“…MYOCARDIAL COOLING For many surgeons, myocardial cooling is a complete substitute for perfusion; the duration of its protection depends on its degree (Angell et al, 1969). It has been used with success for seven hours (Lower et al, 1962) and, by some, is preferred to perfusion (Robicsek et al, 1970). Used with ether anaesthesia (Barnes, Mohri, and Merendino, 1968) or slow pacing (Mohri, 1965), fibrillation may be avoided, though this is not damaging over short periods (Martino et al, 1969).…”
Section: Resultsmentioning
confidence: 99%
“…Moreover, the provision of coronary perfusion does not prevent ischaemic enzyme changes during aortic valve surgery (Littler et al, 1972). The dangers of coronary perfusion may thus outweigh its benefits (Robicsek et al, 1970). HYPOTHERMIA Even perfusion of the heart from the aorta may be overdone, with resulting myocardial damage, when the cooling of the heart or the presence of ventricular fibrillation disturbs the autoregulation of coronary flow (Vasko, 1967).…”
Hedley Brown, A., Braimbridge, M. V., Darracoft, Sally, Chayen, J., and Kasap, H. (1974). Thorax, 29,[38][39][40][41][42][43][44][45][46][47][48][49][50]. An
“…MYOCARDIAL COOLING For many surgeons, myocardial cooling is a complete substitute for perfusion; the duration of its protection depends on its degree (Angell et al, 1969). It has been used with success for seven hours (Lower et al, 1962) and, by some, is preferred to perfusion (Robicsek et al, 1970). Used with ether anaesthesia (Barnes, Mohri, and Merendino, 1968) or slow pacing (Mohri, 1965), fibrillation may be avoided, though this is not damaging over short periods (Martino et al, 1969).…”
Section: Resultsmentioning
confidence: 99%
“…Moreover, the provision of coronary perfusion does not prevent ischaemic enzyme changes during aortic valve surgery (Littler et al, 1972). The dangers of coronary perfusion may thus outweigh its benefits (Robicsek et al, 1970). HYPOTHERMIA Even perfusion of the heart from the aorta may be overdone, with resulting myocardial damage, when the cooling of the heart or the presence of ventricular fibrillation disturbs the autoregulation of coronary flow (Vasko, 1967).…”
Hedley Brown, A., Braimbridge, M. V., Darracoft, Sally, Chayen, J., and Kasap, H. (1974). Thorax, 29,[38][39][40][41][42][43][44][45][46][47][48][49][50]. An
“…In heart surgery topical hypothermia is still used for myocardial protection (1)(2)(3). There are only sporadic publications on the experimental use of topical hypothermia to protect skeletal muscle, for example: musculo-cutaneous flaps (4,5); isolated gracilis muscle (6); and post-ischemic hypothermia to diminish ischemic damage (7,8).…”
Severe lower limb ischemia TASC IIB/III with sensory and motor neurologic deficiencies leads to prolonged hospital care, amputation, and death in 20-70 % of cases. We present our first clinical experience of the use of preoperative topical hypothermia to improve muscular viability in these patients. Two hours after onset of symptoms, six 4-liter plastic bags were filled with snow and packed against the ischemic leg which was protected from frost injury by a layer of towels. After surgical revascularization four hours later muscular and neural functions in the leg were completely restored. A maximum serum myoglobin of 6500 ng/L (median 12000 ng/L in similar but untreated patients) postoperatively decreased to 1400 ng/L after 27 hours.
“…These include continuous hypothermic coronary perfusion (Hirose and Bailey, 1969); intermittent coronary perfusion with hypothermic blood (Ebert et al, 1962) or with normothermic blood (Benzing et al, 1973); low-pressure coronary perfusion (Brown et al, 1969); and topical cardiac hypothermia (Robicsek et al, 1970), although its prolonged application may result in myocardial and pericardial damage. In direct myocardial revascularization retrograde perfusion through the coronary sinus has been employed satisfactorily (Hammond, Davies, and Austen, 1967).…”
. (1975). Thorax, 30,[371][372][373][374][375][376][377][378][379][380][381] Myocardial ultrastructural changes during extracorporeal circulation with anoxic cardiac arrest and its prevention by coronary perfusion. Experimental study. This experimental work has been carried out with the aim of studying the ultrastructural myocardial changes caused by prolonged anoxic cardiac arrest during cardiopulmonary bypass, and their prevention by means of two different techniques of coronary perfusionsystemic-pressure continuous and low-pressure intermittent perfusion.After 30 minutes of cardiac anoxia, the ultrastructural changes of the myocardial cell were reverted to normal by coronary perfusion; when anoxic cardiac arrest was prolonged up to 60 minutes there was severe myocardial damage, with marked mitochondrial changes and dehiscence of intercalated discs, which persisted in spite of restoring coronary flow. These morphological data were in accordance with the fact that no dog which underwent anoxic cardiac arrest for 60 minutes recovered.Both intermittent and continuous coronary perfusion were effective in preventing anoxic damage; cardiac muscle cells were better preserved by low-pressure intermittent perfusion than by systemic-pressure continuous perfusion, which caused intracellular and intramitochondrial oedema.
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