Editorial: Cardiomyopathies.
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Cardiomyopathies↗
Biomedical subjects
G Rona
Publications and source records attributed to G Rona.
Experimental studies on cardiac muscle cell adaptation to insult.
Studies were carried out in rats on myocardial adaptation to injury produced by left coronary artery ligation. In the ischemic zone, open collaterals were present as shown by studies using the fine structural extracellular protein tracer, horseradish peroxidase (HRP). This phenomenon may explain the inhomogeneous cardiac muscle cell alteration in the early phase of coronarogenic myocardial injury. Reperfusion, as evidenced by the influx of HRP into the damaged cells, unmasked sarcolemmal membrane injury. Cardiac muscle cell stimulation modifies the binding of macromolecules to cell components and may influence the repair processes. In the surviving myocardium, correlative enzyme histochemical and ultrastructural studies demonstrated the development of alternative metabolic pathways and morphological signs of adaptation explaining increasing resistance of such cardiac muscle cells to subsequent insult.
Adaptation, Physiological↗
Lymphoma in a pelvic spleen: CT features.
A case of recurrent lymphoma presenting as a pelvic mass on CT is described. At surgery this proved to represent an ectopic spleen with lymphomatous infiltration.
Female↗
Coronary microcirculatory factors and cardiac muscle cell injury.
Coronary artery ligation with or without reperfusion was carried out in Wistar rats to study the role of coronary microcirculatory factors and membrane permeability alteration of cardiac muscle cell in the evolution of cardiac muscle cell injury by using the fine structural extracellular protein tracer, horseradish peroxidase (HRP). The findings were compared with those obtained in noncoronarogenic myocardial injury models following administration of norepinephrine, a pressor, and isoproterenol, a depressor catecholamine. Following left coronary artery ligation lastingfor 10 and 20 minutes, some of the collaterals in the ischemic zone were perused by the tracer, but the numer of patent capillaries decreased during 60-min ligation. The inhomogeneous involvement of cardiac muscle cells in ischemic injury correlated well with these microcirculatory findings. In comparison to permanent ischemia, an abrupt deterioration of the cardiac muscle cell alteration occured after reperfusion with influx of HRP into the damaged cells. The binding of tracer to myofilaments was, however, a later event as compared to that seen in the catecholamine models. The latter observation implies that, in addition to microcirculatory factors, direct cardiac muscle cell stimulation should also be considered in the evolution of noncoronarogenic myocardial injury.
Animals↗