GUIDELINES FOR MANAGEMENT OF ACCIDENTAL HYPOTHERMIA IN A UNIVERSITY HOSPITAL IN NORTHERN NORWAY.

Accidental hypothermia is defined as a trauma. Collaboration on the treatment of victims of accidental hypothermia shouldfollow a communication protocol for the seriously injured. Aim is to establish earliest possible contact with the doctor on duty at the regional University hospital to enable participation in the further communication and decision making process with relevance to technical and logistical issues. Victims of accidental hypothermia with adequate circulation and core temperature < 35°C can be treated with active remote heating (hot air blanket) at all hospitals providing emergency surgical care; active external warming should be started during transport to the nearest hospital. Hypothermic patients showing no signs of life, patients with inadequate circulation or hypothermia-induced circulatory arrest with core temperature < 32°C and serum K⁺ < 12 mmol-l⁻' should be transported directly to University hospital. Advanced life support in all these cases should be started immediately and continued without interruption during transportation until the patient is connected to a heart-lung machine for rewarming. If core temperature is < 28°C and/or the patient has inadequate circulation contact should be taken with the regional University hospital to discuss extracorporeal rewarming.

Mepacrine protects the isolated rat heart during hypoxia and reoxygenation--but not by inhibition of phospholipase A2.

Mepacrine (quinacrine) has in a number of studies been shown to protect the heart from ischemic injury, a protection commonly claimed to be due to inhibition of phospholipase A2. The aim of the present study was to investigate the effect of mepacrine 1 microM on isolated, buffer perfused rat hearts subjected to 60 min hypoxia and 30 min reoxygenation. We also wanted to clarify whether any cardioprotective effect was due to inhibition of phospholipase A2 or to other effects of the drug. Mepacrine led to a substantial fall in left ventricular developed pressure (LVDP) and coronary flow (CF) during normoxic perfusion. Treated hearts showed less increase in LVEDP and less fall in LVDP during the hypoxic period, and significantly fewer hearts stopped beating compared to untreated controls. Release of CK during hypoxia and reoxygenation was reduced in treated hearts compared to controls (19.9 +/- 3.8 vs. 73.1 +/- 13.3 IU, p < 0.05). Lipid analyses of the myocardium showed a significant increase in the total amount of non esterified fatty acids (NEFA) in both untreated and mepacrine treated hypoxic hearts compared to normoxic controls, but to a significantly lower level in the mepacrine treated hearts. However, contribution of polyunsaturated NEFAs to total NEFAs did not differ between the groups. Also, neither total amount of fatty acids nor amount of polyunsaturated fatty acids obtained from the 2-position of the phospholipid fraction differed between the treated and untreated groups. In an enzyme assay, mepacrine 1 microM did not inhibit phospholipase A2 activity. We conclude that in our model mepacrine protects the heart from hypoxic injury, but probably by another mechanism than inhibition of phospholipase A2 induced membrane damage.