Rate of rise of myocardial PCO2 during early myocardial ischemia in the dog.

Abstract

SUMMARYWe have investigated the rate of rise of myocardial Pco» (Pmco») after coronary artery occlusion using a new method for this measurement. Previous studies of Pmcch have been limited by the slow response of the only available method, and no increase in Pmcoi prior to 3 minutes after occlusion has been found. We have implanted a miniature PcOj electrode, with a 63% response time of 14 seconds, into the left ventricle of 14 open-chest dogs. After abrupt coronary occlusion, Pmcoi began to rise in 13.6 ± 1.1 seconds in heparinized dogs and in 7.5 ± 0.7 seconds in unheparinized dogs. The subsequent magnitude of the increase in Pmcoi was 24, 88, 171, and 222 mm Hg at 2, 5, 10, and 15 minutes after occlusion. The rate of rise of Pmcoi was essentially linear from 1 minute to 10 minutes at a rate of 18.3 mm Hg/min. The rate of rise was slower during the first 30 seconds after occlusion (6.1 mm Hg/min) and also from 30 seconds to 1 minute (9.7 mm Hg/min). This rate of rise is much greater than that previously observed and reflects the severe myocardial acidosis developing during ischemia. A rise in Pmco, is one of the earliest metabolic changes that has been observed during myocardial ischemia. Ore Res 45:324-330, 1979

Contribution of shrinkage of extracellular space to extracellular K+ accumulation in myocardial ischaemia of the rabbit.

“…This is because rapid net efflux of cellular K+ concomitantly with anion efflux, for example, will in part serve to minimize osmotic cell swelling (Steenbergen, Hill & Jennings, 1985) and (Aksnes, 1992), it is generally accepted that suppression of sarcolemmal Na+-K+-ATPase is not the primary mechanism (Rau, Shine & Langer, 1977;Kl6ber, 1983;Wilde & Kl6ber, 1986). Recent experimental data suggest that cellular K+ efflux coupled to lactate efflux (Weiss, Lamp & Shine, 1989;Kantor et al 1990, Shieh, Goldhaber, Stuart & Weiss, 1994 Case, Felix & Castellana, 1979) from an ischaemic zone is expected not only to modify extra-and intracellular pH (Yan & Kl6ber, 1992) but osmolarity as well. This is because any molar quantity of C02, which is formed from HCO,-, is expected to decrease osmolarity, and, consequently, the increase in osmolarity (lactate and phosphate) is partially compensated by the decrease in HCO3-.…”

The significance of the late fall in myocardial PCO2 and its relationship to myocardial pH after regional coronary occlusion in the dog.

“…Case described a different method for the measurement of Pmco 2 which employed what was essentially a miniature Sevringhaus electrode (Coon, 1976;Case, 1979a). Utilizing this electrode, he observed a rise in Pmco 2 9.6 ± 0.7 seconds (mean ± SEM) after regional coronary occlusion (Case, 1979b). He stated that he did not observe a subsequent fall in Pmco 2 with prolonged occlusions, although his observations in that study did not extend beyond 15 minutes postocclusion (Case, 1979b).…”

“…This late fall in Pmco 2 has not been observed during global myocardial ischemia (Mc-Gregor et al, 1974;Lange et al, 1983). Neither did Case et al (1979b), who utilized a different Pmco 2 measuring system, observe such a fall during re-gional ischemia. Since we had observed this late fall, invariably, in all the regional occlusion experiments we had performed, we elected to examine this phenomenon further, aided by a new tissue pH electrode that we had evaluated in our laboratory (Khuri et al, 1979b).…”

The consequences of simulated ischaemia on intracellular Ca2+ and tension in isolated ferret ventricular muscle.

“…(i) Volatile products of metabolism will not accumulate for any significant time in this model. Specifically CO2, which can reach a tissue partial pressure of 400 mmHg after 20 min of ischaemia (Case, Felix & Castellana, 1979), will not accumulate in our model. This large rise in Pco, in the intact heart is probably caused mainly by lactic acid displacing HC03-into CO2 which can only leave the ischaemic tissue by diffusion (Ichihara, Haga & Abiko, 1984).…”