Key result
Hibernating hamster hearts showed altered autoregulatory capacity possibly due to intrinsic differences, while responses to adenosine and global ischemia were largely temperature-dependent.
The altered ability of hibernating hamster hearts to autoregulate is likely due to intrinsic differences from hibernation, whereas responses to adenosine and global ischemia are temperature-dependent.
Hibernating hamster data suggest intrinsic autoregulatory adaptations; leaves open whether similar mechanisms inform human cardioprotection during hypothermia.
We have investigated the influence of temperature, acute global ischemia, adenosine administration, and alterations in perfusion pressure on the coronary circulation of isolated, perfused spontaneously beating hearts from hibernating, normothermic, and cold-acclimated (nonhibernating) hamsters. No differences in heart rates were observed among groups at either 9 or 38 degrees C. Hearts from hibernating hamsters showed some differences in autoregulatory capacity at both the low and normal temperatures. All hearts exhibited similar responses to 30 s of global ischemia at both temperatures, with a marked reduction in the response at 9 degrees C. Similarly, the magnitude of the vasculature response to adenosine (250 micrograms) at 38 and 9 degrees C was equal in both normothermic and hibernating hearts perfused at 38 degrees C. Responses were abolished in all groups at 9 degrees C. We conclude that the altered ability of hibernating hearts to autoregulate is possibly due to intrinsic differences initiated by hibernation, while the responses to adenosine, and global ischemia are largely temperature-dependent effects.
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Merrill et al. (1981) studied this question. Temperature, acute global ischemia, adenosine administration, and alterations in perfusion pressure vs. Normothermic and cold-acclimated hamsters was evaluated on Coronary circulation responses (heart rate, autoregulatory capacity, response to global ischemia and adenosine). Hibernating hamster hearts showed altered autoregulatory capacity possibly due to intrinsic differences, while responses to adenosine and global ischemia were largely temperature-dependent.
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