Paper Information

Title: 

HYPOREACTIVITY TO VASODILATOR AND VASOCONSTRICTOR AGENTS IN ENDOTOXIN INDUCED SEPTIC SHOCK IN RAT

Type: POSTER
Author(s): GHOLAMNEZHAD Z.*,AGHAEI AZITA,FATEHI HASANABAD Z.
 
 *DEPARTMENT OF PHYSIOLOGY, PHARMACOLOGICAL RESEARCH CENTER OF MEDICINAL PLANTS, MASHHAD UNIVERSITY OF MEDICAL SCIENCES, MASHHAD, IRAN
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2009Volume 19
 
 
Abstract: 

In hospitalized patients septic shock is the second most important cause of death. In septic patients and animals, the vasculature responsiveness to different vasoconstrictors and vasodilators alters, which suggest that different degree of endothelial and vasculature damage is present. Therefore, the present study was undertaken to investigate the degree and kind of this hyporesponsiveness after endotoxin induced septic shock. In this study, control rats (n=5) received saline (1ml kg-1) and endotoxemic rats (n=7) received a bolus injection of endotoxin (10mg kg-1) intraperitoneally. After 5 hour animals were anaesthetized with sodium pentobarbital (60 mg kg-1) and arterial blood pressure, heart rate and responses to different vasoconstrictor (phenylephrine 0.1 and 0.3 μg kg-1) and vasodilator (acetylcholine 5 and 50 μg kg-1; sodium nitroprusside 0.1 and 0.01 μg kg-1) were studied. Also the responsiveness of the isolated kidneys removed either from control or endotoxemic rats to vasoconstrictor and vasodilators agent were investigated in the absence and presence of L-NAME, 10-5M and chelerythrine (10-5M). After 5 hours, rat in endotoxemic group showed shock symptoms like rapid respiration and diarrhea. Endotoxin injections caused a marked hypotension and bradycardia (P<0.001). The contractile response to phenylephrine and also vasodilatory response to, acetylcholine and sodium nitroprusside were decreased both in vivo and in isolated perfuse kidney (p<0.05 control vs. endotoxemic). L-NAME and/or chelerythrine pretreatment improved the renal vascular responses to different agents. In conclusion, the significant hypotension induced by endotoxin was accompanied by a pronounced decrease in systemic vascular reactivity to vasoconstrictors and also an increase in renal vascular resistance. Our results suggest that inhibition of inducible nitric oxide and/or protein kinas C may be beneficial in an endotoxemic state.

 
Keyword(s): ENDOTOXIN, VASOCONSTRICTOR, VASODILATOR, KIDNEY, RAT
 
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