Zinc protoporphyrin aggravates cerebral ischemic injury following experimental subarachnoid hemorrhage.

Authors: Sun, BL  An, W  Xia, ZL  Zheng, CB  Li, WX  Yang, MF  Zhao, T  Ye, WJ 
Citation: Sun BL, etal., Clin Hemorheol Microcirc. 2006;34(1-2):241-6.
Pubmed: (View Article at PubMed) PMID:16543643

This study was aimed to evaluate the influence of an antagonist of heme oxygenase, zinc protoporphyrin IX (ZnPPIX), on the production of endogenous carbon monoxide (CO) and the secondary cerebral injury after subarachnoid hemorrhage (SAH). Wistar rats were divided into non-SAH, SAH, and ZnPPIX groups. Autologus arterial hemolysate was injected into rat cisterna magna to induce SAH. CO and cyclic guanosine monophosphate (cGMP) levels in the brain, and lactate dehydrogenase (LDH) activity in serum were determined 24 hours and 72 hours after cisternal injection. It was found that 24 hours and 72 hours after SAH, the CO contents in SAH group were increased by 20.76% and 37.36%, respectively. CO content in ZnPPIX group was statistically lower than that in SAH group. No obvious change of cGMP content in SAH group was found. However, cGMP content in ZnPPIX group was lower than that in SAH group. Serum LDH activity increased significantly after induction of SAH. LDH activity in ZnPPIX group increased to a greater extent. It was concluded that ZnPPIX aggravates the cerebral injury secondary to experimental SAH by inhibiting the production of endogenous CO. The activation of HO/CO pathway is an intrinsic protective mechanism against cerebral ischemic injury after SAH.

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CRRD Object Information
CRRD ID: 1582702
Created: 2006-11-17
Species: All species
Last Modified: 2006-11-17
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.