The infusion of 900 μmoles of calcium chloride into the pancreaticoduodenal artery for 10 min resulted in a significant fall in the secretion of pancreatic glucagon. When 90 μmoles of calcium chloride were injected into the pancreatic artery for 10 sec, the plasma insulin in the pancreatic vein rose transiently and the plasma glucagon decreased significantly. The injection of either calcium gluconate or lactate brought about the same results as produced by the calcium chloride injection with respect to the insulin and glucagon levels in the pancreatic vein. The suppressive effect of calcium on pancreatic glucagon was prominent when calcium was infused into the pancreatic artery during arginine infusion. By the infusion of organic salts, arginine-induced hyperglucagonemia was blunted. The present experiment demonstrates the direct effect of calcium upon pancreatic glucagon secretion.
Replicas from complementary freeze-fracture faces of the rabbit rod outer segments were examined in an electron microscope. By this method two dissimilar faces, A and B, were visualized in a disc. The A face, toward the intradisc space, was characterized by densely packed particles, about 10 nm in diameter, rising on it; and the B face, toward the interdisc space, appeared smooth with minute unevennesses. An A face always formed a complementary set with a B face, and vice versa. No evidence has been obtained to suggest that a disc membrane may split along two or more different fracture planes.
Seventy patients admitted to the Tohoku University Hospital during the period from 1959 to 1973 with renal cell carcinoma were studied with regard to clinical and histologic features. Angiography, pyelography and scintigraphy were most contributory to diagnosis. The overall survival rate was 44% at 3 years, 39% at 5 years, and 35% at 10 years. Excluding those patients who exhibited metastasis at the beginning of treatment, the 3-year-survival rate was 78%, 5-year 69%, and 10-year 61%. Concerning clinical symptoms, prognosis was unfavorable for patients with a combination of fever and raised ESR. Although the pathologic staging of tumor growth correlated better with survival rate than the histologic grading of malignancy, both were important determinants in predicting prognosis of individual cases.
Blood pH, serum sodium and potassium, urinary pH, sodium, potassium and ammonia, and glutaminase I and glutaminase II activities in the kidney were studied in 10 control, 20 nephrotic, 12 aldosterone administered and 6 ammonium chloride administered rats. Urine pH of the animals with nephrosis or hyperaldosteronism ranged from 6 to 7.5, whereas that of acidosis ranged from 5.2 to 5.6. All of the experimental animal groups excreted significantly larger amounts of urine ammonia than did the control animals. The activities of glutaminase I in the cortex and glutaminase II in the medulla were elevated in the nephrotic and aldosterone administered animals. In acidotic rats increases in glutaminase I and glutaminase II activities were only noted in the cortex, and the more prominent increase was found in glutaminase I.
Direct perfusion of the sinus node artery at constant pressure of 100 mmHg was performed in eleven canine hearts in situ. The injection of desmethylimipramine (DMI) into the sinus node artery caused an initial short deceleration followed by markedly long-lasting acceleration of the heart rate. The initial deceleration was not influenced by treatment with atropine. The secondary acceleration was inhibited by propranolol, and, furthermore, suppressed by tetrodotoxin. After the treatment with propranolol or tetrodotoxin, DMI produced only a negative chronotropic effect dose-relatedly. It was difficult to observe the blocking effect of DMI on tyramine action, because DMI alone induced marked sinus acceleration. On the other hand, tyramine action was not influenced by tetrodotoxin. Therefore, the use of both DMI and tetrodotoxin is beneficial to observe blocking effect of DMI on tyramine-like action in the in situ SA node preparation.
Clofibrate treatment for 15-20 days (1500 mg/day) of diabetic patients with endogenous hypertriglyceridemia produced a significant increase in the plasma post-heparin lipolytic activity. Single administration of the drug (500 mg) did not affect the lipolytic activity though it resulted in an elevation of plasma clofibrate level similarly to the repeated administration for days. The relationship between changes of the lipolytic activity and plasma triglyceride concentration was not fully reciprocal in these patients. It is concluded that clofibrate increases plasma post-heparin lipolytic activity indirectly. However, it remains obscure whether the increase in the activity may have major role in the triglyceride lowering action of the drug.
Magos (1971) reported a new method of atomic absorption spectrometry for selective and simple determination of inorganic and organic mercury. To investigate the reliability of Magos's method, the content of inorganic and organic mercury in human hair was measured by Magos's method, and the results were compared with the value of organic mercury content by atomic absorption spectrometry with oxidized HCl-extract solution of hair, and with the value of total mercury content by neutron activation analysis. The comparison of the levels of organic mercury determined by Magos's method with that obtained with the HCl-extract gave a good coincidence (r=0.839) and the comparison between the total mercury, inorganic and organic, by Magos's method and that by neutron activation analysis did too (r=0.985). The extent of correlation was considered to be large enough to accept Magos's method for further use.
Effects of dibutyryl cyclic AMP (D-cAMP) on contractile performance of isolated dog heart muscle were investigated with special reference to its effectiveness for the reversal of myocardial depression produced by sodium thiamylal and halothane. D-cAMP increased the velocity of shortening at 0.4 g preload (V'max) and isometric force dose-dependently at concentrations over 1×10-3 M and net-shortening over 2×10-3M. However, the time course of its action was slow, with the peak effect about 70 min after the administration of the drug. This was a sharp contrast to a very rapid onset of action of epinephrine. When V'max was depressed to about 75% of the control by 3.3 mg% of thiamylal or 7.1 mg% of halothane, 3×10-3M of D-cAMP counteracted the depression produced by thiamylal and V'max was increased to 160% of the control, but it failed to reverse the depression produced by halothane and V'max remained 90% of the control. When the concentrations of halothane were lower than 5 mg%, however, D-cAMP at this concentration increased V'max more than the control level. The different responses to D-cAMP of the myocardium depressed by thiamylal and halothane suggest that there may be some differences between these two anesthetic agents in the mechanism for depressing myocardial contractility.
The effects of dibutyryl cyclic AMP (D-cAMP) on the pulmonary hemodynamics were studied in dogs. D-cAMP was administered intravenously in a dose of 30 mg/kg. The measurements of the parameters were made before and 5, 10 and 20 min after the administration of the agent. D-cAMP produced an increase in cardiac output, mean pulmonary arterial pressure and its driving pressure, but pulmonary arterial diastolic pressure and mean left atrial pressure remained almost unchanged throughout the experiments. Although pulmonary vascular resistance decreased gradually, a ratio of pulmonary vascular resistance to total peripheral vascular resistance rather increased after D-cAMP. Pulmonary vascular tension and mean pulmonary intravascular pressure also tended to increase. Pulmonary vascular compliance did not change significantly. Such changes in the pulmonary hemodynamics as produced by D-cAMP seemed to be due to secondary effects on cardiac output rather than to primary pulmonary vasoconstric-tion or vasodilatation.
Sediments from the bile of mice fed a lithogenic diet, and of patients with cholesterol stones were observed under a scanning electron microscope. In the murine bile, single cholesterol crystals appeared at 1 week after the start of lithogenic diet. At 2 weeks, clusters of a few cholesterol crystals were seen. They gradually grew into clusters of many cholesterol crystals in 6 weeks, and finally into cholesterol stones at 20 weeks. In the sediment of the bile from cholesterol stone patients, single cholesterol crystals and clusters of various sizes were observed. From these results, the process of cholesterol stone formation in the bile of man and mouse was presumed as follows: Single cholesterol crystals appear as the first step, then clusters of crystals are formed by the process of new crystal growth on the surface of older crystals or by the coagulation of crystals by cohesive force, and finally cholesterol stones are formed through a repetition of these processes.
Immunoassay for renin in human kidneys was undertaken by a hem-agglutination inhibition technique using high titer antirenin produced in rabbits. Human renin, highly purified by DEAE-cellulose and CM-sephadex column chromatography, was used for sensitization of sheep blood cells. Renin was extracted from kidneys of 11 normotensive and 27 hypertensive subjects through the five steps of the purification procedure described by Haas et al. The inhibition titer of antirenin was found to have a linear relationship with the concentrations of renin. However, in assay of lower concentrations of renin, such as plasma renin, there was some difficulty in reading the end-point of reactions since much diluted antirenin serum had to be used. The pressor effect of renin on unanesthetized dogs estimated by the direct method was compared with the results obtained by the hemagglutination inhibition method. Excellent agreement was obtained between results by both methods. The limits of estimation were 0.05 (Goldblatt) unit per gram of kidney tissue for dog assay and 0.001 unit per gram for the hemagglutination inhibition method. The mean value of renin for normal kidney was 0.105±0.033 U/g. The renin content was slightly higher in essential hypertension (0.222±0.066), greatly elevated in malignant hyperten-sion (0.560±0.376), and low in hypertension caused by chronic glomerulonephritis (0.054±0.020), chronic pyelonephritis (0.040), polycystic kidney (0.006), and Cushing's syndrome (0.008).
In separated preparations of smooth muscle layers, the electrical stimulations with 0.5 msec pulses have been utilized to reveal the nature of motor neurons in the dog urinary bladder. In the outer longitudinal muscle layer, contraction elicited by pulses was depressed after exposure to atropine (5×10-7 g/ml). In the middle circular muscle layer, however, atropine caused no diminution of contraction due to pulses, despite massive atropinization (5×10-6 g/ml). Contraction due to pulses was abolished by tetrodotoxin, but was not reduced by hexamethonium in both muscle layers. These results imply that there exist two kinds of parasympathetic motor neurons in the dog urinary bladder; atropine-sensitive neurons in the outer longitudinal muscle layer and atropine-resistant neurons in the middle circular muscle layer.
Hepatitis B antigen (HBsAg) in human plasma was purified by affinity chromatography through a column of Sepharose 4B which had been charged with anti-HBs. Eight different elution buffers were examined for better recovery by determining the antigen titers by solid-phase radioimmunoassay (Ausria-125). Among the buffers tested, 5M NaI, 1M acetic acid (AcOH) containing 1M NaCl (pH 2.5), and 3.5 M sodium thiocyanate (NaSCN) gave good recoveries and the mast preferable result was obtained with 1M AcOH containing 1M NaCl (pH 2.5).