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Biomedical subjects

R A Goldman

Publications and source records attributed to R A Goldman.

27 records · Page 2Linked to original sources
PubMed1978

Effect of potassium cardioplegia on myocardial ischemia and post arrest ventricular function.

To assess the effects of moderate potassium cardioplegia (37 mEq/l KCl) on the severity of myocardial ischemia during arrest and on post arrest ventricular function, 32 isolated, isovolumic feline hearts were studied before, during and 1 hour after ischemic arrest. Normothermia (37 degrees C) was maintained in the remaining 16 hearts, eight without KCl and eight with KCl. Hypothermia (27 degrees C) was maintained in the remaining 16 hearts, eight with KCl and eight without KCl. Myocardial oxygen (PmO2) and carbon dioxide tensions (PmCO2) were measured by mass spectrometry. Maximum developed intraventricular pressure (max DP) and max dP/dt were used as indices of performance. Compared with normothermic or hypothermic arrest alone, the addition of potassium cardioplegia resulted in a significant reduction in the peak PmCO2 measured during the arrest period. Hypothermia alone resulted in morphologic evidence of improved myocardial preservation and a significant reduction in peak PmCO2 compared with normothermia. Post arrest ventricular function was best with the combination of hypothermic arrest and potassium cardioplegia (max DP = 96 +/- 6% of control and max dP/dt = 99 +/- 5% of control). These data suggest that the beneficial effects of postassium cardioplegia and 27 degrees hypothermia are additive, and that reduction in myocardial ischemia as evidenced by a reduction in peak PmCO2 correlated with improvement in ventricular performance in the post arrest period and with preservation of myocardial structure.

Animals↗
PubMed1978

Effects of procaine-induced cardioplegia on myocardial ischemia, myocardial edema, and postarrest ventricular function. A comparison with potassium-induced cardioplegia and hypothermia.

The extent of myocardial protection afforded by a procaine cardioplegic solution during cardiac ischemia has been evaluated and compared with the protection seen using a potassium cardioplegic solution. An isolated cat heart model was employed, and ventricular function parameters, intramyocardial gas tensions, and postischemic myocardial edema were measured and compared following 60 minutes of induced ischemia at 37 degrees C. and 27 degrees C. There was no significant improvement in recovery of postarrest ventricular function when procaine cardioplegia was used during normothermic ischemia. When used at 27 degrees C., however, both cardioplegic solutions were associated with significantly better recovery of postarrest ventricular function, although there was less myocardial edema formation in the potassium-treated hearts. Results of this study indicate that procaine-induced cardioplegia provides myocardial protection during anoxic cardiac arrest which is additive to that afforded by hypothermia alone. In addition, procaine cardioplegia results in postarrest functional recovery which is similar to that seen with potassium cardioplegia.

Animals↗
PubMed1976

Myocardial reperfusion, a cause of ischemic injury during cardiopulmonary bypass.

Reperfusion following myocardial ischemia has been postulated to cause myocardial edema resulting in increasing interstitial pressure and retardation of the microcirculation. If ischemia then is repeated, the additional insult results in increasing edema and possible infarction. In order to test this hypothesis, 15 pigs were placed on cardiopulmonary bypass with coronary perfusion maintained at 100 mm. Hg by a separate pump through the clamped aortic root. Coronary flow and vascular resistance were recorded. Distribution of coronary blood flow was monitored by injection of radioactively labeled microspheres (15 mu). Myocardial extravascular water was measured by simultaneously determining myocardial intravascular water with radioactive iodinated serum albumin (RISA) and total myocardial water with tritiated water (THO). Three 30 minute periods of myocardial ischemia and 5 minutes of coronary perfusion produced (1) a loss of the reactive hyperemic response to ischemia (coronary vascular resistance increased--from 0.295 +/- 0.024, control, to 0.366 +/- 0.042, after anoxia--rather than decreasing with reactive hyperemia induced vasodilatation); (2) a significant maldistribution of coronary flow away from the endocardium (endocardial: epicardial perfusion ratio 1.10 +/- 0.05, control, to 0.69 +/- 0.08, following ischemia, p less than 0.05); and (3) significant myocardial edema. Myocardial extravascular water rose from 46.4 +/- 1.7 ml. per 100 Gm., control, to 52.6 +/- 2.0 ml. per 100 Gm., after ischemia (p less than 0.05), whereas intravascular myocardial volume did not change significantly. Both light and electron microscopic examination of the postischemic myocardium shows interstitial and intracellular edema with typical ischemic changes at a cellular and subcellular level. The significant increase in myocardial extravascular water content associated with this injury supports the concept that myocardial reperfusion plays a role in its development.

Animals↗