Biomedical subjects

J Nakano

Publications and source records attributed to J Nakano.

At least 91 records · Page 5Linked to original sources

PubMed1976

Studies on the isothermal crystallization of D-glucose and cellulose oligosaccharides by differential scanning calorimetry.

Isothermal crystallization from the glassy state of D-glucose and cellulose oligosaccharides (e.g., cellobiose, cellotriose, and cellotetraose) has been studied by differential scanning calorimetry. The crystallization of amorphous D-glucose and oligosaccharides was very difficult in the absence of traces of water. Amorphous cellobiose and cellotetraose crystallized far more rapidly than amorphous D-glucose and cellotriose. The activation energy for the crystallization of cellobiose and cellotetraose was approximately 10-12 kJ. mol(-1), while that for D-glucose and cellotriose was approximately 1-2 kJ. mol(-1). An odd-even effect seemed to be associated with the crystallization process of these saccharides.

Calorimetry↗

PubMed1976

Reflex bradycardia and hypotension produced by prostaglandin F2alpha in the cat.

1 Intravenous administration of prostaglandin F2alpha results in a dose-dependent increase in pulmonary arterial pressure, decrease in systemic arterial pressure and a delayed bradycardia. Pulmonary vasoconstriction was observed at doses as low as 0.1 and 0.3 mug/kg. The systemic depressor and heart rate lowering effects were observed at 1 mug/kg doses and above. 2 A moderate bradycardia was still observed after atropine blockade but was abolished following bilateral vagotomy. Neither of these procedures affected the pulmonary vascular response. 3 Injections of submaximal doses of prostaglandin F2alpha (1--4 mug/kg) produced a greater and longer lasting bradycardia when injected into the left atrium than was observed following intravenous administration. In addition the latency of onset was much shorter following left atrial injection. These doses resulted in no change in heart rate and a minimal hypotension when injected into the brachiocephalic artery or into the aortic arch. 4 Small doses of prostaglandin F2alpha administered at the level of the origin of the coronary arteries produced marked decreases in heart rate and blood pressure whereas no change occurred following injection of the same amount into the ascending aorta at more distal sites. 5 These results suggest that prostaglandin F2alpha produces bradycardia and hypotension in the cat by activating 'receptors' located in the left heart or by acting on structures perfused by means of the coronary arteries.

Animals↗

PubMed1975

Effect of prostaglandins E1, E2 and F2alpha and pentagrastin on the gall bladder pressure in dogs.

The effect of prostaglandins E1, E2 and F2alpha on the gall bladder pressure was studied in anesthetized dogs with and without clamping of the cystic duct. Both PGE1 and PGE2 lowered the gall bladder pressure when the initial pressure was higher than 5 mm Hg, but caused no significant change when the initial pressure was lower than 3 mm Hg. On the other hand, PGF2alpha increased the gall bladder pressure regardless of its initial pressure. When the cystic duct was clamped, PGF2alpha markedly increased the gall bladder pressure while both PGE1 and PGE2 increased it slightly. This observation suggests that the smooth muscle in the gall bladder is markedly stimulated by PGF2alpha and stimulated to a lesser degree by PGE1 or PGE2. Furthermore, PGF2alpha appears to constrict, and PGE1 or PGE2 appears to relax the sphincter of Oddi. Pretreatment with indomethacin did not affect or slightly potentiated the cholecystokinetic effect of the three prostaglandins but abolished that of pentagastrin, suggesting that prostaglandins are possible mediators for the cholecystokinetic action of the gastrointestinal hormones.

Animals↗

PubMed1974