Paper Information

Title: 

EFFECTS OF CHRONIC EXERCISE TRAINING AND DETRAINING ON CUTANEOUS MICROVASCULAR RESPONSES IN STREPTOZOTOCIN-INDUCED DIABETIC RATS

Type: POSTER
Author(s): HEYDARIANPOUR A.,HAJIZADEH S.,KHOUSHBATEN A.,NAZEM FARZAD,BARABADI Z.
 
 
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Abnormalities of the modulatory roles played by the endothelium and/or smooth muscle may be critical and initiating factors in the development of diabetic vascular disease. Decreased the L-argenein/ NO pathway activity, and thus impaired vascular relaxation may play pivotal roles in the diabetes-induced vascular dysfunction. During exercise, as core temperature rises, skin blood flow (SkBF) increases to facilitate the convective transfer of heat from core to skin. Although physical conditioning enhances cutaneous microvascular responsiveness, the mechanisms of this training effect on the control of skin blood flow remain unclear.
Method: Male wistar rats (220±10 g, N=60) were made diabetic by streptozotocin (60mg/kg, s.c). After 1 week of diabetes induction, animal were submitted to exercise training for 10 weeks on treadmill and then detrained for 8 weeks. We used laser Doppler flowmetery technique to characterize cutaneous microvascular responses.
Results: 1) Ach- induced cutaneous perfusion were increased significantly by training and attenuated by detraining and L-NNA in the diabetic groups; 2) Cutaneous microvascular responses to SNP did not alter in control and diabetic by training but decreased significantly by Detraining in diabetic rats; and 3) Local microinjection of L- argenein increased cutaneous blood flow in diabetic and normal rats. However this effect augmented by training in diabetic compared to age-matched normal rats.
Conclusions: Chronic exercise improves endothelium-dependent dilatation and potantiate L-argenein/ NO pathway activity in diabetic rats.

 
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