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BACKGROUND AND PURPOSE:Hemodynamics is thought to play an important role in the mechanisms of cerebral aneurysm initiation, progression, and rupture. The purpose of this study was to present a hemodynamic study of a cerebral aneurysm immediately before its rupture to assess whether previously identified hemodynamic characteristics would classify this aneurysm in the high-risk category.

Long chain free fatty acids (FFA) are the preferred metabolic substrates of myocardium under aerobic conditions. However, under ischemic conditions long chain FFA have been shown to be harmful both clinically and experimentally. Serum levels of free fatty acids frequently are elevated in patients with myocardial ischemia. The proposed mechanisms of the detrimental effects of free fatty acids include: (1) accumulation of toxic intermediates of fatty acid metabolism, such as long chain acyl-CoA thioesters and long chain acylcarnitines, (2) inhibition of glucose utilization, particularly glycolysis, during ischemia and/or reperfusion, and (3) uncoupling of oxidative metabolism from electron transfer. The relative importance of these mechanisms remains controversial. The primary site of FFA-induced injury appears to be the sarcolemmal and intracellular membranes and their associated enzymes. Inhibitors of free fatty acid metabolism have been shown experimentally to decrease the size of myocardial infarction and lessen postischemic cardiac dysfunction in animal models of regional and global ischemia. The mechanism by which FFA inhibitors improve cardiac function in the postischemic heart is controversial. Whether the effects are dependent on decreased levels of long chain intermediates and/or enhancement of glucose utilization is under investigation. Manipulation of myocardial fatty acid metabolism may prove beneficial in the treatment of myocardial ischemia, particularly during situations of controlled ischemia and reperfusion, such as percutaneous transluminal coronary angioplasty and coronary artery bypass grafting.

Gene transfer to modify donor heart function during transthe ␤ 2 -AR agonist, zinterol. Treatment with the ␤ 2 -AR virus plantation has significant therapeutic implications. Recent resulted in global myocardial gene transfer with a six-fold studies by our laboratory in transgenic mice have shown increase in mean ␤-AR density which corresponded to a that overexpression of ␤ 2 -adrenergic receptors (␤ 2 -ARs) significant increase in basal contractility (LV + dP/dt max , leads to significantly enhanced cardiac function. Thus, we control: 3152.1 ± 286 versus ␤ 2 -AR, 6250.6* ± 432.5 investigated the functional consequences of adenovirusmmHg/s; n = 10, *P Ͻ 0.02). ␤ 2 -AR overexpressing hearts mediated gene transfer of the human ␤ 2 -AR in a rat heteroalso had higher contractility after zinterol administration topic heart transplant model. Donor hearts received 1 ml compared with control hearts. Our results indicate that of solution containing 1 × 10 10 p.f.u. of adenovirus encomyocardial function of the transplanted heart can be ding the ␤ 2 -AR or an empty adenovirus as a control. Five enhanced by the adenovirus-mediated delivery of ␤ 2 -ARs. days after transplantation, basal left ventricular (LV) pressThus, genetic manipulation may offer a novel therapeutic ure was measured using an isolated, isovolumic heart perstrategy to improve donor heart function in the postfusion apparatus. A subset of hearts was stimulated with operative setting.