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M M Bersohn

Publications and source records attributed to M M Bersohn.

8 recordsLinked to original sources
PubMed1992

Measurement of sarcolemmal vesicle orientation by beta-adrenergic receptor binding.

To assess the orientation (inside-out vs. outside-out) of purified cardiac sarcolemmal vesicles, we developed a new method utilizing the known outward-facing binding site of the beta-adrenergic receptor. We compared the binding of the lipid-insoluble ligand 3H-CGP-12177, which binds to beta-adrenergic receptors on outside-out sarcolemmal vesicles only, to the binding of the lipid soluble ligand 125I-iodocyanopindolol, which binds to beta-adrenergic receptors in sarcolemmal vesicles of either orientation. The ratio of CGP to ICYP binding is equal to the fraction of outside-out sarcolemmal vesicles. Sidedness measurements by beta-adrenergic receptor-binding showed similar mean values but less scatter than sidedness assessments by measurement of 3H-ouabain-binding or Na+,K(+)-ATPase activity in the presence or absence of membrane permeabilizing agents.

Animals↗
PubMed1991

Effect of temperature on sodium-calcium exchange in sarcolemma from mammalian and amphibian hearts.

We have investigated temperature dependence of Ca2+ uptake by the cardiac sarcolemmal Na(+)-Ca2+ exchanger from dog, rabbit and bullfrog. In native rabbit sarcolemmal vesicles, Ca2+ affinity of the Na(+)-Ca2+ exchanger is unchanged from 7 to 37 degrees C; however, the initial velocity of Ca2+ uptake declines much more steeply below 22 degrees C than above 22 degrees C. In native dog sarcolemma, the temperature dependence of Na(+)-Ca2+ exchange velocity is similar to that of native rabbit. However, in frog heart the velocity of Na(+)-Ca2+ exchange declines much more slowly with decreasing temperature at both temperature ranges. Reconstitution of the Na(+)-Ca2+ exchanger into artificial lipid vesicles consisting of either asolectin or phosphatidylserine, phosphatidylcholine, and cholesterol has little effect on temperature dependence of Na(+)-Ca2+ exchange velocity in any of the three species. We conclude that the lesser temperature sensitivity of the cardiac sarcolemmal Na(+)-Ca2+ exchanger of a poikilothermic species is at least partly an intrinsic property of the transport protein.

Animals↗
PubMed1991

Lysophosphatidylcholine and sodium-calcium exchange in cardiac sarcolemma: comparison with ischemia.

Lysophosphoglyceride accumulation in ischemic myocardium has been hypothesized to be a mechanism for altered sarcolemmal properties that underlie electrophysiological changes and Ca2+ accumulation in ischemia. We find that in vitro application of lysophosphatidylcholine to normal canine sarcolemmal vesicles at a concentration of 0.3 mumol/mg sarcolemmal protein inhibits Na(+)-Ca2+ exchange. Both maximum velocity (Vmax) for Ca2+ transport and Ca2+ affinity are reduced by lysophosphatidylcholine, whereas in ischemia only Vmax is reduced [M. M. Bersohn, K. D. Philipson, and J. Y. Fukushima. Am. J. Physiol. 242 (Cell Physiol. 11): C288-C295, 1982]. This amount of lysophosphatidylcholine does not affect sarcolemmal passive permeability to either Ca2+ or Na+. Treatment of sarcolemma with phospholipase A2 sufficient to inhibit Na(+)-Ca2+ exchange velocity by 50% causes large increases in sarcolemmal lysophosphatidylcholine and lysophosphatidylethanolamine. On the other hand, 1 h of ischemia in rabbit hearts does not affect sarcolemmal phospholipid composition. Thus, although in vitro treatment with lysophosphatidylcholine or phospholipase A2 has profound effects on sarcolemmal properties, sarcolemmal accumulation of lysophosphatidylcholine cannot account for the effects of ischemia as measured in highly purified sarcolemmal vesicles from ischemic hearts.

Animals↗
PubMed1986

Mechanically mediated pacemaker pseudomalfunction.

A case is described of pacemaker pseudomalfunction caused by intermittent displacement of the ventricular lead. The displacement was shown to be caused by critically timed atrial contractions, dislodging the looped ventricular lead, and resulting in intermittent failure to stimulate the heart.

Aged↗
PubMed1977

Effects of physical training on end-diastolic volume and myocardial performance of isolated rat hearts.

We studied the performance of ventricular muscle and cardiac function of hearts from rats conditioned by swimming (CH) and from sedentary rats (SH) in an isolated working heart apparatus modified to measure end-diastolic volume by dye dilution. Instantaneous aortic flow, left ventricular (LV) pressure and oxygen consumption were measured. Heart rate and mean aortic pressure were kept constant, and atrial filling pressure was varied from 5 to 20 cm H2O. Heart weights of SH and CH were equal and end-diastolic pressures and volumes were similar at all atrial pressures. However, ejection fraction, calculated circumferential fiber velocity, peak systolic pressure, peak aortic flow, cardiac output, and stroke work were all greater in CH than in SH, and the differences increased as atrial pressure was increased. Maximal negative dP/dt was greater in CH than SH at all preloads (P less than 0.001). Oxygen consumption of CH was increased in proportion to the increase in work. These results indicate that the improved pumping performance of CH is due to a change in ventricular muscle function. Faster relaxation is a prominent effect of physical training on the rat heart and may foster more complete filling at high heart rates.

Animals↗