Methods:40 SD rats were randomly divided into control group,injury group,cemetidine treated group and nimodipine treated group,GMBF,pH of gastric juice and mucosal ulcer index were measured on the 72th hour after head injury.
RESULTS:Following burn injury, protein contents of the in-testinal mucosa decreased obviously in both groups. At 24,48 and 72 h postburn, mucosal protein contents in EF groupwere 262±24 mg/m, 283±29 mg/m, and 282±18 mg/mrespectively, significantly higher than those in PN group(195±45 mg/m, 194±41 mg/m, and 143±19 mg/m,respectively).
Over the next 9 hours,PTK activity declined gradually(160.6％ for 12 hours post-injury,vs controls,p<0.01),up regulated again at 24 hours after injury(176.37％,p<0.01)。 At 48 hours post-injury,PTK activity restored to normal level.
Our studies demonstrated an in vivo cardioprotection effect of (N-(3,4,-dimethoxy-2-chlorobenzylideneamino)-guanidine: ME10092) in ischaemic reperfusion injury in the rodent.
Diclofenac (25 mg kg-1) and meloxicam (7.5 mg kg-1) produced 9.3 and 19.6 mm2 ulcer areas in stomachs of rats, respectively, when used alone, but when combined with nimesulide diclofenac and meloxicam did not cause any injury in rat stomachs.
These proteins may be involved in cardiovascular injury, and could play an important role in the treatment of coronary heart disease.
SOD and POD activities declined correspondingly, followed by significant increases of MDA and MP, and leaf injury was finally observed.
Hepatocellular injury was the predominant type in these cases (132 cases, 48%).