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Endotoxin impairs the response of rat anococcygeus muscle to electrical field stimulation
M O Guc1, B L Furman, J R Parratt
1Department of Physiology and Pharmacology, University of Strathclyde, Glasgow, U.K.
Abstract:
Rat anococcygeus muscles were isolated 4 h after treatment with either E. coli endotoxin (20 mg kg-1 i.p.) or saline. The contractile responses of the muscle to electrical field stimulation, and to the alpha 1-adrenoceptor agonist cirazoline were impaired by endotoxin treatment. Inhibition of the L-arginine pathway with L-NG-nitro arginine methylester (3 x 10(-5) M) failed to restore responsiveness to either electrical field stimulation or to cirazoline. Endotoxin impaired inhibitory responses to electrical field stimulation in preparations precontracted with cirazoline. Responsiveness to sodium nitroprusside was also impaired by endotoxin under these conditions. These results show an impairment by endotoxin of both contractile and inhibitory responses of the rat anococcygeus muscle to electrical field stimulation. The impairment appears to be post-junctional. In contrast to the findings in vascular smooth muscle, the endotoxin-induced impairment of contractile responses does not appear to involve the L-arginine pathway.
Insights
E. coli endotoxin impairs rat anococcygeus muscle responses to electrical stimulation and alpha-1 adrenoceptor agonists. This impairment is post-junctional and does not involve the L-arginine pathway, unlike in vascular smooth muscle.
Area of Science:
- Pharmacology
- Physiology
- Smooth Muscle Biology
Background:
- Endotoxemia can cause organ dysfunction.
- The rat anococcygeus muscle is a well-established model for smooth muscle studies.
- The role of the L-arginine pathway in endotoxin-induced smooth muscle dysfunction is not fully understood.
Purpose of the Study:
- To investigate the effects of E. coli endotoxin on the contractile and inhibitory responses of the rat anococcygeus muscle.
- To determine if the L-arginine pathway is involved in endotoxin-induced impairment of smooth muscle function.
- To explore the post-junctional or pre-junctional nature of the observed impairment.
Main Methods:
- Isolation of rat anococcygeus muscles 4 hours post-treatment with E. coli endotoxin or saline.
- Assessment of contractile responses to electrical field stimulation and cirazoline (alpha 1-adrenoceptor agonist).
- Evaluation of inhibitory responses and responsiveness to sodium nitroprusside under endotoxin treatment and L-NG-nitro arginine methylester (L-arginine pathway inhibitor).
Main Results:
- Endotoxin treatment significantly impaired contractile responses to electrical field stimulation and cirazoline.
- Endotoxin also impaired inhibitory responses to electrical field stimulation and responsiveness to sodium nitroprusside.
- Inhibition of the L-arginine pathway did not restore normal muscle responsiveness.
- The observed impairment was post-junctional.
Conclusions:
- E. coli endotoxin impairs both contractile and inhibitory functions of the rat anococcygeus muscle.
- The endotoxin-induced impairment is post-junctional.
- The L-arginine pathway is not involved in the endotoxin-induced impairment of contractile responses in this specific smooth muscle model, contrasting with findings in vascular smooth muscle.