LYMPH ISOLATED FROM A REGIONAL SCALD INJURY PRODUCES A NEGATIVE INOTROPIC EFFECT IN DOGS

Large surface-area burns in patients have been associated with a sever e impairment in cardiac performance, as evidenced by a decline in card iac output. The mechanisms responsible for this profound myocardial dy sfunction are largely unknown. We investigated the effects of lymph is olated from the scalded hind limb of dogs on regional myocardial blood flow, coronary vascular reactivity, and contractile performance. Dogs were instrumented with ultrasonic dimension crystals in the myocardiu m supplied by the left anterior descending (LAD) and by the left circu mflex (LCx) coronary arteries. After cannulating a hind limb lymphatic , lymph was infused directly into the LAD before and after a 10-second 100 degrees C hind limb scald. Scalding alone did not alter myocardia l contractile performance in the LAD or LCx regions, coronary artery b lood flow, or systemic hemodynamics. Interestingly, postburn lymph inf used into the LAD resulted in a 38% decline in LAD zone segment shorte ning (p < 0.01 vs baseline) that lasted throughout the 5-hour observat ion period. In contrast, segment shortening in the (control) LCx regio n was unaffected by postburn lymph injections into the LAD. Regional m yocardial blood flow (radiolabded microspheres) in the LAD and LCx reg ions was unchanged after scald injury or intracoronary injection of po stburn lymph. In addition, LAD coronary artery vascular reactivity to acetylcholine and nitroglycerin was also unaffected by the regional th ermal injury or by injection of lymph into the LAD. These data suggest that a regional scald injury results in the production and release of a potent myocardial depressant factor(s) that produces a direct negat ive inotropic effect on the canine myocardium.