Methylprednisolone in the prevention of cerebral hemodynamic and metabolic disorders during endotoxin shock in the dog.
These results provide evidence that steroid pretreatment and subsequent post-treatment prevent cerebral hemodynamic and metabolic alterations during four hours of Escherichia coli endotoxin shock in the dog. However, in this study, no data are provided on how the steroid prevents an increase in cerebral vascular resistance, and no clear answer is available in the literature. While active vasodilation or alpha-adrenergic blocking properties, or both, have been attributed to glucocorticoids, recent evidence does not support these findings during normal conditions or circulatory shock. If the increase in cerebral vascular resistance is passive, steroids may help by preventing platelet aggregation, cell disruption and subsequent microvascular plugging. Intravenously administered fluids, dextran-saline solution, while in themselves are probably not important to survival, may augment cerebral blood flow during shock through a blood dilutional effect. Finally, it is possible that steroids act to permit normal, long term cerebral auto-regulation, which is apparently impaired during endotoxin shock in the dog.
D000818:Animals; D001921:Brain / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects; D002561:Cerebrovascular Disorders / Q000188:drug therapy* / Q000378:metabolism / Q000517:prevention & control; D004285:Dogs; D004926:Escherichia coli; D005260:Female; D005947:Glucose / Q000378:metabolism; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D008775:Methylprednisolone / Q000494:pharmacology / Q000627:therapeutic use*; D012772:Shock, Septic / Q000188:drug therapy* / Q000503:physiopathology
D005947:Glucose; D008775:Methylprednisolone