Mechanisms of volume-induced increase in left ventricular contractility

Abstract

Volume-induced increases in left ventricular (LV) contractility were studied in 18 anesthetized dogs. Denervation eliminated cardiac reflexes, and hearts were paced at 100 +/- 9 (SD) beats/min. Acute volume loading increased LV end-diastolic pressure from approximately 4 to 14 mmHg within 1 min. Contractility increased over 10 min as measured by a decrease in end-systolic length (ESL) (sonomicrometer) at matched LV end-systolic pressure (ESP) or increase in LVESP measured at matched ESL. Volume-dependent increase in contractility was not attenuated by verapamil (0.3 +/- 0.2 microgram/kg i.v., n = 6) or myocardial stunning (15 min ischemia, 30 min reperfusion, n = 6) but was attenuated by ryanodine (1-16 micrograms/kg i.v., n = 6), which alters calcium release from the sarcoplasmic reticulum. From 1 to 10 min after volume loading, LV anterior ESL (measured at LVESP 132 +/- 12 mmHg) decreased by 6.7 +/- 0.5% before, but only by 4.0 +/- 1.7% after 1 microgram/kg ryanodine (P < 0.05). The LVESP (measured at anterior ESL 11.6 mm) increased 32 +/- 4 mmHg before, but only by 17 +/- 12 mmHg after 1 microgram/kg ryanodine. In conclusion, acute volume loading produces a time-dependent increase in LV contractility, which is mediated in part by an increase in calcium release from the sarcoplasmic reticulum.