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Biomedical subjects

C W Urschel

Publications and source records attributed to C W Urschel.

At least 19 recordsLinked to original sources
PubMed1980

Critical evaluation of indices of myocardial contractility derived from the isovolumic phase of contraction.

The accuracy, sensitivity and reproducibility of several isovolumic force-velocity indices of myocardial contractility were compared. Contractile element velocity was calculated using both two-element (total pressure) and three-element (developed pressure) models of cardiac muscle. While all indices demonstrated comparable sensitivity to inotropic state, only Vmax using developed pressure was independent of preload and appeared to be a useful index of the myocardial contractile state.

Animals↗
PubMed1979

Effects of sodium nitroprusside on function of regional ischemic myocardium.

In the presence of regional myocardial ischemia, a 20% decrease in systemic arterial pressure following nitroprusside caused a 25% decrease in coronary perfusion pressure in animals with normal left ventricular end-diastolic pressures. This pressure decrement resulted in a significant decrease in the shortening of the regionally ischemic segment during the ejection phase of systole. A comparable arterial pressure drop of 21% with nitroprusside infusion during ischemia in the animals with elevated diastolic pressures caused a similar 28% decrease in coronary perfusion pressure, but resulted in a simultaneous increase in regional shortening. For the entire group there was no significant change in stroke volume. Even in the 11 animals where stroke volume increased, systolic regional shortening increased in only 4. An increase in stroke volume cannot be used to infer a parallel increase in the performance of a regionally ischemic segment. Nitroprusside appears to improve regional performance only in the presence of severe failure.

Animals↗
PubMed1976

Experimental myocardial ischemia: dynamic alterations in ventricular contractility and relaxation with dissociation of speed and force in the isovolumic dog heart.

Although the time course of changes in myocardial function during ischemia has been demonstrated for the papillary muscle, this time course in the intact heart is less well understood. Accordingly, in 24 isolated, isovolumic, perfused dog hearts, coronary perfusion pressure (PP) was lowered to various fixed levels. Left ventricular developed pressure (LVP) rapidly fell and reached 63 +/- 3% of control at 1 minute of ischemia 50 +/- 5% at 6 minutes; this was due primarily to an abbreviation of time to peak tension (TPP). dP/dt was 70 +/- 3% of control at 1 minute and 56 +/- 5% at 6 minutes. The rate of relaxation as reflected by negative dP/dt declined as well to 49 +/- 4% of control at 1 minute of ischemia and to 41 +/- 4% control at 6 minutes. These changes were directly correlated with the decrease in PP. When PP was restored to normal, an overshoot of LVP and dP/dt was noted, peaking at 1 minute, returning to control by 5 minutes, and then gradually declining to 90 +/- 2% of control following 25 minutes of recovery. Depression of the rate of relaxation was reduced, but persisted throughout recovery. Diminution of force development early in ishcemia is due primarily to decreased duration of contraction accompanied by a decrease in relaxation rate. Later, the rate of force development also falls, but some preservation of force development may result from the return toward normal of the duration of contraction.

Animals↗
PubMed1975

Detection of latent function in acutely ischemic myocardium in the dog: comparison of pharmacologic inotropic stimulation and postextrasystolic potentiation.

In poorly perfused myocardium with resultant ischemic dysfunction, augmentation of contractility can, under certain conditions, be used to detect viable but ordinarily noncontracting muscle. Two methods of inotropic augmentation, pharmacologic inotropic stimulation and postextrasystolic potentiation (PESP), were studied in acutely ischemic canine myocardium with controlled coronary blood flow. A caliper length gauge to record segmental shortening and left ventricle pressure was used to construct pressure-length loops. Acute regional ischemia depressed segmental function: early segmental shortening decreased (-20 plus or minus 0.02% [SE]) and frequent dyskinesia occurred. Restoring coronary blood flow corrected segmental shortening to control levels. During acute regional ischemia, PESP consistently augmented segmental function (+49 plus or minus 0.03%) and abolished dyskinesia. Pharmacologic inotropic stimulation with isoproterenol or calcium administered into the coronary arteries did not produce a comparable improvement in segmental function (+9 plus or minus 0.05%). Although early shortening markedly increased with pharmacologic stimulation, there was no consistent change in total shortening, and the area of the pressure-length loop decreased. Due to late dyskinesia, there was a decrease in injection shortening. Systemically administered pharmacologic agents accentuated early dyskinesia but caused no consistent change in total shortening. Unlike PESP, pharmacologic agents either worsened segmental function or caused responses that were minimum and inconsistent; such responses clearly cannot be used to identify viable ischemic myocardium.

Acute Disease↗