Hibernation Induction Trigger (HIT), obtained from a variety of winter-hibernating animals such as black bears, has been tested and proven to improve myocardial function recovery, enhance myocardial preservation to help avoid postischemic dysfunction, and inhibit metabolic rates. The chemistry of HIT indicates that it is a small, thermolabile, protease-sensitive, nuclease-insensitive protein which depends on seasonal changes for its effects. This HIT molecule serves many purposes. First, there is evidence to suggest that it has significant metabolic inhibitory effects through specific membrane opioid receptors (Bolling et al., 1998). This aids in a black bear's survival because it can conserve more than 90 percent of the energy it would require if it was in an active state and remained at a normal metabolic rate. Furthermore, studies have further shown that HIT can induce cardiac metabolic changes in non-hibernating animals (Bolling et al., 1998).

Second, and perhaps most important is the property of HIT, is that it serves as a natural cellular protectant to maintain cellular energy status and membrane integrity during hibernation. Some evidence suggests that the HIT molecule and a similar delta opioid DADLE may play a role in the preservation of ATP during ischemia thereby allowing it to augment cellular and myocardial ischemic tolerance. HIT has also been proven most effective when injected before the onset of ischemia (Bolling et al., 1997). Again, HIT has been studied on non-hibernating species and when an animal was given a pre-injection of HIT, contractile function was much better preserved (Bolling et al., 1998). The dual advantageous properties of HIT - its metabolic inhibitory property and myocardial preservation characteristic - favor the survival of black bears and many other species at the organ and cellular level.