THE PHYSIOLOGIC BASIS FOR VASOPRESSOR THERAPY DURING SHOCK*
- SHELDON E. GREISMAN, M.D.
- Requests for reprints should be addressed to Sheldon E. Greisman, M.D., Assistant Professor of Medicine, Department of Experimental Surgery, University of Maryland School of Medicine, Lombard and Greene Streets, Baltimore 1, Maryland.
Excerpt
INTRODUCTION The therapeutic usefulness of vasopressor agents, although employed many years for correction of various shock syndromes, remains highly controversial. Some investigators disapprove of their indiscriminate use;1-3 others have advocated such therapy routinely.4, 5 The basis for the divergence of opinion may be traced to variation in interpretation of the clinical evidence. Conclusions favoring the routine employment of vasopressor therapy often fail to consider that: (1) improvement of the systemic arterial blood pressure is not synonymous with therapeutic benefit; in some instances "cures" have been ascribed to vasopressor drugs although the ultimate outcome was fatal; (2) lessening of cyanosis, though
Summario in Interlingua
Como consequentia del insufficiente numero de controlate studios clinic, le utilitate therapeutic de agentes vasopressori in varie syndromes de choc human remane controverse. Le presente articulo considera certe conceptos physiologic de choc experimental in relation al application de therapia vasopressori in humanos. Es sublineate le facto que le capacitate de animales normal de mantener un adequate tension de sanguine arterial in le circulation systemic in despecto del presentia de un volumine de sanguine considerabilemente inferior al capacitate del vasculatura depende in parte del regulation physiologic per vasomotion peripheric. Iste processo vasomotori es essentialmente un systema dual. Activitate vasomotori in le capillares es le prime linea de defensa e vasomotion arteriolar es le secunde linea de defensa contra le effortio del sanguine de entrar in le reservoir capillar, de distender lo, e de accumular se in illo. Durante le prime phases de choc per reduction del volumine de sanguine, tanto le apparato capillar como etiam le apparato vasomotori arteriolar exhibi un intensification de lor activitate constrictori. A iste stadio le systema capillar es multo responsive al effecto de agentes vasopressori. Durante que le choc progrede, le processo vasomotori capillar—al minus in le area mesenteric—suffre un progressive deterioration e deveni de plus in plus refractori al effecto del agentes vasopressori, durante que le constriction arteriolar es mantenite per un regulation neurogene que es promovite per le activitate de factor humoral. Le disturbation fundamental responsabile pro iste deterioration del vasomotion capillar pare trovar se in ischemia de histo. Le sustenite constriction arteriolar es un importante factor contributori. Ben que le constriction arteriolar servi como mechanismo de salva-vita immediate in caso de rapide e sever perdita de sanguine, le resultante ischemia in altere histos (inter le quales le intestino pare esser specialmente importante) accelera le deterioration del function vasomotori capillar e le progresso verso choc de forma irreversibile. Hypoxia, le liberation de productos del histometabolismo anaerobie, e le absorption de endotoxinas bacterial es probabilemente factores contributori significative. Es presentate un revista del mechanismo de action de agentes vasopressori e antipressori in choc experimental. Usque datos es obtenite ab studios controlate in re le action de agentes vasopressori in choc human, il es recommendate que therapia vasopressori es utilisate solmente in le sequente situationes clinic: Disfallimento circulatori peripheric que es secundari al perdita del function vasomotori arteriolar, disfallimento circulatori central que es secundari a thrombosis de arteria coronari, disfallimento circulatori peripheric que es associate con le suspicion de atherosclerosis coronari o cerebral, e extreme depression del tension de sanguine arterial in le circulation systemic que es associate con signos clinic de un inadequate fluxo de sanguine coronari o cerebral.
Article and Author Information
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↵* Received for publication August 4, 1958.
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From the Departments of Medicine and Microbiology, School of Medicine, University of Maryland, Baltimore, Maryland.
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