Effect of alkali therapy with nahco3 or tham on cardiac contractility. Mazer, C. D., B. Naser, and K. S. Kamel. Departments of Anaesthesia and Nephrology, St. Michael's Hospital, University of Toronto, Toronto, Canada
APStracts 2:0319R, 1995.
We examined the impact of alkali therapy on myocardial contractility in a model of myocardial ischemia in dogs using direct measurements of myocardial contractile function. Myocardial ischemia in the left anterior descending (LAD) artery territory was induced using a perfusion circuit from the internal carotid artery to the LAD artery. Myocardial contractile function was assessed using sonomicrometry for measurement of % systolic shortening (% SS), pre-load recruitable stroke work (PRSW) and end-systolic pressure length relationship (ESPLR). As the blood flow in LAD artery was diminished by about 70 %, there was a significant decrease in O2 delivery and uptake by the ischemic myocardium. Ischemia led to a significant fall in LAD regional contractile function with % SS decreasing from 15 +/- 2% to 7 +/- 2%, PRSW slope from 82 +/- 10 to 37 +/- 5 mm Hg and ESPLR area from 121 +/- 2 to 48 +/- 14 mm Hg.mm (p &LT 0.05). In six dogs, the intracoronary administration of NaHCO3 resulted in a significant increase in pH in LAD arterial and venous blood. There was, however, no significant increase in % SS (6 +/- 2), PRSW slope (43 +/- 10 mm Hg) or ESPLR area (60 +/- 13 mm Hg.mm). Since the administration of NaHCO3 resulted in a significant increase in Pco2 in LAD arterial and venous blood, similar experiments were carried out in five dogs, but with the intracoronary infusion of the amine buffer THAM instead of NaHCO3. Although the administration of THAM resulted in a significant increase in pH and a significant decrease in Pco2, in both LAD arterial and venous blood, there was no significant improvement in any of the parameters used to assess myocardial contractile function. In conclusion, the administration of alkali (NaHCO3 or THAM) does not enhance the contractile function of the ischemic myocardium.

Received 29 June 1995; accepted in final form 27 October 1995.
APS Manuscript Number R386-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95