Ryanodine and left ventricular function in intact dogs: dissociation of force-based and velocity-based indexes
| Autor: | M. M. Rozek, David R. Murray, Sumanth D. Prabhu, Gregory L. Freeman |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Physiology Systole Ventricular Function Left Contractility Dogs Diastole Heart Rate Physiology (medical) Internal medicine Autonomic blockade Carnivora Medicine Animals biology Ventricular function business.industry Ryanodine receptor Ryanodine Fissipedia Hemodynamics Anatomy biology.organism_classification Myocardial Contraction Circulatory system Injections Intravenous Cardiology Female Cardiology and Cardiovascular Medicine business |
| Zdroj: | The American journal of physiology. 273(3 Pt 2) |
| ISSN: | 0002-9513 |
| Popis: | After anesthesia and autonomic blockade, nine dogs chronically instrumented with left ventricular (LV) micromanometers and piezoelectric dimension crystals were studied before and after the intravenous administration of 4 micrograms/kg ryanodine, a specific inhibitor of the sarcoplasmic reticulum Ca2+ release channel. Ryanodine prolonged LV contraction and relaxation (P < 0.001) without changing heart rate, end-diastolic volume (EDV), or end-systolic pressure. Velocity-dependent mechanical parameters were significantly depressed, including the maximal rate of LV pressure rise (dP/dtmax; P < 0.002), the mean velocity of circumferential fiber shortening (P < 0.002), the slope of the dP/dtmax-EDV relation (P < 0.05), and the time constant of LV relaxation (P < 0.01). In contrast, the slopes of the end-systolic pressure-volume (PES-VES) and stroke work (SW)-EDV relations, both force-based parameters, were increased (P < 0.05) or maintained, respectively. Ryanodine reduced overall LV contractile performance, evidenced by significant rightward shifts of the PES-VES, dP/dtmax-EDV, and SW-EDV relations and reduced SW at constant preload (P < 0.02). Thus, in the closed-chest dog, low-dose ryanodine resulted in 1) generalized slowing of LV mechanical events without changes in heart rate or load, 2) dissociation of velocity-based and force-based measures of LV function, with depression of the former but enhancement or maintenance of the latter, and 3) reduced overall LV inotropic performance. These effects are consistent with ryanodine-induced alterations of the Ca2+ transient and altered sarcoplasmic reticulum Ca2+ availability. |
| Databáze: | OpenAIRE |
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