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G A Misbach

Publications and source records attributed to G A Misbach.

25 records · Page 2Linked to original sources
PubMed1981

Effect of the normal pericardium on the left ventricular diastolic pressure-volume relationship.

Closed chest placement of tantalum screws in the endocardium was performed an biplane cineradiography of these markers was used to measure LV dimensions while changing total blood volume. Measurements were then repeated following thoracotomy, pericardiotomy and reclosure of the thorax. The LV pressure-volume curves obtained after pericardiotomy always were shifted down and to the right from curves obtained before thoractomy and pericardiotomy. The divergence between the curves increased as LV volume increased, the curves being identical at small LV volumes and at low diastolic pressures. In each experiment the curves diverged before LV diastolic pressure exceeded 10 mm Hg, however.

Animals↗
PubMed1979

Changes in the diastolic pressure-diameter relation after ventricular function curves.

Systolic performance depends on end-diastolic muscle fiber length, contractility, and afterload. Ventricular function curves are constructed using end-diastolic pressure instead of end-diastolic dimensions, on the assumption that end-diastolic pressure and end-diastolic dimensions (reflecting muscle fiber length) have a constant relation. That assumption has been rejected. Theorectically, ventricular function curves should change with changes in the diastolic pressure-dimension relation as well as with contractility or afterload. We measured pressures and dimensions in ventricles of six open-chest dogs before and after opening the pericardium to alter diastolic pressure-dimension relations with afterload constant. When an indicator of systolic performance (developed pressure times diameter change during systole) was plotted against end-diastolic pressure, data obtained with the pericardium closed and open resulted in two distinct curves, suggesting an increase in contractility with the pericardium open. However, when systolic performance was plotted against end-diastolic diameter, data obtained with the pericardiumclosed and open fell along one curve, indicating no change in contractility. Therefore, changes in the diastolic pressure-dimension relation to shift conventional ventricular function curves.

Animals↗
PubMed1978

A mechanism for shifts in the diastolic, left ventricular, pressure-volume curve: the role of the pericardium.

Attempts to explain acute shifts in the pressure-volume relationship by changes in myocardial stiffness have been unsupported by animal experimentation and discouraged by calculations showing that making half the ventricle rigid would hardly account for the clinically observed upward shifts in the curve. Data collected in open-chest anesthetized dogs during volume loading with the pericardium open and closed indicate that when the pericardium is closed, left ventricular enddiastolic pressure is better predicted by right ventricular pressure than by left ventricular dimensions. These data support the hypothesis that acute, upward shift in the pressure-volume curve may be caused by an increase in pericardial pressure, in turn caused by an increase in the volume of the intrapericardial contents. This follows from the fact that measured left ventricular diastolic pressure is equal to the sum of the pressure differences accross the myocardium and the pericardium. Thus, increases in pericardial pressure raise measured ventricular diastolic pressure without change in ventricular volume: hence, an upward shift in the pressure-volume curve.

Animals↗
PubMedDate not supplied

Diastolic mechanical properties of the left ventricle after global ischemia.

The purpose of this study was to evaluate left ventricular (LV) diastolic mechanical properties after induced global ischemia using reliable new methods. The diastolic function of nonoxygenated crystalloid solution (CC sO2) was compared with those of oxygenated crystalloid (CC cO2) and oxygenated fluorocarbon cardioplegic (FC cO2) solutions. Postischemic ventricular performance was studied in 3 equal (no. 7) groups of dogs subjected to 120 minutes of global ischemia induced at an average myocardial temperature of 18.5 +/- 1.4 degrees C. LV diastolic function (chamber and myocardial stiffness) and relaxation (the exponential fall in LV pressure) were evaluated by sonomicrometry and Millar micrometers before ischemia and at 45 and 60 minutes after ischemia. LV chamber and myocardial stiffness in the CC sO2 group was significantly (p less than 0.05) elevated after ischemia, while the CC cO2 and FC cO2 groups did not show increases in LV chamber and myocardial stiffness after ischemia. LV relaxation before and after ischemia was not changed in any group. The myocardial water content of the CC sO2 group was significantly higher than that of the CC cO2 and FC cO2 groups (p less than 0.05). We conclude that (1) the postischemic increase in LV chamber stiffness in the CC sO2 group was dependent not only on the increase in intrinsic myocardial stiffness but also due to an increase in myocardial edema, and (2) there was no correlation between the LV relaxation rate and the leftward shift of diastolic compliance curves in the CC sO2 group.

Animals↗