Studies of the effects of ventricular fibrillation on the adequacy of regional myocardial flow

Viability of the Myocardium after Twenty-four-hour Heart Conservation - a Preliminary Study

“…Oxygen consumption was 1.9 € 1.7 ml/100 g/min at initial reperfusion and increased continuously to 5.3 € 2.1 ml/100 g/min. This is in accordance to the findings of Hottenrott et al [13] who measured oxygen consumption in the arrested canine heart at 0.3 -1.1 ml/100 g/min. In our previous experiments, we found a myocardial oxygen consumption of 10 -12 ml/100 g/min 3 -6 hours after orthotopic heart transplantation [9].…”

Induced fibrillation is equally effective as crystalloid cardioplegia in the protection of fetal myocardial function

“…The cardioprotective qualities of fibrillation have been extensively studied in mature myocardium. Early studies by Hottentrot and associates 16 demonstrated that fibrillatory arrest caused subendocardial ischemia in adult hearts after ventricular distention. Other authors have found that fibrillation and hyperkalemic cardioplegic arrest provide similar degrees of protection of the adult myocardium.…”

A compare between myocardial topical negative pressure levels of -25 mmHg and -50 mmHg in a porcine model

“…If perfusion pressure is kept above 50 mmHg the ventricular wall will still be perfused[ 19 ], but the myocardial wall tension may become higher than in a beating heart[ 20 ]. Hottenrot et al showed in 1972 that perfusion of a fibrillating dog heart for one to two hours did not damage the subendocardial muscle unless a strong maintained electrical stimulus was used[ 21 ]. In the present study, no sustained electrical stimuli was used, the ventricle was protected from distension with a left ventricular vent, and the perfusion pressure was be kept at 80 mmHg, to avoid subendocardial ischemia in the fibrillating heart [ 22 ].…”