Reference

Effect of selective inhibitor of thromboxane A2 synthetase on experimental cerebral vasospasm

Effect of selective inhibitor of thromboxane A2 synthetase on experimental cerebral vasospasm. Fukumori, Toyokazu; Tani, Eiichi; Maeda, Yukio; Sukenaga, Atsuhiko (Dep. Neurosurg., Hyogo Coll. Med., Hyogo, Japan). Stroke (Dallas), 15(2), 306-11 (English) 1984. CODEN: SJCCA7. ISSN: 0039-2499. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Exptl. cerebral vasospasm was induced in the canine basilar artery by an intracisternal injection of fresh autogenous arterial blood. Delayed vasospasm was defined as a redn. to less than 75% of the caliber of control basilar artery 5 days after the intracisternal blood injection. A selective inhibitor of thromboxane A2 synthetase, (E)-3-[4-(3-pyridylmethyl)phenyl]-2-methyl-2-propenoic acid (I) [75987-08-5], was infused i.v. for 1 or 2 h at 50 mg/kg/min in normal animals and in animals exhibiting vasospasm. Angiog. evidence of cerebral vasospasm was not reversed. Mean regional cerebral blood flow was not significantly increased in normal and vasospastic animals, but a mean difference of regional cerebral blood flow was significantly increased only in vasospastic animals. Mean arterial blood pressure and pulse rate were not seriously changed in normal and spastic animals. Another selective thromboxane A2 synthetase inhibitor, (E)-3-[4-(1-imidazolylmethyl)phenyl]-2-propenoic acid [82571-53-7], showed a similar effect on the caliber of the basilar artery, regional cerebral blood flow, blood pressure, and pulse rate, in vasospastic animals. Venous blood was taken from the internal jugular vein, and the mean platelet aggregation induced by 10 mg/mL of collagen was inhibited by the infusion of either selective inhibitor at 50 mg/kg/min for 2 h. However, mean platelet aggregation rates in vasospastic animals before and after treatment with either selective inhibitor were not significantly different from those in normal animals.

Participation of peroxisomal b-oxidation system in the chain-shortening of a xenobiotic acyl compound

Participation of peroxisomal b-oxidation system in the chain-shortening of a xenobiotic acyl compound. Yamada, Junji; Horie, Shuichi; Watanabe, Takafumi; Suga, Tetsuya (Dep. Clin. Biochem., Tokyo Coll. Pharm., Tokyo 192-03, Japan). Biochem. Biophys. Res. Commun., 125(1), 123-8 (English) 1984. CODEN: BBRCA9. ISSN: 0006-291X. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 4, 13 A model drug, (E)-3-[4-(1-imidazolylmethyl)phenyl]-2-propenoic acid [82571-53-7], was metabolized to 4-(1-imidazolylmethyl)benzoic acid [94084-75-0] by isolated hepatocytes of rats and this metab. was enhanced by pretreatment of rats with clofibrate. With liver homogenates, the formation of the CoA-ester [94666-06-5] of this drug and its subsequent chain-shortening were demonstrated. Acyl-CoA synthetase [9013-18-7], CoA [85-61-0], ATP [56-65-5], and NAD [53-84-9] were required for this metabolic sequence; CN- did not inhibit the reaction. These results indicate that peroxisomes are capable of shortening the acyl side-chains of drugs by the b-oxidn., giving an addnl. suggestion on the functions of peroxisomes.