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S Teramura

Publications and source records attributed to S Teramura.

23 records · Page 2Linked to original sources
PubMed1989

Effect of diethyldithiocarbamate on gastric and duodenal mucosal blood flow and vascular permeability in rats.

Diethyldithiocarbamate (DDC), an inhibitor of superoxide dismutase, produced ulceration in the proximal duodenum of rats, and erosions or ulcers in the stomach. DDC given s. c. at 1.5 g/kg increased duodenal and gastric vascular permeability, and reduced blood flow. The decrease in gastric blood flow caused by DDC was attenuated by pretreatment with superoxide dismutase, and significantly inhibited by a xanthine oxidase inhibitor, allopurinol. It is suggested that the superoxide and other radicals damage the mucosal vasculature, and play a role in the pathogenesis of gastric and duodenal mucosal lesions.

Animals↗
PubMed1989

Effect of plasmin inhibitors on gastric mucosal permeability in rats.

We examined the protective effect of plasmin inhibitors on gastric mucosal vascular permeability in rats. Tranexamic acid and aminocaproic acid significantly inhibited the increase in vascular permeability and macroscopic gastric mucosal lesions induced by 50% ethanol and 1% ammonia. The protective effect afforded by plasmin inhibitors was not affected by pretreatment with indomethacin. Our results show that plasmin inhibitors inhibit the increase in gastric vascular permeability and suggest that plasmin may play an important role in the pathogenesis of gastric mucosal damage.

Aminocaproates↗
PubMed1975

Effects of hardness on the disintegration time and the dissolution rate of uncoated caffeine tablets.

The effects of hardness on disintegration and dissolution characteristics of uncoated caffeine tablets made at eight different pressure levels were studied. The disintegration times were determined using the J.P. VIII procedure with disks and the dissolution rate measurements were performed with the U.S.P.XVIII procedure (U.S.P. method) and the J.P. VIII disintegration test apparatus (J.P. method). A good correlation between the hardness and the disintegration times was obtained. The dissolution rate constants were determined from the equation of Noyes & Whitney (1897) and a good correlation between the hardness and the dissolution rate constants was obtained. The hardness governed the dissolution over all the stages from tablet to the smallest particles after the breakage by disintegration. The dissolution rates of the J.P. method were greater than those of the U.S.P. method.

Caffeine↗
PubMedDate not supplied

[Which time constant of left ventricular relaxation is the most sensitive measure in acute myocardial ischemia?].

To investigate which time constant of isovolumic left ventricular pressure (LVP) decay is the most sensitive measure in acute myocardial ischemia, the time constant of isovolumic relaxation (IR) was calculated by two different models, the semilogarithmic model assuming a zero of LVP decline (TL) and an exponential model (Texp) with an asymptote (extrapolated baseline pressure to which LVP would fall if decay continued indefinitely), in 10 patients before and during ergonovine-induced vasospastic angina. Two time constants were derived from the exponential method as the times for LVP at peak negative dP/dt to decline by 1/e (Texp (1/e)) and by one half (Texp (1/2)). Three changes in LVP during isovolumic relaxation were analyzed and fitted to the two models described above: the LVP from the peak negative dP/dt 1) to when LVP fell to 5 mmHg above LV end-diastolic pressure (EDP), 2) until 40 msec had passed, and 3) to the LVP level 5 mmHg above LVEDP during coronary spasm. There were significant increases in TL, Texp (1/e) and Texp (1/2) in each period of the LVP during vasospastic angina. However, no significant change in Texp or asymptote was observed during angina. We concluded that TL measured by the semilogarithmic model assuming a zero of LVP decline and Texp (1/e) or Texp (1/2) derived from the exponential model are adequately sensitive for detecting acute myocardial ischemia due to coronary spasm.

Adult↗