A new canine myocardial infarction model using thrombi induced by closed-chest injection of thrombin and autogenous blood with fibrinogen into coronary arteries was developed. Occlusive thrombi were formed in all treated animals. Occluded vessels did not spontaneously reperfuse 1 day after occlusion, but did so within 3 days. Infarction was confirmed by increased levels of creatine kinase-MB, glutamate-oxaloacetate transaminase and -hydroxybutyrate dehydrogenase. Additionally, the left ventricular ejection fraction (LVEF) decreased within 0.5 h after occlusion and had not improved 4 weeks later. After 1 week, extensive transmural anteroinferior myocardial infarction was observed and heart mass had increased. By 4 weeks after occlusion, pulmonary capillary wedge pressure and central venous pressure were increased, and oxygen pressure was decreased. Dropout of nuclei in cardiomyocytes and increased amount of collagen fiber were observed in myocardial infarct regions of hearts excised 4 weeks after occlusion. This canine model may be useful and convenient in evaluating treatment efficacy and the long-term outcome of acute myocardial infarction. (Jpn Circ J 1999; 63: 900 -905)

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Vitellogenesis in many insect species is triggered by juvenile hormone (JH) where other factors such as neural or endocrinological ones also play a important roles. Newly emerged adult females of the American cockroach, Periplaneta americana were injected with indoleamines such as tryptamine (Tn), N-acetyltryptamine (NATn), serotonin (5-HT), N-acetylserotonin (NAS) and melatonin (ME) at 20, 30 and 40 µg in the abdomen. Tn and NATn stimulated Vg synthesis, while 5-HT, NAS and ME inhibited it. These amines may exert the effect on either directly on Vg synthesis in the fat body, Vg receptor, follicle cells, or JH synthesis. We first cloned the genes encoding juvenile hormone acid O-methyltransferase (JHAMT) and farnesoic acid O-methyl transferase (FAMeT) which are involved in JH biosynthesis. qRT-PCR analysis revealed that indoleamines affected the expression of JHAMT and FAMeT in the Br-CA complex. 5-HT, NAS and ME inhibited JHAMT and FAMeT transcription, while Tn and NATn stimulated their transcription. The oocyte length and yolk accumulation showed that, Tn, more likely NATn induced oocyte maturation. Here, the result suggests that intricate mutual interactions induced Vg synthesis in the fat body during oocyte maturation between neurotransmitters/modulator pathway and JH synthesis pathways.

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Subacute prognosis of cardiac function after thrombolysis with a modified tissue-type plasminogen activator (t-PA) YM866 was determined in dogs with coronary artery thromboses induced by injection of a thrombin, fibrinogen and autogenous blood mixture. The left ventricular ejection fraction (LVEF) decreased 30 min after occlusion and had not improved 1 week later. Examination after sacrifice revealed myocardial infarction as well as increases in both the left ventricular myocardial area and heart mass. Occluded coronary arteries reperfused by YM866 (0.1 mg kg(-1) i.v.) treatment 30 min after occlusion, by contrast, had improved LVEF and inhibited myocardial infarction development. In addition, the left ventricular myocardial area and heart mass were significantly reduced compared with the vehicle control group 1 week after administration. Although occluded coronary arteries reperfused by YM866 (0.1 mg kg(-1) i.v.) treatment 3 h after occlusion did not show an improvement in the LVEF or inhibition of myocardial infarction development, the left ventricular myocardial area and heart mass decreased significantly compared with the vehicle control group 1 week after administration. In conclusion, early reperfusion by t-PA treatment 30 min after occlusion improved the ventricular function and cardiac hypertrophy, whereas late reperfusion by t-PA treatment 3 h after occlusion did not improve the ventricular function but did inhibit hypertrophy in dogs with coronary artery thrombi.