Sudden death may occur in man and animals with psychological stress, physiological stress, and sublethal. A large literature correlates stress with endogenous catecholamine release and myocardial lesions in sudden death. The term contraction band necrosis (CBN) describes focal hyper contraction and lysis of small groups of myocardial cells. CBN may develop after transient myocardial ischemia and reperfusion, and is the characteristic lesion seen in the myocardium with exogenous administration or elevated endogenous levels of catecholamines (epinephrine and norepinephrine). The exact mechanism by which catecholamines cause CBN is not understood, although the damage is generally thought to be due to a defect in the supply of energy necessary for the maintenance of essential cellular processes.

We have found focal and occasionally more diffuse CBN in 50 of 52 (96.2%) cetaceans stranded along the western coast of the Gulf of Mexico. This study included 44 Tursiops truncatus, 1 Physeter catodon, 1 Lagenodelphis hosei, 1 Globicephala macrorhynchus, 1 Stenella attenuata, 1 Stenella coeruleoalba, 1 Mesoplodon europaeus, and 1 Pseudorca crassidens. The cause of stranding in each of these cetaceans was different and sometimes multifactorial, including acute or chronic disease, and/or trauma. We hypothesize that cetaceans, under stress due to disease, trauma, and/or stranding, release excess catecholamines into the circulation thereby producing CBN. This endogenous myocardial injury may contribute to the high mortality rate of stranded cetaceans.

Rises in serum glucose, glutamate-pyruvate transaminase, glutamate-oxaloacetate transaminase (aspartate aminotransferase), lactate dehydrogenase, and creatine phospho signal the initial stages of catecholamine-induced myocardial necrosis. Several different pharmacological, hormonal, and metabolic interventions have been shown to lessen the seventy of CBN in humans and other animals. Recognition of the role of massive endogenous catecholamine release in cetaceans subjected to a great variety of physiological and psychological stressors raises the prospect that early treatment with appropriate drugs to block the stimulatory effects of catecholamines, reduce cardiac work, improve oxygen supply to myocarchal cells, and counteract ionic shifts, may reduce the severity of CBN in stranded cetaceans. Potential treatment re for CBN in stranded cetaceans should be investigated to improve the success rate of rehabilitation of these animals.