Der Einfluß des koronaren Perfusionsdruckes auf die Druck-Volumenbeziehung und die Kontraktilität des linken Ventrikels

Hagl, S.; Neuhaus, K. L.; Hinglais, J; Mayr, Norbert; Meisner, H; Sebening, F

doi:10.1055/s-0028-1102781

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References 5 publications

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“…The loss of sympathetic tone, in addition to its slight direct effect on myocardial contractility, results in a loss of vasomotor tone, decreased vascular resistance, and a significant fall in diastolic aortic blood pressure, and therefore coronary perfusion pressure. It was shown that coronary perfusion pressure is a significant determinant of left ventricular function [32], especially at low pressure levels [33]. In recent pilot experiments [34], we showed that brain death-related cardiac dysfunction could be reversed by restoration of coronary perfusion pressure and blood flow.…”

Section: Discussionmentioning

confidence: 73%

Influence of Brain Death and Cardiac Preservation on Systolic and Diastolic Function and Coronary Circulation in the Cross‐circulated Canine Heart RID="" ID="" This International Society of Surgery (ISS)/Société Internationale de Chirurgie (SIC) article was presented at the 37th World Congress of Surgery International Surgical Week (ISW97), Acapulco, Mexico, August 24–30, 1997.

et al. 1999

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Previous studies have demonstrated hemodynamic instability and cardiac dysfunction in the brain-dead organ donor. It remains unclear if primary cardiac dysfunction is responsible for hemodynamic deterioration or decreased cardiac function is secondary to brain death-associated altered loading conditions. Therefore in the present study the effects of brain death on hemodynamics and cardiac function were analyzed in vivo in an open chest model and ex vivo in a cross-circulated heart preparation. In a second protocol, the impact of brain death-associated hemodynamic changes on postischemic graft function was investigated. Brain death was induced injecting saline in a subdural Foley catheter. Induction of brain death led to a hyperdynamic reaction followed by hemodynamic deterioration with a decrease of systemic vascular resistance and myocardial contractility. If the hearts were explanted and assessed ex vivo, no differences were found between control and brain-dead hearts. Furthermore, both control and brain-dead hearts showed full functional recovery after 4 hours of hypothermic ischemic storage. Despite hemodynamic deterioration in situ after brain death, there were no differences between the postischemic function of control and brain-dead hearts. These results indicate that myocardial dysfunction is not irreversible and may be secondary to altered loading conditions, and that the recovery of cardiac function after long-term hypothermic storage is not impaired by the hemodynamic changes observed in situ after brain death induction. These data may also indicate that potential donor hearts might not be excluded from transplantation on the basis of impaired hemodynamic characteristics, especially if they are evaluated by load-dependent parameters.

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