Abstract
The key mechanisms associated with irreversible hemorrhagic shock have no so far been elucidated. The involvement of mast cells in this phenomenon, however, has already been studied. On the other hand, β-endorphin and various opiates, or any stressful stimuli mediated by endogenous opiates, cause mast cell degranulation and histamine release, as the study of the related literature shows. Hemorrhagic shock is one such stressful stimulus that leads to an increase in the plasma levels of endogenous opioids, especially β-endorphin. During hemorrhagic shock, therefore, mast cells can be activated by an elevation of the β-endorphin level; and the degranulated products of mast cells, histamine in particular, may contribute to the progress of hemorrhagic shock to the irreversible state. The investigation of the effect of hemorrhage on mast cell degranulation has shown that there is a positive correlation between the two phenomena. In addition, it has been established that the administration of vasoactive intestinal peptide (VIP) prevents such degranulation. Depending on these results, the effects of VIP have been studied in the treatment of severe experimental hemorrhagic shock in combination with other therapeutic means used in this type of shock, such as naloxone, hypertonic saline infusion and/or blood reperfusion. A combination of VIP and naloxone has yielded the best results on survival when it is used either alone or in conjunction with volume replacement after a severe hemorrhage. The important prospect of a combination of VIP and naloxone is that it has apparently the most potent inhibitory effect on mast cell degranulation. In the light of the related experiments, we may conclude that the inhibition of mast cell degranulation has a beneficial effect on severe hemorrhagic shock; mast cell degranulation may thus be accepted as a physiopathological mechanisms contributing to the progression of hemorrhagic shock state. Biomedical Reviews 1993; 2: 37-46.
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