chronic heart failure (NYHA Class III or IV). At the highest drug doses, sodium nitroprusside significantly increased stroke volume index (+ 6.63 ml/m 2, p = 0.045), whereas quinaprilat induced only a minor increase (+ 1.79 ml/m 2, n.s.).

A Comparison of Fenoldopam with Dopamine and Sodium Nitroprusside in Patients Undergoing Cross-Clamping of the Abdominal Aorta

Fenoldopam, a selective dopamine-1-receptor agonist, decreases arterial blood pressure rapidly, with a brief duration of action similar to sodium nitroprusside (SNP), but in contrast to SNP, it increases renal blood flow. We compared the hemodynamic and renal effects of fenoldopam in patients undergoing abdominal aortic surgery requiring cross-clamping of the aorta with another therapeutic option, dopamine and SNP. Fenoldopam or 2 mcg x kg(-1) x min(-1) of dopamine and SNP was infused before incision in 60 randomly selected patients in a double-blind fashion. Hemodynamic variables were recorded before incision, immediately before clamping the aorta, 5 min after cross-clamp release and upon completion of surgery. Urine output, serum creatinine, and creatinine clearance were measured intraoperatively and postoperatively. Characteristics were compared between groups using two-sample rank sum test for continuous variables and Fisher's exact test for discrete variables. The occurrence of severe hypotension, maximum systolic blood pressure, and need for additional antihypertensive drugs were not different between the groups. Most intraoperative hemodynamic variables and all indices of renal function did not differ according to treatment. Therefore, fenoldopam has no therapeutic advantage compared with similar therapies in patients undergoing major vascular surgery involving cross-clamping of the aorta.

Microvascular Function, Metabolic Syndrome, and Novel Risk Factor Status in Women With Cardiac Syndrome X

To characterize microvascular function, candidate risk pathways, and metabolic syndrome prevalence in women with cardiac syndrome X, 52 nondiabetic women with angiographically normal epicardial arteries but >1 mm of planar ST depression during exercise testing (patients) and 24 healthy controls of similar age were recruited. In addition to fasting blood samples and anthropometric measurements, forearm cutaneous microvascular function after iontophoresis of acetylcholine and sodium nitroprusside was assessed by laser Doppler imaging. Despite body mass index correction and a larger proportion on statin therapy, patients had high levels of insulin (p=0.016), triglycerides (p=0.018), intercellular adhesion molecule-1 (p=0.021), von Willebrand factor (p=0.005), and leptin (p=0.005) and lower levels of high-density lipoprotein cholesterol (p=0.042) compared with controls. Consistent with these data, 30% of patients but only 8% of controls fulfilled criteria for the metabolic syndrome as defined by the National Cholesterol Education Program (p=0.015). Endothelium-dependent and -independent microvascular functions were markedly impaired in patients (p<0.001), and the odds ratio for cardiac syndrome X was 7.38 (95% confidence interval 2.2 to 24.7) if the acetylcholine response was <8,710 flux units. In conclusion, women with cardiac syndrome X more commonly have metabolic syndrome and related adiposity, metabolic, and inflammatory derangements. They also have significantly impaired skin microvascular function as assessed by laser Doppler imaging, consistent with generalized vascular dysfunction, a finding with potential diagnostic implications.

Low-Renin Hypertension With Relative Aldosterone Excess Is Associated With Impaired NO-Mediated Vasodilation

Recent studies suggest that hypertension associated with low renin status and hyperaldosteronism is associated with increased risk for end-organ damage and cardiovascular events compared with other forms of hypertension. Additionally, experimental studies have demonstrated impaired nitric oxide-mediated bioactivity in these states. To investigate the relation between renin/aldosterone status and resistance vessel function, we examined plasma renin activity, serum aldosterone level, and forearm blood flow responses to the endothelium-dependent vasodilator methacholine and the endothelium-independent vasodilators sodium nitroprusside and verapamil using venous occlusion plethysmography in 130 volunteers (43 hypertensive, 87 normotensive). Low renin status was associated with impaired responses to methacholine and nitroprusside in patients with hypertension. Peak methacholine response was 8.7+/-5.6 mL/min per dL in the lowest renin quartile (0.1 to 0.3 ng/mL per hour) versus 14.3+/-7.3 mL/min per dL in the highest 3 renin quartiles combined (0.4 to 4.6 ng/mL per hour; P<0.001). Peak nitroprusside response was 5.6+/-2.3 mL/min per dL in the lowest renin quartile versus 13.3+/-4.1 mL/min per dL in the highest 3 renin quartiles combined (P<0.001). Blood pressure and other clinical characteristics were similar in all 4 quartiles. Vasodilator responses to verapamil did not relate to renin activity. Methacholine and nitroprusside responses did not relate to renin status in normotensive controls (P=0.34). Importantly, hypertensive patients with a high aldosterone/renin ratio also had impaired responses to methacholine. This study demonstrates that low-renin hypertension is associated with marked impairment of nitric oxide-mediated vasodilation of resistance vessels in the forearm vasculature of humans. This impairment could contribute to adverse outcomes in patients with low-renin hypertension and relative aldosterone excess.

Effects of sevoflurane and isoflurane on the efficacy of rewarming from hypothermic cardiopulmonary bypass

Effects of sevoflurane and isoflurane on the efficacy of rewarming from hypothermic cardiopulmonary bypass

Part 6: Advanced Cardiovascular Life Support

Part 6: Advanced Cardiovascular Life Support

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 μg · kg–1 · min–1) for the first 60 minutes of reperfusion. Interleukin 6, interleukin 8, and tumor necrosis factor α 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 α (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. (J Thorac Cardiovasc Surg 2000;119:566-74)

The Effects of Clonidine on Sensitivity to Phenylephrine and Nitroprusside in Patients with Essential Hypertension Recovering from Surgery

Clonidine reduces postoperative circulatory instability in patients with essential hypertension.It also increases the sensitivity to vasopressors before and during anesthesia. We investigated blood pressure responses to phenylephrine and nitroprusside pre- vs postoperatively and the effect of clonidine on these responses in patients with essential hypertension. Twenty patients received clonidine 6 [micro sign]g/kg orally 120 min before anesthesia and 3 [micro sign]g/kg IV over the final hour of surgery or an identical placebo. During increasing bolus doses of phenylephrine and nitroprusside (30-300 [micro sign]g), the maximal systolic pressure responses were recorded at baseline on the day before surgery, before the induction of anesthesia, and 1 and 3 h postoperatively. Sensitivity to phenylephrine and nitroprusside was interpolated from linear regression of the data. There was no difference between preoperative and postoperative sensitivity to phenylephrine or nitroprusside in either group. Clonidine increased sensitivity to phenylephrine versus placebo before and after surgery (response to dose of 1.5 [micro sign]g/kg: 42 +/- 14 vs 27 +/- 8 mm Hg preinduction, 37 +/- 10 vs 26 +/- 8 mm Hg 3 h postoperatively; both P < 0.01), but not to nitroprusside (38 +/- 6 vs 37 +/- 10 mm Hg preinduction and 40 +/- 6 vs 39 +/- 8 mm Hg postoperatively). Clonidine increases the sensitivity to phenylephrine but not nitroprusside at baseline and postoperatively in hypertensive patients. Implications: Clonidine increases the sensitivity to bolus injections of the vasoconstrictor phenylephrine, but not the vasodilator sodium nitroprusside, before and after surgery in patients with preexisting hypertension. The doses of vasopressors should be reduced accordingly in hypertensive patients receiving perioperative clonidine. (Anesth Analg 1999;88:1239-43)

Is inhaled nitric oxide a better pulmonary vasodilator than sodium nitroprusside in patients with advanced heart failure?

Is inhaled nitric oxide a better pulmonary vasodilator than sodium nitroprusside in patients with advanced heart failure?

Endothelium-dependent vasodilatation is not selectively impaired in patients with chronic heart failure secondary to valvular heart disease and congenital heart disease.

This study examined possible selective impairment of endothelial dysfunction in the peripheral vascular bed in patients with chronic heart failure in the absence of confounding factors influencing endothelial function (i.e. hypertension, hypercholesterolaemia and diabetes mellitus). Several recent studies have suggested that endothelium-dependent peripheral vasodilation is impaired but endothelium-independent vasodilation is preserved in patients with chronic heart failure. However, a classical paper has demonstrated that sodium nitrite-mediated calf blood flow is clearly depressed in patients with valvular heart disease and cardiomyopathy. We examined forearm blood flow changes mediated by acetylcholine and nitroprusside in patients with valvular heart disease (n = 55) or congenital heart disease (n = 13), and a comparison was made with healthy volunteers (n = 21). The blood flow changes mediated by acetylcholine and nitroprusside were significantly impaired in both patient groups (P < 0.01). When blood flow responses were collected from all patients, two types of vasodilatory capacity were found to have decreased significantly with increasing clinical severity of heart failure (New York Heart Association functional class; P < 0.01). This suggests that the peripheral vasodilatory responses mediated by endothelium-dependent and endothelium-independent vasodilators are significantly impaired in patients with symptomatic chronic heart failure due to non-ischaemic heart disease.