[The effect of halothane on the somato-sympathetic reflex].
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Biomedical subjects
Publications and source records attributed to S Saeki.
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The contribution of enterohepatic circulation of cholesterol and bile acids in the hypocholesterolemic activity of soybean protein isolate (SPI) was compared with the activity of casein. Intact, sham-operated, jejunectomized or ileectomized adult rats were fed a cholesterol-free, purified diet containing either 20% casein or 20% SPI for 7 or 10 d. For the subsequent 7 d the diets were reversed. In intact rats the plasma cholesterol concentration (p-chol) was significantly higher when the casein diet was fed than when the SPI diet was fed. Within 3 d after the diet crossover, p-chol in each group of intact rats reached rapidly the same level as that in its previous counterpart. These rapid inherent responses of p-chol to the casein and SPI diets remained unchanged even when the jejunum or the ileum was resected, and p-chol in jejunectomized or ileectomized rats was similar to that found in sham-operated rats. The extent of the change in p-chol induced by exchanging dietary proteins was almost the same among intact, sham-operated, jejunectomized and ileectomized rats. These findings indicate that the interruption of enterohepatic circulation of cholesterol and bile acids is not the major factor involved in the differential effects of dietary proteins on p-chol.
1. Metabolism in vivo of 3,4,3',4'-tetrachlorobiphenyl (TCB) and toxicological assessment of the metabolites were investigated in the rat. 2. Four metabolites were isolated from faeces of rats dosed with 3,4,3',4'-TCB. Two were identified as 5-hydroxy-3,4,3',4'-TCB and a chlorine-shift metabolite, 4-hydroxy-3,5,3',4'-TCB, by comparison of melting points, chromatographic mobilities and spectral features with those of the synthetic samples. A dihydroxy-TCB and monohydroxy-trichlorobiphenyl were also indicated by mass spectrometry to be excreted in faeces as minor metabolites. 3. Faecal excretion of unchanged 3,4,3',4'-TCB, 5-hydroxy-3,4,3',4'-TCB and 4-hydroxy-3,5,3',4'-TCB was 0.8%, 19.6% and 11.6% of dose, respectively, in 5 days after i.p. injection of 3,4,3',4'-TCB at a dose of 50 mg/kg. 4. From the inability to cause the liver hypertrophy and thymus atrophy, both monohydroxy-metabolites of 3,4,3',4'-TCB are much less toxic than the parent 3,4,3',4'-TCB. In addition, these phenolic metabolites did not induce the activities of benzo[a]pyrene hydroxylase and DT-diaphorase, whereas 3,4,3',4'-TCB greatly induced these activities. These results indicated that unlike PCB congeners with phenobarbital-type inducing ability, 3,4,3',4'-TCB, a prototype of 3-methylcholanthrene-type inducers, is detoxified by metabolic hydroxylation.
The role of renomedullary lipids in the hypotensive effect of captopril was studied in spontaneously hypertensive rats, one-kidney, one clip hypertensive rats and two-kidney, one clip hypertensive rats using inhibitors of acetyl glyceryl ether phosphorylcholine and prostaglandins, and chemical medullectomy. Our experiments indicate that it is unlikely that renomedullary lipids contribute to the hypotensive action of captopril.
A new surgical method for internal biliary drainage was devised, consisting of percutaneous transhepatic cholangio-drainage (PTCD) and Roux-en-Y anastomosis. The PTCD fistula is connected to the jejunostomy by a drainage catheter buried in the subcutaneous space. As compared with conventional methods for surgical internal biliary drainage, this method has the following advantages: It can be easily performed even when other types of internal drainage are not feasible, the catheter can readily be changed if it becomes obstructed, and percutaneous cholangiography, irrigation or drug infusion can be performed at any time via the drainage catheter.
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An enzyme immunoassay for serum 18-hydroxycorticosterone was established using alkaline phosphatase as a label. The antiserum for 18-hydroxycorticosterone was produced by immunization of rabbits with 18-hydroxycorticosterone 3-(o-carboxymethyl) oxime conjugated to bovine serum albumin. Sephadex LH-20 column chromatography was used to separate 18-hydroxycorticosterone from other steroids in serum samples. The minimal detectable amount of 18-hydroxycorticosterone was 50 pg/tube, and the measurable range was from 5 to 1000 ng/dl when a 1.0 ml serum sample was used. Intra- and inter-assay coefficients of variance were 5.0% (n = 6), and 5.8% (n = 6), respectively. In normal controls the serum 18-hydroxycorticosterone level was 4.8 approximately 34.0 ng/dl (mean +/- S.D. = 17.1 +/- 9.0 ng/dl) on an unrestricted diet. Seven out of 8 patients with aldosterone-producing adenoma had above-normal serum 18-hydroxycorticosterone levels. Serum 18-hydroxycorticosterone increased and decreased significantly following ACTH and dexamethasone administration, respectively. In essential hypertensive patients, serum 18-hydroxycorticosterone was high during a low-sodium diet and was suppressed remarkably by captopril. These observations support the previous reports that adrenal 18-hydroxycorticosterone synthesis is dependent on both ACTH and the renin-angiotensin system. The present method is sufficiently sensitive and producible, avoids the use of radioisotopes and is quite satisfactory for clinical use.
The direct cardiac action of 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (PAF) was studied in isolated perfused guinea-pig heart preparations. PAF produced a fall in left ventricular pressure, decreases in the rate of rise of the left ventricular pressure (dp/dt) and coronary flow, but had no effect on heart rate. These results indicate that PAF is a cardiodepressant with inotropic selectivity and this effect on heart is blocked by CV-3988, a specific PAF antagonist.
One-O-hexadecyl-2-O-acetyl-sn-glycero-3-phosphorylcholine (AGEPC) was intravenously administered to anesthetized dogs to study the effects on hemodynamics and several endocrine factors. The effect of AGEPC on local blood flow was also studied by direct intra-arterial injection. Following intravenous injection, blood pressure and cardiac output decreased significantly (p less than 0.001). Changes in total peripheral resistance (TPR) and heart rate were biphasic. TPR increased significantly (p less than 0.01) after an initial slight reduction. Heart rate decreased significantly (p less than 0.01) with only a transient slight elevation. Femoral blood flow was increased (p less than 0.001) by intraarterial injection and decreased (p less than 0.05) by intravenous administration. Plasma norepinephrine (p less than 0.001), epinephrine (p less than 0.01), thromboxane B2 (p less than 0.001), 6-0-PGF1 alpha (p less than 0.01), aldosterone (p less than 0.001) and cortisol (p less than 0.001) were elevated, but plasma renin activity did not change. These results suggest that the hypotensive mechanism of AGEPC is due to both cardiosuppression and vasodilation. AGEPC increased plasma catecholamines, thromboxane A2, PGI2, aldosterone and cortisol which, in turn, may modify hemodynamics.
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