[Effect of cigarette smoking on the gastric hemodynamics.--Analysis by reflectance spectrophotometry (author's transl)].
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Biomedical subjects
Publications and source records attributed to M Shichiri.
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Two patients had hypouricemia due to increased uric acid clearance. Their daily urinary uric acid excretions were normal. In both patients, pyrazinamide decreased urinary uric acid clearance to almost while probenecid increased it markedly. No other renal tubular or metabolic abnormalities were found. The serum electrolytes and the urinary electrolytes excretions showed no abnormalities. It appears that increased secretion of uric acid in the renal tubule is most probably responsible for hypouricemia in these patients. This report adds to the list of hypouricemic conditions due to a new isolated renal tubular abnormality.
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Utilizing reflectance spectrophotometry, hemoperfusion, rate of oxygen consumption and redox level of mitochondrial cytochrome c (+c1) in livers in situ of anesthetized rats were measured. The transition to the anoxic state was induced by raising the pressure on the liver surface to more than the hepatic blood pressure by pressing with the tip of the optical guide of the reflectance spectrophotometer. During this transition, the average oxygen saturation of hemoglobin in the liver in situ decreased linearly with time until it became 10--20% of the total. This was followed by reduction of mitochondrial cytochrome c (+c1), which reached completion in 10--20 s. The measured O2 consumption rate remained constant until the percentage of oxyhemoglobin in situ decreased to a critical level. There was then a decrease in the rate of O2 consumption which was accompanied by a progressive reduction of cytochrome c (+c1). It was shown that amounts of hemoglobin and mitochondrial respiratory chain cytochromes in the liver in situ could be measured non-invasively and could provide important signals for vital cellular functions. The changes in hemoperfusion and rate of O2 consumption of the liver in situ following ethanol ingestion were also shown in rats, and are briefly discussed with respect to possible application of this method to study the pathophysiology of tissues.
To determine a possible relation of hepatic oxidative activity to glucose metabolism, the rates of oxygen consumption of liver slices from patients with chronic liver diseases were polarographically measured. The livers from patients with chronic (persistent and aggressive) hepatitis and with normal glucose tolerance showed almost the same respiratory activity as those from patients with normal livers and normal glucose tolerance, whereas the livers from patients with chronic hepatitis and with diabetic glucose tolerance (ie, diabetes mellitus secondary to chronic hepatitis) showed only a half the normal level. The decreased rate of respiration was also observed in liver slices from cirrhotics with glucose intolerance. The decrease in respiration was found in patients with normal or hyperinsulinemia as well as hypoinsulinemia responding to oral glucose load. No liver tests so far examined, except the oral glucose tolerance test, correlated with hepatic respiratory activity. It is concluded that in patients with chronic liver diseases the defect of liver respiration has a close relation to the glucose metabolism and is not necessarily associated with histological change of the liver.
Six alloxan-diabetic dogs with fasting plasma glucose levels above 200 mg/100 mL were treated with rectal administration of insulin suppositories twice a day for 6--9 days. The effectiveness was compared with that of subcutaneous insulin injections. In three diabetic dogs with fasting plasma glucose levels below 300 mg/100 mL, both insulin suppository at a dose of 20 U (2.3 U/kg) and subcutaneous insulin at a dose of 0.2 U/kg showed a similar effect in reducing fasting glucose levels and daily urinary glucose amounts. In dogs with higher fasting glucose levels, 0.5 U of subcutaneous insulin/kg is less effective in reducing fasting glucose than 50 U (5.2 U/kg) suppositories, in spite of the same effects on daily urinary glucose output. Postprandial glucose responses were significantly lessened with rectal administration of insulin suppositories. The integrated area of increase in peripheral insulin concentration after subcutaneous infection of 0.2 or 0.5 U insulin/kg was significantly greater than that after rectal administration of an insulin suppository (2.3 or 5.2 U/kg, respectively). These results indicate that diabetes could be controlled by the daily rectal administration of an insulin suppository instead of the conventional subcutaneous injection.
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Scintiphotosplenoportography (SSP) was performed in 190 instances in 161 patients. No significant complications, such as severe pain or splenic haemorrhage, were encountered in any of the patients studied. Flow patterns of SSP were classified into nine groups according to the direction of collateral flow. Hepatopetal collateral flow was frequently observed in pancreatic cancer. In portal hypertension, cephalic collateral flow was more frequently observed than caudal flow. In detecting oesophageal varices, both SSP and endoscopy were performed in 81 patients. In four out of 46 patients with cephalic flow, oesophageal varices could not be observed by endoscopy. Conversely, in three out of 44 patients with oesophageal varices, SSP failed to show cephalic flow. The combined use of SSP and endoscopy would therefore provide more useful information in the management of patients with portal hypertension.
To elucidate the precise significance of pancreatic A-cell hypersecretion in the pathogenesis of diabetes mellitus, the change in the immunoreactive glucagon (IRG) response to intravenous arginine was studied in both nonobese, hypoinsulinemic non-insulin-dependent (NIDDM) and insulin-dependent diabetic (IDDM) subjects whose blood glucose responses and plasma immunoreactive insulin (IRI) simulated those of healthy subjects with the aid of the artificial beta-cell system that we originally developed. In both five NIDDM and five IDDM subjects, blood glucose responses and plasma IRI after arginine challenges were made equivalent to those seen in healthy subjects by infusing insulin in response to blood glucose, revealing that previously exaggerated IRG responses were made completely similar to the responses in healthy subjects. In summary, these results clearly demonstrate that the exaggerated response of A-cell secretion against arginine challenges in insulin-deficient diabetics is secondary to insulin lack, and the perfect normalization of its response is achieved only when both plasma insulin concentration and glycemic control simulate those of healthy subjects.
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An instrument for the control of blood glucose in a closed-loop fashion has been developed. This artificial beta cell consists of 4 subunits: a Glucose Monitor, a Microcomputer, an Insulin Infusion Pump and a Printer. Its internal control algorithm was derived from the modeled dynamics of glucose-induced insulin secretion, and includes the effects of both the proportional and derivative actions of blood glucose concentration, and is expressed as: IIR = Kp . BG + Kd . deltaBG + Kc, where IIR is insulin infusion rate, BG and deltaBG are blood glucose concentration and rate of change in glycemia, respectively. Kp and Kd are individual coefficients and Kc is a constant of basal insulin secretion. The performance of this system was studied with various kinds of glucose challenges on anaesthetized depancreatized dogs. Its notable characteristics were: 1) the insulin infusion rate was such as to maintain physiological insulin levels, and 2) dextrose or glucagon infusions were not required.
An artificial endocrine pancreas has been developed by adding a glucose infusion system to the artificial beta cell system. In this computer algorithm, glucose is infused on the basis of proportional and derivative actions to blood glucose concentration with the time delay constant between blood withdrawal and initiation of glucose infusion. When glucose was infused on the basis of proportional action with a 20-minute time delay, the prompt restoration to normoglycemia from the hypoglycemic state with a smaller amount of glucose was shown in depancreatized dogs. These results indicate that the artificial endocrine pancreas thus prepared is not only a useful device to safely control blood glucose, but also is an efficient research tool for the analysis of the blood glucose regulatory mechanism.
The dynamic property of insulin secretion in relation to glucose tolerance was investigated quantitatively during iv glucose tolerance tests in 237 cases. The following results were obtained; 1) Glucose clearance constant (k-value) was not constant but variable with time and should be expressed as a function of time, K(t). In normal glucose tolerance, K(t) became greater with time. 2) Glucose-induced insulin secretion was expressed as the function of a proportional plus derivative response to glucose concentration. A weighting function of derivative response, reflecting the insulin secretion per unit of rate of change in blood glucose concentration, was calculated from blood glucose concentration (input) and insulin concentration (output) by the deconvolution method. It was clearly shown that the gain in weighting function was small and the response was slow even in the individual whose glucose tolerance was slightly impaired. 3) The greater the weighting function, the larger the change in K(t).