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Pulmonary hypertension in congestive heart failure causes medial hypertrophy in pulmonary vessels and thickening of the endothelial basement membrane. In this study, the functional consequences of such pulmonary vascular adaptations were evaluated. Heart failure was induced in dogs by rapid ventricular pacing (240 beats per minute) for 28 days, at which time left ventricular shortening fraction was decreased by 57% compared with that at baseline. Lung lobes from paced (n=56) and control dogs (n=68) were isolated and perfused with autologous blood. Total, arterial (Ra), and venous (Rv) vascular resistances were significantly increased and vascular capacitance decreased in lobes from paced animals compared with controls. Increments in Ra and Rv after intra-arterial boluses of norepinephrine were measured before and after sequential addition of the al-and a2-receptor antagonists prazosin (16 ,umol/L) and yohimbine (0.1 gmol/L) in the presence or absence of propranolol (5 ,umol/L). Nor-epinephrine (1 to 40 jig) had little effect on Ra in the absence of propranolol, a pattern that persisted in control lobes after propranolol. However, when lobes from paced animals were pretreated with propranolol, norepinephrine increased Ra. Rv was increased after norepinephrine in control lobes, an effect that was enhanced in the paced group. In both groups, the increment in Rv was greater after propranolol. Irrespective of propranolol pretreatment, prazosin significantly attenuated, if not abolished, the response to norepinephrine. The enhancement in venous vascular reactivity in lobes from paced animals remained when venous pressure was elevated to 20 cm H20. In control lobes under conditions of elevated tone or when endothelium-dependent relaxing factor was blocked, responses to norepinephrine did not mimic those observed in the paced group. Microvascular permeability, as measured by the capillary filtration coefficient, was not altered in the paced group. We conclude that the pulmonary adaptations to 4 weeks of rapid ventricular pacing include functional changes in pulmonary hemodynamics and vascular reactivity but not in microvascular permeability. (Circ Res. 1994;75:347-356.) Key Words * congestive heart failure * pulmonary venous hypertension * pulmonary circulation * isolated lung * yohimbine * prazosin * propranolol C ongestive heart failure is associated with chronic exposure of the lung to high pulmonary vascular pressures. In part, this may be due to the increased circulating levels of humoral vasoconstrictors such as catecholamines and angiotensin II observed in animal models of heart failure and in humans with congestive heart failure.1-3 Although pulmonary capillary pressure (Pc), and therefore transcapillary fluid flux, would be predicted to be increased as a result, not all patients with congestive heart failure or high pulmonary vascular pressures secondary to mitral stenosis develop pulmonary edema.3 Several mechanisms could potentially contribute to protection of the lung against edema formation and a...

For unclear reasons, myocardial infarction is rare in childhood sickle cell disease, whereas lung, bone, and brain infarcts are more common. During vasoocclusive crisis and infection, acute myocardial ischemia and chronic volume overload from anemia may result in myocardial dysfunction. We report a child who had reversible cardiac dysfunction that mimicked myocardial infarction.

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