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DEVELOPMENTS IN OCCUPATIONAL MEDICINE
Author(s) -
Carl Zenz
Publication year - 1970
Publication title -
medical journal of australia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 131
eISSN - 1326-5377
pISSN - 0025-729X
DOI - 10.5694/j.1326-5377.1970.tb116811.x
Subject(s) - citation , psychology , computer science , library science
demonstrating that fibrinolytic mechanisms normally degrade the fibrin which circulates in the plasma. Fibriilolytic inhibition reduced the survival time of animals infused with adrenaline. Whitaker and McKay' have also shown that rapid infusion of thrombin into Iprimates to induce acute disseminated intravascular coagulation, causes transient hypotension. Following rapid infusion of thrombin, some animals die promptly, but the remainder almost always recover fully within a short time. In unstressed animals it is difficult to induce hypotension by a slow continuous infusion of thrombin, and most will recover in spite of almost complete conversion of circulating fibrinogen into fibrin and a profound coagulation defect. In contrast, once shock has been induced by infusing adrenaline, the administration of a very small quantity of thrombin is 'often rapidly lethal. Considered together, these data on catecholamine shock and thrombin infusion indicate that, as a rule, disseminated intravascular coagulation does not independently lead to shock, but that it is nevertheless a component of refractory shock which is both lethal and potentially reversible. 'I'he adreno-sympathetic system and hsemostatic mechanism, which are alike of value in maintaining homreostatic processes during acutely stressful situations, and in their capacity to lead to harmful sequelse if their action is perpetuated. appear to interact synergistically in the evolution of shock. Additionally, alpha-adrenergic stimulation can itself trigger the hremostatic mechanism. With experimental hremorrhagic shock R. M. Hardaway and his associates' have found that pretreatment witb phenoxybenzamine inhibits disseminated intravascular coagulation. There are grounds for believing that inhibition of the hremostatic mechanism, as by heparin administration, may be a-valuable adjunct to the therapy and prophylaxis of shock, although clinical studies are as yet too sparse and fragmentary to o;Jermit any conclusions to be made. Preliminary trials of fibrinolytic therapy with streptokinase have also produced encouraging results in refractory shock.

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