The purpose of this study was to develop a hypothesis to explain patterns of findings at necropsy of dolphins stranding on beaches or killed by net entanglement.
Study parameters included histologic examination, clinical-pathologic correlation where feasible, reference to the literature on diving physiology, and pathology.
Over a number of years of examining beach stranded and net-caught dolphins at necropsy we have observed recurring patterns of changes in organs and tissues. The changes are consistent with injury caused by massive release of endogenous catecholamines (escape response) or by ischemia and reperfusion. The observations are contraction band necrosis of cardiac4 and smooth muscle, ischemic injury to the intestinal mucosa, especially the mucosa of the small intestine, and acute tubular necrosis (ATN) of the proximal tubules of the nephron.
Conclusions and Hypothesis
A common feature of all the lesions described is vasospasm leading to ischemic injury, followed by reperfusion and reperfusion injury. We also suspect endogenous catecholamine injury to the myocardium, well known in human medicine as an extreme “stress” response. A secondary effect of intestinal ischemia is to permit seeding of the blood with bacteria normally resident in the intestine, producing an often-mixed bacteremia and sepsis.
A dolphin in free dive (voluntary dive) undergoes certain physiologic adjustments reflective of exercise, including a reflexive apnea, with voluntary over-ride, minimal cardiovascular adjustments, and a general maintenance of aerobic metabolism.2 Blood flow is reduced to the gut and kidneys, but maintained in the heart, brain, and to a degree, exercising muscles. The animal is able to surface and dive repeatedly (foraging dive pattern), as there is little lactic acid build-up. These together have been termed the “dive response.” A dolphin in an involuntary dive situation undergoes a somewhat different set of adjustments, which have been termed the “dive reflex,” but which may better be termed an “alarm reaction.” These include not only the reflexive apnea, but also decreased heart rate (diving bradycardia), reduction of cardiac output, vasoconstriction with markedly decreased perfusion of gut, liver, kidneys, and skeletal muscle, with substantial increase in production of lactic acid in these tissues, which is reflected in marked rise in blood levels on surfacing.1,3 The clear implication of the distinctive reactions to voluntary and involuntary diving is that the dolphin is responding to the environment as it is perceived; the triggering of the alarm reaction is a reaction to a situation interpreted by the dolphin as a dire threat, and is responded to by a marked autonomic reaction. Since the major threats to an aquatic, air breathing mammal are drowning and predation, the alarm reaction is an accentuation of the physiologic dive and escape responses.
The histopathologic findings cited above suggest that the reflexive response of a dolphin to any major perceived threat, the alarm reaction, is to activate all the physiologic adaptations to diving or escape to an extreme or pathologic level, resulting, if greatly prolonged, in widespread ischemic injury to tissues. A dolphin in extreme physical or psychologic distress will exhibit an extreme, protracted alarm reaction.
We offer these observations as a tentative explanation of the mechanism whereby sensitive species die abruptly from handling or transportation, why the mortality of highly stressed beach stranded animals is very high, and why many beached dolphins bloat with gas forming in tissues very shortly after death.
1. Butler PJ. Respiratory and cardiovascular control during diving in birds and mammals. J Exp Biol. 1982;100:195–221.
2. Butler PJ, Jones DR. Physiology of diving birds and mammals. Physiol Rev. 1997;77:837–899.
3. Ridgway SH. Diving by cetaceans. In: Brubakk AO, Kanwisher JW, Sundes G, eds. Diving in Animals and Man. Trondheim, Norway: The Royal Norwegian Society of Science and Letters; 1986:33–62.
4. Turnbull BS, Cowan DF. Myocardial contraction band necrosis in stranded cetaceans. J Comp Path. 1998;118:317–327.