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IS RAFTING, SINKING, AND SLEEPING BEHAVIOR OF CHASED AND PURSE-SEINED

GLUCOCORTICOID-POTENTIATED ENDORPHIN ANALGESIA?

K.L. Seve=lbergen and A.C.Myrick, Jr.

Southwest Fisheries Science Center, U.S. Department of Commerce, La Jolla, California, U.S.A.

DOLPHINS CAUSED BY

For years scientists have tried to understand why many wopical Pacific dolphins, foreed-chased and captured by purse-seiners to catch tuna that

follow them, assume unusual behaviors and postures in the net. They may float in motionless "rafts" of two to four animals at the surface,

sink vertically to hang in the water below the surface, or descend passively to the bottom of the net, to lie as though asleep or dead. Most

dolphins are released alive but some ave found dead for no apparent reason. Unsupported conjectures for the behavior have included the notions

that such dolphins are: 1. "decoupling" in fear from aversive stimuli, 2. exhibiting learned behavior of waiting for release, 3. using the

behavior to reduce risk of entanglement in the net, and 4. operating under some degree of cataleptic shock. Recent studies have suggested that

many purse-seined dolphins are under continuous acute stress frem the fishing method of chase and capture, a response that includes

hypersecretion of glucocortiensteroids and lowering of blood calcium. Advances in stress and endorphin physiology now allow us to suggestthat

elevated serum glucocorticoids suppress tolerance to serum opioids and enhance the opioids' analgesic effect. Thus, acutely stressed dolphiusmay

enter a state of narcosis, producing various degree of temporary or prolenged ataxia and semiconsciousness. Deep narcosis preempts a dolphin's

unaique voluntary control of respiration and may lead to asphyxia and death. Several studies am planned to test hypotheses derived from this

physiological appmw~ to the question.

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ROLE OF NITRIC OXIDE IN STRESS ULCER K. Ogino, Y. Takeyama, H. Ishiyama, H. Kobayashi, T. Hobara Department of Public Health, Yamaguchi University School of Medicine, Kogushi Ube, Japan

The mechanism of stress-induced gastric mucosal injury has long been investigated. The reduction of gastric mucosal blood flow and active oxygen generation are regarded as important factors for the formation of gastric mucosal injury. Therefore, we have proposed the significance of superoxide dismutase (SOD), a scavenger of superoxide, and vasoregulin, which inhibits increase in permeability of the blood vessels and is inactivated by active oxygen, in the protection of stress-induced gastric mucosal injury. Recently, endothelium-derived relaxing factor (EDRF) has been identified as nitric oxide (NO) derived from L-arginine by the NO synthase. NO is destroyed by superoxide anions. In this study, we investigate a role of NO on stress-induced gastric mucosal injury.

Male Wlstar rats were fasted overnight and were immersed into the water at 23" C. Seven hours later the rats were killed and the stomach was removed. The total length of gastric mucosal lesions were measured and expressed as ulcer index. The activities of SOD (Cu, Zn-SOD and Mn-SOD) were measured at critical times. Prior to the experiment, SOD (60,000 U/kg), catalase (60,000 U/kg), SOD plus catalase, vasoregulin (0.1 mg/rat and 0.5 mg/rat) and N-nitro-L- arginine methyl aster(NAME) (100 mg/kg) were injected subcutaneously. Vasoregulin was extracted from culture medium of Namalva cells (derived from human Burkitt's lymphoma) after the addition of dexamethasone.

Gastric mucosal SOD activities decreased at 0.5 hr and 7 hr after the treatment. SOD and SOD plus catalase inhibited ulcer index by 15% and 26%, respectively. But catalase alone had no effect. Vasoregulin (0.1 mg and 0.5 mg) inhibited ulcer index by 41% and 48%, respectively. The administration of inhibitor of NO synthase (L-NAME) augmented ulcer index by 30%.

These results suggested that SOD, vasoregulin and NO may play an important role in the protection of gastric mucosal damage by active oxygen.

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