Despite careful clinical, noninvasive, and hemodynamic assessment of patients with constrictive/restrictive physiology, the differentiation of restrictive cardiomyopathy from constrictive pericarditis remains difficult. We examined the role of right ventricular endomyocardial biopsy in defining the underlying process in 54 patients with evidence of constrictive/restrictive physiology, including 38 patients with profound symptoms of heart failure in whom diagnostic/therapeutic thoracotomy was contemplated (group I) and 16 patients with milder symptoms (group II). All patients in group I had NYHA class III or IV heart failure with depressed cardiac index (mean 2.5 liters/minIm2), right atrial hypertension (mean 15 mm Hg), and normal left ventricular ejection fraction (mean 59%). Endomyocardial biopsy identified a specific source of restrictive cardiomyopathy in 15 of 38 patients (39%) (1 1 amyloid, four myocarditis). Of the 23 remaining patients with either normal biopsy findings or nonspecific abnormalities on biopsy, 18 had intraoperative or autopsy evaluation of their pericardium, and constriction was found in 14 (77%). A specific form of restrictive cardiomyopathy was also identified in four of the 16 patients with milder symptoms (group II). We conclude that endomyocardial biopsy is useful in patients with severe constrictive/restrictive physiology. It identifies a large subset of patients with specific forms of restrictive cardiomyopathy in whom thoracotomy should be avoided. It supports the need for thoracotomy and the likelihood of finding pericardial constriction in patients without specific pathologic findings.

A B S T R A C T Acetylcholine produces venoconstriction of isolated vein strip preparations. However, the effect of acetylcholine on overall vascular capacity is not known. To investigate this effect and to elucidate the mechanisms involved, 38 anesthetized dogs were placed on total cardiopulmonary bypass, splenectomized, and given intraarterial infusions of acetylcholine. Almost all of the effect on vascular volume was found to be in the splanchnic circulation, because in four eviscerated animals there was no significant change in capacity. In the animals in which the mesenteric arteries were cannulated to provide constant inflow, and the hepatic vein was cannulated to measure splanchnic venous outflow, acetylcholine infusion for 5 and 21 min increased splanchnic vascular capacity in all animals by 107±28 (SEM) ml (P < 0.01) and 291±132 ml (P < 0.05), respectively. This increase in splanchnic vascular volume was associated with a rapid and sustained increase in transhepatic resistance to portal blood flow for the duration of the infusions (P < 0.01). In the animals in which the portal vein was vented proximal to the liver, no significant volume change occurred in the splanchuiic vasculature with acetylcholine infusion. Increasing hepatic venous pressure to elevate portal venous pressure to the same level as that achieved with acetylcholine resulted in a similar increase in splanchnic vascular volume. Atropine, but not adrenergic blockade, blocked the acetylcholine-induced volume retention, indicating that the effect of acetylcholine was direct. Substantial volume retention was also achieved by stimulation of the distal ends of the sectioned cervical vagi. Thus, acetylcholine administration directly increases transhepatic resistance and is associated with a pooling of volume in the splanchnic vasculature that would, in the intact animal, result in a decrease in venous return to the heart.

Introduction

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SUMMARY The role of a r adrenergic receptor stimulation in the regulation of systemic vascular capacity and venous return, a major determinant of cardiac output, is not well understood. With the influence of the central nervous system isolated from the systemic circulation, the direct peripheral vascular effects of two specific, chemically distinct a 2 -adrenergk receptor agonists, UK 14,304 and B-HT 920, were investigated in 19 dogs on total cardiopulmonary bypass with constant arterial perfusion and central venous pressure. Five-minute intra-arterial infusions of UK 14,304 (200 /ig/min) resulted in increased arterial resistance (mean arterial pressure increased 18 ± 4 [SEM] mm Hg; p<0.01) and a decrease hi systemic vascular capacity (81 ± 20 ml; p<0.01). This decrease in systemic vascular capacity appears to result from vasoconstriction, since there was no decrease in transhepatic resistance to portal flow and no significant change in hepatic vein flow to suggest redistribution of arterial blood flow. Yohimbine abolished both the arterial and systemic capacity effects, whereas prazosin did not. Intra-arterial administration of B-HT 920 (200 Oglmin) in five dogs produced similar changes in arterial resistance and systemic capacity. These findings provide direct evidence for /^-adrenergic control, not only of arterial resistance but also of systemic vascular capacity, which in the intact nnlmnl would increase venous return to the heart. (Hypertension 11: 352-359, 1988) KEY WORDS • UK 14,304 • B-HT 920 • yohimbine • canine T HE importance of the regulation of systemic vascular capacity, which in turn determines venous return to the heart and thus cardiac output, has been a subject of recent investigation. l~* /3-Adrenergic receptor stimulation has been shown to decrease vascular capacity, 1 " 3 and acetylcholine infusion and parasympathetic nerve stimulation have been shown to increase vascular capacity. 4 The role of aadrenergic stimulation in the regulation of systemic vascular capacity is less well understood. Postsynaptic cr 2 -adrenergic receptors have been demonstrated in the