scholarly journals Comments on "Factors which affect the diastolic pressure-volume curve".

1979 ◽  
Vol 44 (4) ◽  
pp. 589-592
Author(s):  
W Grossman ◽  
W H Barry
1978 ◽  
Vol 42 (2) ◽  
pp. 171-180 ◽  
Author(s):  
S A Glantz ◽  
W W Parmley

1994 ◽  
Vol 266 (4) ◽  
pp. H1373-H1385 ◽  
Author(s):  
H. Shintani ◽  
S. A. Glantz

The reversible upward shift of the diastolic pressure-volume curve that occurs during pacing-induced ischemia has not been fully explained by increases in passive chamber stiffness or reductions in relaxation rate. We measured the fully relaxed pressure-volume relation defined by both filling and nonfilling beats and the isovolumic relaxation time constant in nonfilling beats before and during demand ischemia using our in situ left ventricular volume clamping technique in 10 dogs. Pacing-induced ischemia shifted the diastolic pressure-volume curves in filling beats upward compared with the end-diastolic pressure-volume relation of the normally perfused heart. In contrast, the end-diastolic points for nonfilling beats during pacing-induced ischemia fell on the fully relaxed pressure-volume relation defined by the normally perfused heart. Left ventricular filling per se was necessary for the upward shift of the diastolic pressure-volume curve observed during pacing-induced ischemia. We speculate that active force developed during diastole induced by stretch activation or, perhaps, length-dependent changes in calcium sensitivity of the myofilaments in the ischemic myocardium due to stretch of the myocardium during rapid diastolic filling may contribute to the upward shift of the diastolic pressure-volume curve observed during pacing-induced ischemia.


Circulation ◽  
1997 ◽  
Vol 96 (12) ◽  
pp. 4408-4414 ◽  
Author(s):  
Thomas J. Fraites ◽  
Akio Saeki ◽  
David A. Kass

1998 ◽  
Vol 274 (6) ◽  
pp. H2100-H2109 ◽  
Author(s):  
Masao Tayama ◽  
Steven B. Solomon ◽  
Stanton A. Glantz

The diastolic pressure-volume curve shifts upward during demand ischemia, most likely because of changes in Ca2+ dynamics within the sarcomere. It is possible that agents that affect Na+/Ca2+exchange, such as lidocaine, a class 1b-type Na+-channel blocker that decreases intracellular Na+, could affect the diastolic pressure-volume relationship because of indirect effects on intracellular Ca2+. Lidocaine is a drug widely used to treat arrhythmias in patients with myocardial ischemia. We studied the effects of lidocaine on diastolic dysfunction associated with demand ischemia. We compared diastolic (as represented by the shift in the diastolic pressure-volume relationship) and systolic function during demand ischemia before and after lidocaine injection. We created demand ischemia in pigs before and after administering lidocaine (5 mg/kg) in eight open-pericardium anesthetized pigs. Demand ischemia was induced by constricting the left anterior descending coronary artery and then pacing at 1.5–1.8 times the baseline heart rate for 1.5–3 min. Hemodynamics were recorded during baseline, demand ischemia, baseline after lidocaine injection, and demand ischemia after lidocaine. Lidocaine did not affect systolic function or the time constant of isovolumic relaxation, but it increased the upward shift of the diastolic pressure-volume curve during demand ischemia compared with the increase that occurred before lidocaine was administered. This result suggests that lidocaine could aggravate diastolic dysfunction in patients with ischemic heart disease.


1991 ◽  
Vol 52 (5) ◽  
pp. 1052-1057 ◽  
Author(s):  
Joseph S. Auteri ◽  
Valluvan Jeevanandam ◽  
Mark R. Bielefeld ◽  
Juan A. Sanchez ◽  
Henry M. Spotnitz

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