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1.
J Trauma ; 33(2): 321-5, 1992 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-1380565

RESUMO

Class I and II hemorrhage has been routinely treated clinically with 2-2.5 times the volume of shed blood as balanced electrolyte solution. Although this regimen has been shown to adequately restore arterial pressure in trauma patients, it is not clear that it uniformly restores regional perfusion. Since it is becoming apparent that the gut plays a major role in the development of the posttraumatic septic state, we studied the effects of graded doses of balanced electrolyte resuscitation on the mesenteric microcirculation. Regimens consisting of one (1 x LR), two (2 x LR), or three (3 x LR) times the volume of shed blood as lactated Ringer's (LR) solution or 7.5% hypertonic saline and 6% dextran (HSD) equal to one seventh the volume of shed blood were given to groups of anesthetized (urethane-chloralose) male Sprague-Dawley rats after 30 minutes of hemorrhage to 50% of baseline mean arterial blood pressure. The microcirculation of the distal ileum was observed using an in vivo video microscope. Mean arterial pressure and ileal A1 diameters returned to baseline values with HSD within 20 minutes following this moderate hemorrhage. Additionally, A1 diameters returned to baseline in the 2 x LR and 3 x LR groups. A1 vessels remained significantly constricted in the 1 x LR group. Mean arterial pressure remained significantly lower than the baseline value in all of the LR groups. We conclude that in this model, HSD is superior to LR for restoration of blood pressure. In restoring A1 diameters, LR is equivalent to HSD only when volumes of balanced electrolyte two and three times shed blood volume are given.


Assuntos
Dextranos/uso terapêutico , Eletrólitos/uso terapêutico , Solução Salina Hipertônica/uso terapêutico , Choque Hemorrágico/fisiopatologia , Choque Hemorrágico/terapia , Circulação Esplâncnica , Animais , Arteríolas/fisiologia , Pressão Sanguínea , Soluções Isotônicas/uso terapêutico , Masculino , Microcirculação , Insuficiência de Múltiplos Órgãos/etiologia , Ratos , Ratos Endogâmicos , Lactato de Ringer
2.
Am J Physiol ; 262(5 Pt 2): H1449-57, 1992 May.
Artigo em Inglês | MEDLINE | ID: mdl-1590450

RESUMO

Differential recovery of prostacyclin and endothelium-derived relaxing factor after vascular injury. Am. J. Physiol. 262 (Heart Circ. Physiol. 31): H1449-H1457, 1992. The recovery of prostacyclin (prostaglandin I2, PGI2) synthesis and endothelium-derived relaxing factor (EDRF) activity, as demonstrated by acetylcholine (ACh)-induced relaxation, by rabbit aorta was examined up to 8 wk after balloon catheter-induced injury. Following injury, basal 6-keto-PGF1 alpha formation was decreased acutely; however, after 3 wk it was not different from control. Arachidonic acid-stimulated 6-keto-PGF1 alpha formation was decreased, returning to control levels at 3 and 8 wk for thoracic and abdominal aorta, respectively. ACh-induced relaxation did not return to control levels over the 8-wk study. Initiation of reendothelialization with a layer of hyperplastic endothelial cells overlying subendothelial fibrosis and intimal hyperplasia were present at 2-3 wk. Intimal hyperplasia appeared 2 wk after injury and progressed throughout the period of the study. These data indicate that following balloon catheter-induced injury the formation of both PGI2 and EDRF is reduced and that recovery follows a differential time course. In addition, the recovery of PGI2 formation did not coincide with the attenuation of intimal hyperplasia, whereas the relationship between EDRF formation and intimal hyperplasia is uncertain.


Assuntos
Aorta/lesões , Epoprostenol/metabolismo , Óxido Nítrico/metabolismo , Acetilcolina/farmacologia , Animais , Aorta/metabolismo , Aorta/patologia , Ácido Araquidônico/farmacologia , Cateterismo , Eicosanoides/metabolismo , Hiperplasia , Nitroglicerina/farmacologia , Endoperóxidos Sintéticos de Prostaglandinas/farmacologia , Prostaglandina H2 , Prostaglandinas H/farmacologia , Coelhos , Vasodilatação , Ferimentos e Lesões/etiologia
3.
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