Abstract:Global Ischemia in Dogs: Cerebrovascular COi Reactivity and Autoregulation• One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO 2 , and (2) cerebral blood flow (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO 2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing Paco 2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant Paco 2 . These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO 2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.

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The culture conditions of Polyporus tuberaster K2606 were investigated to find conditions with which much benzaldehyde and benzyl alcohol would be obtained. Strain K2606 reduced benzoic acid as well as L-phenylalanine to benzaldehyde and benzyl alcohol in high yield. The conversion rate of benzoic acid was about 60%. Two other metabolites of L-phenylalanine, 3-phenylpropionic acid and 3-phenylpyruvic acid, were reduced to benzaldehyde and benzyl alcohol as well. Veratryl alcohol, a secondary metabolite of L-phenylalanine, was not detected. Benzaldehyde produced by strain K2606 was reduced to benzyl alcohol, which was slowly converted again into benzaldehyde when culture with shaking continued. The maximum concentrations of benzaldehyde and benzyl alcohol produced by strain K2606 were 7.89 and 11.93 mM when L-phenylalanine was added to the culture medium at concentrations of 90 and 45 mM, respectively.

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