ATP-sensitive potassium channels (K(ATP)) have been thought to be a mediator of cardioprotection for the last ten years. Significant progress has been made in learning the pharmacology of this channel as well as its molecular regulation with regard to cardioprotection. K(ATP)openers as a class protect ischemic/reperfused myocardium and appear to do so by conservation of energy. The reduced rate of ATP hydrolysis during ischemia exerted by these openers is not due to a cardioplegic effect and is independent of action potential shortening. Compounds have been synthesized which retain the cardioprotective effects of first generation K(ATP)openers, but are devoid of vasodilator and cardiac sarcolemmal potassium outward currents. These results suggest receptor or channel subtypes. Recent pharmacologic and molecular biology studies suggest the activation of mitochondrial K(ATP)as the relevant cardioprotective site. Implications of these results for future drug discovery and preconditioning are discussed.

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This review is focused on the composition and organization of the junctional subsarcolemmal cytoskeleton of adult muscle fibers. The cytoskeleton of muscle fibers is organized in functionally distinct compartments and the subsarcolemmal cytoskeleton itself can be broadly divided into junctional (myotendinous junction, neuromuscular junction and costameres) and non-junctional domains. In junctional zones three different multimolecular cytoskeletal complexes coexist: the focal adhesion-type, the spectrin-based and the dystrophin vs utrophin-based membrane skeleton systems. These complexes extend over several levels, from intracytoplasmic to subsarcolemmal and transmembranous; their common feature is the anchorage of actin filaments emanating from the intracytoplasmic level. The different cytoskeletal proteins, their putative roles and their interactions with various signaling pathways are presented here in detail. The subsarcolemmal cytoskeleton complexes are thought to play distinct physiological roles (membrane stabilization, force transmission to extracellular matrix, ionic channel anchorage, etc) but their colocalization on the three sarcolemmal junctional domains strongly suggests interrelated or common functions.

The association between chronic alcohol consumption and alcoholic heart disease in human beings is well recognized. Chronic alcohol consumption is the leading cause of secondary cardiomyopathy, a heart muscle disease associated with long-term alcohol consumption. Both acute and chronic alcohol consumption have a negative inotropic effect on the myocardium, precipitate arrhythmias, and may provoke angina pectoris. There are numerous reports that alcohol changes many subcellular processes that are involved in excitation-contraction coupling. However, the exact mechanism(s) underlying these changes in the heart are still poorly understood. Despite the recent presumptive protective reports that moderate alcohol consumption protects against the risk of coronary artery disease, nurses and physicians must educate all patients about the many other adverse effects of alcohol on the cardiovascular system. The purpose of this article is to review and discuss the mechanism(s) that may underlie changes in contractile function after long-term alcohol consumption and identify current trends in identification and treatment of alcoholic heart disease.

The main results obtained by the author and collaborators in 25 years\' work about the type of sialic acid determined in some materials from the animal kingdom are summarized, with the respective references to the original papers and the indication of the reviews in which they have generally been quoted. The high number of publications on sialic acids from the time of their discovery reflects the increasing interest on these acids in areas such as their chemical composition (16 different sialic acids are now recognized), their distribution in Nature (a not yet well explained topic), their metabolism (which shows differences between bacteria and animal cells) and their biological roles, mainly as a part of glycoproteins and gangliosides (as receptors, markers of the cytoplasmic membrane, viscosity agents of the glycoproteins, life regulators of some substances, etc.).

In this review we present the effects of a well-known antianginal drug, prenylamine (PNL), in experimental models of acute myocardial damage induced by a beta-agonistic drug, isoproterenol (ISP), in several trials conducted in our laboratory in both rats (n = 204) and monkeys (n = 26). PNL significantly inhibited ISP-induced lesions, protecting the majority of animals studied. Studies dealing with the site of action of the drug, such as 45Ca, 3H-PNL and 3H-ISP trials, showed a clear membrane effect slowing down Ca transport. Correlation between ECG (inhibition of ST depression after ISP) and pathological findings in monkeys was also obtained in one of our experiments. These series of assays were useful in obtaining a more complete idea of activity and site of action of the drug. It seems that, in acute models, PNL acts as a calcium antagonistic drug rather than an adrenergic moderator.

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