[The role of nitric oxide on the dysfunction of intestinal motility in rats subjected to hemorrhagic shock].
OBJECTIVE
To determine the role of nitric oxide (NO) in intestinal motility dysfunction in rats subjected to hemorrhagic shock (HS).


METHODS
Sixteen male Wistar rats were randomly and equally divided into two groups. The HS model of rat was induced by bleeding from femoral artery. After animal models were made, different inducers were added, and duodenum samples were harvested for the determination of contractile response to acetylcholine (ACh) in vitro, activities of inducible nitric oxide synthase (iNOS), contents of NO in tissue, and morphological changes.


RESULTS
The spontaneous contraction of intestinal smooth muscle and contractile response induced by ACh were significantly decreased at 180 minutes in HS group, compared with control group, the contractile response induced by ACh of intestinal smooth muscle was decreased by almost 60% (0.40±0.11 g×mm(-2)×s(-1) vs. 1.00±0.20 g×mm(-2)×s(-1), P<0.01). The inhibitor of iNOS N(G)-nitro-L-arginine methyl ester hydrochloride (L-NAME) could significantly restore the suppressed contractile response of smooth muscle strips obtained from HS rats (0.97±0.25 vs. 0.40±0.11, P<0.01). Moreover, the inhibitor of soluble guanylyl cyclase 1H-[1,2,4] Oxadiazolo [4,3-a] quinoxalin-1-one (ODQ) also improved the contractility of HS muscle strips significantly (0.79±0.17 vs. 0.40±0.11, P<0.01). But the blocker of ATP-sensitive potassium channel glibenclamide had no effect on the contractility of HS muscle strips (0.47±0.14 vs. 0.40±0.11, P>0.05). Compared with those of control group, iNOS activities (2.295±0.310 U/g vs. 1.319±0.322 U/g) and NO contents (2.880±0.353 μmol/g vs. 1.505±0.387 μmol/g) in duodenum of HS rats were both significantly increased (both P<0.01). Under light microscopy, the most significant morphological change in duodenum following HS was the infiltration of obvious inflammatory cells.


CONCLUSIONS
The NO produced by the overexpression of iNOS induced by HS involves in the motility dysfunction of intestine through the mechanism of cyclic guanosine monophosphate (cGMP) system. Moreover, NO-mediated infiltration of inflammatory cells in tissue may also contribute to the development of motility dysfunction of intestine following HS.
Department of Pathophysiology, Preclinical College of Hebei North University, Zhangjiakou 075000, Hebei, China. Corresponding author: Zhang Yu-ping, Email: zhangeping@sina.com.
Yu-ping
YP
Zhang
Xiao-rong
XR
Wang
Xiao-qi
XQ
Zhao
Hai-xia
HX
Qiao
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D006152:Cyclic GMP / Q000378:metabolism; D005769:Gastrointestinal Motility; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009569:Nitric Oxide / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012771:Shock, Hemorrhagic / Q000378:metabolism* / Q000503:physiopathology*
D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D006152:Cyclic GMP; D000109:Acetylcholine