Effect of hyaluronidase on experimental cerebral infarct size and mortality.
The goal of this investigation was to determine whether hyaluronidase administration can alter the size, morbidity, and mortality of experimental acute cerebral infarctions. Accordingly, the left common carotid artery was occluded in 1205 ether-anesthetized Mongolian gerbils. The gerbils were randomized into hyaluronidase-treated (4000 National Formulary units per kg., intravenously, 5 minutes after occlusion) or control groups. All were examined for clinical signs of cerebrovascular accident three times during the 24 hours and then decapitated, and each hemibrain was analyzed for its total creatine kinase activity. In the control group, 90 of 601 gerbils died, whereas in the hyaluronidase-treated group only 61 of 604 gerbils died. This reduction in mortality was highly significant (chi 2 = 6.53, p less than 0.02). In the surviving gerbils with cerebrovascular accidents, infarct size was calculated by creatine kinase depletion (normal right hemibrain creatine kinase minus infarcted left hemibrain creatine kinase divided by right hemibrain creatine kinase and corrected for "residual" (nondepletable) creatine kinase). In controls, infarct size was 36.5 +/- 1.8 per cent (n = 105), and in the hyaluronidase-treated gerbils it was significantly lower, 31.4 +/- 1.7 per cent (n = 117, p less than 0.05). Thus, in gerbils with experimental cerebrovascular accidents, hyaluronidase significantly reduced mortality (by one-third) and reduced "enzymatic" infarct size by 14.0 +/- 4.6 per cent (p less than 0.01).
D000818:Animals; D002544:Cerebral Infarction / Q000188:drug therapy* / Q000401:mortality / Q000473:pathology; D003402:Creatine Kinase / Q000378:metabolism; D004195:Disease Models, Animal; D005849:Gerbillinae; D006821:Hyaluronoglucosaminidase / Q000627:therapeutic use*; D011379:Prognosis
D003402:Creatine Kinase; D006821:Hyaluronoglucosaminidase