[Role of the adrenal medulla in elevation of blood pressure induced by sodium loading].
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Biomedical subjects
Publications and source records attributed to H Ijichi.
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The influence of exercise training on left ventricular performance was investigated by exercise two-dimensional echocardiography in 12 top-ranking Japanese volleyball players and 10 untrained subjects. Left ventricular wall thickness and dimension were greater in the athletes than in the nonathletes. The left ventricular wall thickness-internal radius ratio, however, was nearly the same in both groups. At rest, heart rate, the stroke area index, % fractional area and the cardiac index were significantly lower in the athletes than in the nonathletes. During exercise, heart rate was slower in the athletes at every exercise stress stage. The stroke area index, % fractional area and the cardiac index increased linearly in the athletes, although these indices of the nonathletes reached a plateau at the moderate exercise stage. The double product at the last stage was greater in the athletes than in the nonathletes. Both groups did not differ as to segmental fractional area change of left ventricular contraction at rest and during exercise. Serum norepinephrine concentration was significantly lower in the athletes than in the nonathletes at rest. After exercise, however, the difference between the two groups was not apparent. It is suspected that exercise training increased the exercise capacity due to an increase in the left ventricular systolic function reserve, the increment of cardiac VO2 max, and the change of blood flow distribution, and generalized aerobic metabolism in various organs.
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Evaluation of regional contractile reserve and the viability of an infarcted segment of the myocardium is very important in determining the indications for aorto-coronary bypass after myocardial infarction and in predicting the prognosis. Regional wall motion of the left ventricle after postextrasystolic potentiation (PESP) was studied in 18 patients with old myocardial infarction, and compared with indices of redistribution of thallium after exercise. Equilibrium radionuclide angiocardiography (RNA) using Tc99m HSA was performed at rest and after PESP produced by a programmable cardiac stimulator via a right ventricular catheter. Regional ejection fractions (REF) were determined, and wall motion was observed visually. The relative thallium activity (RTA) and washout rate (WOR) were obtained from exercise myocardial scintigraphy performed 10 minutes, and 3 hours after thallium-201 injections. Wall motion improved in 12 of 23 infarcted segments after PESP. Regional ejection fraction and relative thallium activity (in three hours, or the difference between the activities of the initial and three hours after exercise) in the improved segments were significantly higher (p less than 0.001) than in the unchanged segments. Washout rate was lower (p less than 0.02) in the improved segments. Significant correlation was observed between the change in regional ejection fraction and relative thallium activity (3 hours after exercise) (r = 0.654, p less than 0.05). Thus, the wall motion of some infarcted regions of the myocardium improved after PESP, and thallium was redistributed during three hours after exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
Bethanidine, a chemical analog of bretylium, increased the plateau phase of the action potential of guinea-pig papillary muscle in 2.7 mM K+ Tyrode solution without changing other electrophysiological parameters. In 25 mM K+ Tyrode solution, the amplitude, duration and Vmax of the Ca2+-dependent action potential were increased in a dose-dependent manner by bethanidine. It is speculated that the mechanism of antiarrhythmic effect of bethanidine might be due to the prolongation of action potential by an increase of the slow inward current.
The effects of a calcium channel blocker, diltiazem, on central cardiovascular regulation were investigated by injecting it intracerebroventricularly (i.c.v.) in urethane-anaesthetized rats. The blood pressure decreased immediately after the injection returning to baseline level 20-30 min later. Both heart rate and abdominal sympathetic nerve activity decreased correspondingly. Diltiazem injected intravenously (i.v.) decreased both blood pressure and heart rate without affecting sympathetic nerve firing. Although the central pressor responses to carbachol and prostaglandin E2 were not affected by i.c.v. pretreatment with diltiazem, diltiazem attenuated the pressor responses to angiotensin II. Furthermore, electrical lesioning of the anteroventral third ventricle (AV3V) area significantly attenuated the depressor responses to diltiazem injected i.c.v. These results suggest that diltiazem injected i.c.v. affects the central nervous system to decrease sympathetic outflow, and thereby to attenuate the central vasopressor effects of angiotensin II in the brain AV3V area.
The effects of taurine on central cardiovascular regulation were investigated by intracerebroventricular (ICV) injection of taurine in urethane-anesthetized rats. Blood pressure fell gradually to attain the maximum level at 10 to 15 min after the injection of 50 micrograms taurine and returned to the basal level 20 min later. After injecting 200 micrograms of taurine, blood pressure began to fall within 30 seconds and attained the maximum level at 2 to 5 min and did not return to the basal level by 20 min. Both heart rate and abdominal sympathetic nerve activity decreased as the blood pressure fell, However, the similar amount of taurine injected intravenously did not affect the blood pressure, the heart rate or the abdominal sympathetic nerve activity. These results suggest that taurine causes the central nervous system to lower the blood pressure by decreasing the sympathetic nerve outflow.
The present study was undertaken to determine the central effect of adrenaline. Adrenaline was administered to the cisterna magna in urethane anesthetized rats. Following the intracisternal injections, the blood pressure dropped and reached a plateau after 15 min, the hypotensive effect continuing for at least 30 min. The heart rate also slowed concomitantly with the depressor effect. The vehicle treated rats did not show any cardiovascular responses. The cardiovascular responses in the experimental rats were accompanied by an inhibition of the sympathetic nerve activity. Pressor responses to electrical stimulation of the posterior hypothalamus were partly inhibited, while pressor responses to intravenous injections of noradrenaline remained unchanged. In DOCA hypertensive rats, the depressor responses to intracisternal injections of adrenaline were augmented. These findings suggest that adrenaline in the brain could contribute to the inhibitory mechanism of the cardiovascular system accompanied by inhibition of the sympathetic nerve system, and that this mechanism may be attenuated in DOCA hypertensive rats.
The role of the renal nerve in influencing the hypothalamo-sympathetic nerve system to regulate the cardiovascular system was studied in normotensive Wistar and spontaneously hypertensive rats (SHR). Renal denervation attenuated pressor and sympathetic nerve responses to electrical stimulation of the hypothalamus without lowering the basal blood pressure at 48 hours after denervated operation. These findings suggest that renal denervation could inhibit the hypothalamo-sympathetic nerve system in normotensive rats. The development of hypertension in SHR was completely inhibited by renal denervation during 2 weeks of observation (from 7 to 9 weeks of age) without increasing water intake and urine volume. Pressor responses to intravenous injection of norepinephrine were not affected by renal denervation. The results show that the antihypertensive effect of renal denervation was not due to the changing of vascular reactivity. Pressor and sympathetic nerve responses to hypothalamic stimulation were strongly diminished in renal denervated rats. These results suggest that renal denervation strongly inhibited they hypothalamo-sympathetic nerve system. It is also suggested that the renal afferent nerve may facilitate the hypothalamo-sympathetic nerve system in regulating blood pressure and that this facilitation may contribute to the development of hypertension in SHR.
High ferritin levels in the aspirate of thyroid cyst (Six yellow clear, 4 yellow turbid and 10 chocolate colored turbid) without apparent sings of malignancy were found. The mean concentration in the 3,000 X g supernatant of the fluid was 40,116 ng/ml, and the 3,000 X g precipitate was 11,147 ng/ml. All cases showed normal levels of serum ferritin. Con A binding with ferritin was distributed from low to high. These ferritins showed a molecular weight of approximately 450,000 which was the same as found in human spleen and liver. The continuous increase in ferritin levels in thyroid cyst fluid was found by a chronological study in some cases. When tumor markers such as CEA, NCA, CA 19-9 and alpha 1-acid glycoprotein (alpha 1-AG, acute phase reactant) were examined simultaneously, an increase in some of the cyst fluid was observed. However, the incidence and the rate of increase of these tumor markers and acute phase reactant were low compared to ferritin. Neither a correlation between ferritin and CEA, nor between ferritin and CA 19-9 was found. The increase in ferritin in thyroid cyst fluids may be due to the increased synthesis, release and storage by the inflammatory cells.
The effects of d1-2-(3'-t-butylamino-2'-hydroxypropylthio)-4-(5'-carbamoyl-2'-thi enyl) thiazole hydrochloride (S-596) were evaluated in 9 normal volunteers. Exercise echocardiography was performed in the semi-supine position before and 2, 4 and 24 hours after the oral administration of 15 mg of S-596. Two hours after administration, resting heart rate was unchanged, compared with control, but systolic blood pressure at rest was slightly decreased (114 +/- 6 vs 106 +/- 10 mmHg, p less than 0.05). Left ventricular dimensions were unchanged, but shortening fraction was increased in the resting state (30.3 +/- 4.6 vs 33.1 +/- 4.8%, p less than 0.05). During exercise on oral S-596, heart rate and systolic blood pressure responses were reduced (127 +/- 11 in control vs 108 +/- 6 beats/min on S-596, 198 +/- 25 vs 168 +/- 23 mmHg, p less than 0.001 and 0.05, respectively). Left ventricular end-diastolic dimension was not significantly altered by S-596 compared with the preceding control exercise test; however, end-systolic dimension was significantly larger after beta blockade with S-596 (2.6 +/- 0.4 vs 3.0 +/- 0.4 cm, p less than 0.05). Shortening fraction and cardiac output decreased significantly (43.7 +/- 3.7 vs 40.0 +/- 5.7%, 9.5 +/- 1.4 vs 8.4 +/- 1.3 L/min, p less than 0.05 and 0.01, respectively). These effects of S-596 were maximal at 2 hours after oral administration with reduced response of heart rate to exercise lasting for 24 hours. Compared with the effects of propranolol (30 mg, given orally) in the same subjects, beta-adrenergic blockade during exercise with S-596 was equivalent to or greater than that of propranolol. Thus, S-596 has little, if any, effect on resting left ventricular performance, but demonstrates potent negative chronotropic and inotropic effects during exercise in normal human subjects. Its beta-adrenergic blocking action also has long acting properties, especially its chronotropic effect.
As both hormonal and hemodynamic alterations similar to those occurring during exercise can also be produced in humans by hypoglycemia, the present study explored changes in hemodynamic parameters during hypoglycemia and the effects of the alpha 1-adrenergic blocker, prazosin, on those responses in hypertensive patients. In the control group, which did not receive prazosin, plasma epinephrine, plasma norepinephrine and plasma renin activity (PRA) all increased along with a rise in blood pressure during hypoglycemia. On the other hand, the blood pressure decreased despite similar increases in plasma catecholamine levels and PRA in the prazosin treated group. The hemodynamic parameters, analyzed using M-mode echocardiography, changed in both the control and prazosin groups during hypoglycemia; stroke volume and cardiac output showed similar increases. However, while the total peripheral resistance did not change significantly in the control group, it decreased in the prazosin group during hypoglycemia. In accord with the changes in total peripheral resistance, the increment in mean-velocity of circumferential fiber shortening (m-Vcf) during hypoglycemia was greater in the prazosin group than in the control. These results suggest that: hypoglycemia stimulates the sympatho-adrenal axis which then releases catecholamines leading to a rise in blood pressure and tachycardia; In contrast, the blood pressure decreases during hypoglycemia in the prazosin group despite an increase in plasma catecholamines, because the alpha-receptors are blocked by prazosin and the unopposed beta-adrenergic effects of the catecholamines are pronounced enough to reduce the total vascular resistance.
Hepatic hydrothorax occurred in a 38-year-old woman of severe hepatic failure complicated with pulmonary tuberculosis. The transdiaphragmatic passage of ascitic fluid to the pleural cavity was visually shown with a scintigram using technetium-99m macroaggregated albumin and also shown with a tracer analysis using indocyanine green. The ascites was suggested to be transported to the pleural cavity via the defect in the right diaphragm.
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