Hemodynamic changes during prolonged carbon monoxide inhalation in the rat

49 HEMODYNAMIC CHANGES DURING PROLONGED CARBON MONOXIDE INHALATION IN THE RAT. D. G. Penney, P. C. Sodt and A. F. Cutilletta. Dept. of Physiol., Wayne State Univ. School of Med., Detroit, Mich., School of Med., Northwestern Univ., Chicago, Ill., and Johns Hopkins Hospital, Baltimore, Md. Adult male rats were exposed to 500 p.p.m. CO (38 - 42% COHb) for periods of time from 1 - 42 days. Hematocrit rose gradually from 49.8% to 69.7%. Using an open chest anesthetized preparation (R. T. Dowel1 --et al. J. Appl. Physiol. 2, 1043, 1975), stoke index, mean stroke power and mean cardiac output were seen to increase sharply upon initial CO exposure and remained elevated for the duration of exposure. Concurrently, both total systemic peripheral resistance and total pulmonary resistance fell sharply and remained depressed. Both left ventricle (LV) and right ventricle (RV) systolic pressure and mean aortic pressure rose modestly, but non-significantly over the first 14 days of exposure, declining somewhat thereafter. Maximum rate of heart muscle contraction (dP/dt) tended to rise above control levels during the first two weeks of exposure. Neither LV or RV end-diastolic pressure changed significantly during CO exposure. There was no consistent change in heart rate. Enhanced cardiac output via increased stroke volume is seen as a compensatory mech anism to provide adequate tissue oxygen delivery during CO intoxication. The greater continuous heart work involved may be the major factor responsible for development of cardiomegaly. (this research was in part supported by Grant HL-16367 from the National Heart, Lung & Blood Institute)

REDUCTION OF MYOCARDIAL RESISTANCE TO EDEMA FORMATION BY STRETCH M.B. Pine, J.B. Caulfield, and W.H. Abelmann. Harvard Medical School and Beth Israel Hospital, Boston, MA., U.S.A. Exposure to high K+, low Na+ solution results in marked swelling of kidney, atrium and diaphragm, but only small increases in ventricular The resistance of --in vitro oxygenated contracting myocardial water. rat papillary musc)es (PM)+to swelling was further characterized by comparing water, K and Na in unstretched (unstr) PM, PM stretched (str) to Lmax and renal cortical slices after 1 hr in modified KrebsHenseleit solution (K-H) in which K+ completely replaced Na', ion for ion (K-sub), and after 1 hr recovery in K-H. PM (N=24) were also Water contents were (ml/g examined by light and electron microscopy. dry weight; meanfSEM; N=16 per group): unstr PM str PM kidney Control 2.86k.04 3.77k.06 3.78A.06 K-sub 4.07k.07 4.53+.10 6.80?.08 Recovery 3.76+.08 3.74k.06 3.26k.08 Extracellular water by 3H-inulin was similar after each intervention. K-sub resulted in similar reductions in Na+, while changes in K+ paralleled changes in water. K+ returned to control levels with 1 hr Microscopy confirmed the resistance of PM to swelling, but recovery. did not detect differences in water between str and unstr PM. Thus, mechanical stretch reduces but does not abolish ventricular myocardial resistance to edema formation in high K+ medium.