Department of Pathology and the Marine Biomedical Institute, The University of Texas Medical Branch and Texas Marine Mammal Stranding Network, Galveston, TX, USA
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. 1982. Respiratory and cardiovascular control during diving in birds and mammals. J
Exp. Biol 100:195-221 .
2. Butler PJ, DR Jones. 1997. Physiology of diving birds and mammals. Physiol Rev 77:837-899.
3. Ridgway SH. 1986. Diving by cetaceans.In: Diving in Animals and Man, A. Brubakk O, JW.
Kanwisher, G Sundness, eds. The Royal Norwegian Society of Science and Letters, Trondheim, Norway. pp 33-62.
4. Turnbull BS, Cowan DF. 1998. Myocardial contraction band necrosis in stranded cetaceans. J Comp