Related Experiment Video
Updated: Sep 23, 2026
Developing a Clinically Relevant Hemorrhagic Shock Model in Rats
Published on: March 22, 2024
[Therapeutic efficiency of nitric oxide synthase inhibitor on traumatic shock in rats]
Gao-bin Sun1, Zong-hai Huang, Ying-gang Sun
1Department of Surgery, Zhujiang Hospital, First Military Medical University, Guangzhou 510282, Guangdong, China.
Objective:
To evaluate the effects of aminoguanidine (AG) used as a selective inhibitor of the inducible form of nitric oxide synthase (iNOS) and N-nitro-L-arginine methyl ester (L-NAME) used as a non-selective inhibitor of nitric oxide synthase (NOS) on traumatic shock.
Methods:
Thirty SD (Sprague-Dawley) rats were used to create a animal model of traumatic shock. Both shaft of femurs were crashed and bled to mean arterial pressure of 35-45 mm Hg (1 mmHg=0.133 kPa) via femoral artery. Hypotension was maintained 30 minutes, the shed blood was then returned, followed by an infusion with Ringer's solutions. Animals were randomly divided into three groups: traumatic shock group (n=10), AG group (AG 8 mg/kg was infused at resuscitation, n=10), L-NAME group (L-NAME 8 mg/kg was infused at resuscitation, n=10). Plasma levels of nitric oxide (NO) were determined before and after shock, immediately after resuscitation and 0.5, 2 and 4 hours after resuscitation. The 24 hours survival rates were recorded. Lung, liver and kidney, intestine tissues were obtained 24 hours after shock for microscopic examination.
Results:
The plasma level of NO markedly increased after shock. The plasma level of NO markedly decreased and less tissue damages with highly survival rates in AG group. Lower plasma level of NO and survival rates and highly tissue damages were seen in L-NAME group.
Conclusion:
NO plays an important role in development of pathologically traumatic shock. AG is beneficial of treatment in traumatic shock, but L-NAME can only decrease the plasma level of NO and can not improve the outcome of shock.
