Abstract

To study in rats the effect of S(+) ketamine on the renal histology after intraoperative hemorrhage. Twenty male Wistar rats, anesthetized with sodium pentobarbital, were randomly divided in 2 groups: G1 - control (n=l0) and G2 - S(+)-ketamine (n=10), both submitted to arterial hemorrhage of 30% of volemia in 3 moments (10% each 10 min) 60 min after anesthesia. G2 received S(+)-ketamine, 15 mg. kg-1, i.m., 5 min after anesthesia and 55 min before the 1st hemorrhage moment (Ml). Medium arterial pressure (MAP), rectal temperature (T) and heart rate were monitored. The animals were sacrificed in M4, 30 min after the 3rd hemorrhage moment (M3) and the kidneys and blood collected from hemorrhage were utilized for histological study and hematocrit (Ht) determination. There were significant reduction of MAP, T, and Ht. The histological study verified G1 = G2 for tubular dilation, congestion, and necrosis. The total score addition were significantly different and G2 > G 1. Hemorrhage and hypotension determined changes in kidney histology. The rise in catecholamine blood concentration probably was the cause of S(+)-ketamine-induced higher score of histological changes.

Highlights

  • S(+)-ketamine, a ketamine S(+)-enantiomer, is a noncompetitive N--methyl-D-aspartate (NMDA) receptor ion channel blocker

  • Twenty male Wistar rats, anesthetized with sodium pentobarbital, were randomly divided in 2 groups: Gl - control (n=l0) and G2 - S(+)ketamine (n=10), both submitted to arterial hemorrhage of 30% of volemia in 3 moments (10% each 10 min) 60 min after anesthesia

  • The animals were sacrificed in M4, 30 min after the 3rd hemorrhage moment (M3) and the kidneys and blood collected from hemorrhage were utilized for histological study and hematocrit (Ht) determination

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Summary

Introduction

S(+)-ketamine, a ketamine S(+)-enantiomer, is a noncompetitive N--methyl-D-aspartate (NMDA) receptor ion channel blocker It is a short acting anesthetic used as an inducing agent or during surgical and short diagnostic procedures, providing rapid dissociative anesthesia followed by rapid recovery. Anesthetics should be chosen to protect renal function for those patients with coexisting renal disease, under some type of surgical procedures or with risk factors for development of perioperative renal failure, but the ideal anesthetic has not been developed to protect renal function These patients are predisposed to perioperative morbidity and mortality. Ketamine inhibits cytokines-induced mesangial cells (MC) proliferation. Angiotensin II affects acute renal hemodynamics under pathological conditions and induces cell proliferation in a cultured murine MC line[3] and stimulates

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