Why the study?
Does experimental hemorrhagic shock followed by reinfusion depress myocardial performance in dog and primate models?
Does experimental hemorrhagic shock followed by reinfusion depress myocardial performance in dog and primate models?
The study provides direct evidence for a factor that seriously depresses myocardial performance during the postinfusion period of experimental hemorrhagic shock despite maintenance of coronary driving pressure and arterial oxygen content.
Highlights post-reinfusion myocardial depression in animal shock models; leaves open relevance to human resuscitation and requires clinical validation.
Myocardial performance was investigated in nine dogs and six monkeys during experimental hemorrhagic shock under conditions of constant afterload. Left ventricular function curves were obtained by opening an aorta to left atrial bypass, and simultaneous recordings of stroke volume, peak stroke power, maximal dP/dt, maximal dF/dt, heart rate, atrial pressure and end-diastolic pressure were made. Total plasma catecholamine content was also measured in the monkeys during the control period and at death. The dogs showed a marked increase in performance, in contrast to the control group, 0-2 hours after reinfusion. Performance then deteriorated significantly by 2-4 hours, although it was still comparable to control levels. However, higher atrial and end-diastolic pressures were obtained, and in most cases cardiac failure developed soon thereafter. Two additional dogs were subjected to all stresses except the hypotension for 10 hours without evidence of deterioration. The monkeys did not withstand the surgical procedure as well as the dogs did and survived a maximum of 136 minutes after reinfusion. Catecholamine levels decreased in five of the six monkeys but not below normal levels, which indicates that failure was not due to depletion of myocardial stores. The data are interpreted as direct evidence for a factor(s) seriously depressing myocardial performance during the postinfusion period of experimental hemorrhagic shock in the dog and the monkey despite the high levels of performance in the early postinfusion period and the maintenance of coronary driving pressure and arterial oxygen content.
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Abel et al. (1973) studied this question.
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