Search PubMed⌕ Search

Biomedical subjects

T Ogihara

Publications and source records attributed to T Ogihara.

At least 775 records · Page 43Linked to original sources

Platelet-activating factor and anti-platelet-aggregating factor in acute reduction of blood pressure following percutaneous transluminal renal angioplasty in patients with renovascular hypertension.

The mechanism of the acute fall of BP following percutaneous transluminal renal angioplasty (PTRA) was studied in four patients with renovascular hypertension caused by fibromuscular dysplasia. One hour after PTRA, systemic blood pressure and plasma renin activity in the ipsilateral renal venous blood decreased significantly (P less than 0.05), but the plasma noradrenaline level in ipsilateral renal venous blood increased significantly (P less than 0.05). At the same time, a platelet-activating factor (PAF) and an unidentified factor that inhibited the aggregation of rabbit platelets induced by PAF, arachidonic acid or ADP were detected in the ipsilateral renal venous blood, but were not found in the contralateral renal venous blood. Plasma noradrenaline level in cubital venous blood decreased significantly (P less than 0.05) after 24 hours as compared with that before PTRA and BP also maintained the normal level. These results suggest that the reduction in plasma renin activity is associated with the acute reduction in BP following PTRA. PAF and an unidentified factor blocking the aggregation of platelets may be involved in ipsilateral renal venous blood following PTRA in patients with renovascular hypertension. The reduction in plasma noradrenaline level is an additional mechanism involved in maintaining normal BP following PTRA in the late stage.

Adult↗

Changes in plasma lipids and uric acid with sodium loading and sodium depletion in patients with essential hypertension.

The short-term effects of manipulating dietary salt intake on plasma levels of cholesterol, lipoproteins and uric acid were studied in two groups of patient with essential hypertension. With dietary salt restriction in 8 patients (10 g to 2 g salt/day for five days), plasma total cholesterol, esterified cholesterol, beta-lipoprotein, low density lipoprotein and uric acid rose significantly. With salt repletion (2 g salt/day to 20 g/day for five days) in 17 patients, plasma total cholesterol, esterified cholesterol, beta-lipoprotein, low density lipoprotein and uric acid fell significantly. Total/HDL cholesterol ratio increased significantly with salt restriction and decreased significantly with repletion. However, very low density lipoprotein, HDL-cholesterol, triglyceride, phospholipid, chylomicron and non-esterified fatty acid were not influenced by the changes in salt intake. These results indicate that the severe restriction of dietary salt raises plasma cholesterol and uric acid levels in patients with essential hypertension in the short term.

Blood Pressure↗

Normalization of high plasma level of ouabain-like immunoreactivity in primary aldosteronism after removal of adenoma.

Plasma ouabain-like immunoreactivity, which has been supposed to be associated with hypertension, was significantly higher in five patients with primary aldosteronism than in age-matched normotensive subjects. High plasma levels of ouabain-like immunoreactivity decreased to normal after removal of adenoma. Extracts of adenoma tissue did not contain any apparent ouabain-like immunoreactivity. Anti-ouabain antibody used in this study did not cross-react with aldosterone, cortisol, corticosterone, arachidonic acid or lysophosphatidylcholine. Hypertension, hypokalemia, a high plasma aldosterone level and low plasma renin activity were also normalized after surgery. These results indicate that hyperaldosteronism induces the high plasma level of ouabain-like immunoreactivity and this is associated in part with high blood pressure (BP) in primary aldosteronism.

Adenoma↗

Effects of oral and intravenous administrations of dopamine and L-dopa on plasma levels of two isomers of dopamine sulfate in man.

The levels of two isomers of dopamine sulfate, dopamine-3-O-sulfate (DA3S) and dopamine-4-O-sulfate (DA4S), in human plasma were measured by HPLC-fluorometry. The basal plasma levels of DA3S and DA4S in the early morning were 13.8 +/- 1.9 and 3.2 +/- 0.5 pmoles/ml, respectively (means +/- S.E.M.). Oral administrations of dopamine (50 mg/body) and 1-dihydroxyphenylalanine (L-DOPA, 250 mg/body) increased the plasma levels of these dopamine sulfates almost 100-fold to 1807 +/- 266 and 1674 +/- 195 pmoles/ml of DA3S, and 466 +/- 83 and 321 +/- 76 pmoles/ml of DA4S. Intravenous dopamine infusion (5 micrograms/kg/min for 30 min) markedly increased the plasma free dopamine concentration, as expected, but increased the levels of DA3S and DA4S only slightly to 110 +/- 32 and 25 +/- 9 pmoles/ml, respectively. In contrast, intravenous L-DOPA (25 mg/body) resulted in a slight increase of free dopamine followed by marked increases of DA3S and DA4S to 691 +/- 219 and 139 +/- 40 pmoles/ml, respectively. These data indicate that O-sulfation of dopamine, especially 3-O-sulfation, is the main pathway for metabolism of intravenously and orally administered L-DOPA and orally ingested dopamine. This sulfation is suggested to occur in the gut wall.

Administration, Oral↗

Optical birefringence of phosphatidylcholine liposomes in gel phases.

A simple and rapid method for studying optical anisotropic properties of liposomes was proposed. Intensities of transmitted light through one spherical liposome of dipalmitoylphosphatidylcholine placed between two polarizers were measured at various wavelengths by a microscopic spectrophotometer. Large increases in the intensities were observed at the prephase-transition temperature, which were caused by an increase in the birefringence of the multilayer of the liposome. The birefringence values obtained from the intensity data were about 0.020 below the pretransition temperature and 0.028 above that temperature. These values are in good agreement with the results reported for the plane samples in which lipid bilayers are stacked. The obtained values of the birefringence were far lower than the values estimated from polarizabilities. This lower birefringence is attributed to disordering of the tilt direction in the multilayer. The degree of order of the liposome multilayers calculated from the birefringence increased by 38% at the pretransition. This simple method is applicable to the study of the multilayer structure of liposomes in water.

1,2-Dipalmitoylphosphatidylcholine↗

Plasma atrial natriuretic peptide level as an index for the severity of congestive heart failure.

Human atrial natriuretic peptide (hANP) is a vasodepressor and a natriuretic hormone. The levels of plasma hANP increase during extracellular volume expansion. In the present study, we investigated whether plasma levels of hANP were associated with the severity of congestive heart failure (CHF), and whether such an association could be used as a diagnostic aid. Plasma hANP levels in 102 patients with various heart diseases and correlation between the plasma hANP levels and the left ventricular ejection fraction (EF) determined from echocardiography in 43 patients were examined. The plasma levels of hANP were high during the state of extracellular fluid overloading and atrial distention as determined by high right atrial pressure and pulmonary capillary wedge pressure. The high plasma hANP levels decreased in CHF patients whose clinical state improved, but remained high in those patients who were refractory to treatment. Plasma hANP levels correlated inversely with left ventricular EF (r = -0.41, p less than 0.01). In 9 patients reexamined during the course of treatment the plasma hANP levels decreased with an increase in EF. These data indicate that the level of plasma hANP is a practical diagnostic indicator of the severity of CHF, and can also be used as a means for assessing the efficacy of the treatment.

Adult↗

Hemodynamic, renal, and hormonal responses to alpha-human atrial natriuretic peptide in patients with congestive heart failure.

Hemodynamic, renal, and hormonal effects of intravenous bolus injection of 50 micrograms synthetic alpha-human atrial natriuretic peptide (alpha-hANP) were studied in eight patients with congestive heart failure. alpha-hANP caused significant reductions in mean blood pressure and systemic vascular resistance. These responses were sustained up to 90 minutes and not accompanied by reflex tachycardia. Cardiac index and stroke volume index increased significantly at 90 minutes and pulmonary capillary wedge pressure, pulmonary arterial pressure, and mean right atrial pressure remained unchanged. Urine volume, urinary sodium excretion, creatinine clearance, and fractional excretion of sodium increased significantly, but fractional excretion of potassium and phosphate did not change. Elevated plasma renin activity, plasma aldosterone, and norepinephrine were suppressed after the injection of alpha-hANP. The bolus injection of this peptide has moderately hypotensive, vasorelaxant, and natriuretic effects in patients with congestive heart failure.

Aged↗

Selective pharmacological effects of triprolyl and pentasarcosyl angiotensin II.

Among the various biological effects of angiotensin II (AII), both pressor activity and aldosterone stimulation appear to be mediated by functionally different receptors. With this in mind, we compared pressor and aldosterone-stimulating activities of AII with those of triprolyl [(Pro)3] AII and pentasarcosyl [(Sar)5] AII. In conscious male Wistar rats (Pro)3 AII and (Sar)5 AII produced 48 and 46% of the pressor activity of AII. After intravenous infusion (conscious unrestrained rats, 125 pmol/kg/min for 30 min), plasma aldosterone concentrations were not significantly different from those of control rats which were infused with saline. However, when the rats were infused with AII (125 pmol/kg/min for 30 min), plasma aldosterone concentrations increased significantly (1,306 +/- 80 pg/ml). This study indicates that (Pro)3 AII and (Sar)5 AII may prove to be useful tools to elucidate biological actions of AII.

1-Sarcosine-8-Isoleucine Angiotensin II↗

Changes in plasma atrial natriuretic polypeptide concentration during head-out water immersion and saline infusion in normal men.

The physiological mechanism regulating secretion of human atrial natriuretic polypeptide (hANP) was examined by measuring plasma hANP by a specific radioimmunoassay during head-out total body water immersion (WI) and saline infusion in normal men. Seven healthy men were immersed in water for 1 hour, 6 normal men and women were given an infusion of 1 liter of normal saline over 1 hour and 8 normal men were given a similar infusion over 2 hours. During WI, the urinary volume (UV) and urinary Na excretion (UNaV) increased significantly, and the plasma hANP level increased significantly from 246 +/- 12 (mean +/- SE) pg/ml to 392 +/- 32 pg/ml after 35 +/- 5 min, but returned to the basal level after 90 min. The increase in hANP level was correlated with an increased UNaV between 30 to 60 min during WI. The plasma norepinephrine, renin activity, aldosterone and cortisol levels also decreased during WI. Saline infusion caused variable increases in the hANP level: the mean peak values of hANP and times of the peaks from the start of saline infusion were respectively 305 +/- 30 pg/ml after 30 +/- 3 min of infusion at a rate of 1L/1 hr and 285 +/- 25 pg/ml after 69 +/- 15 min of infusion at a rate of 1L/2 hrs. The time of the peak of plasma hANP during infusion at 1L/2 hrs was significantly longer than the peaks for WI or an infusion of saline at 1L/1 hr. Moreover, the peak hANP level was significantly smaller during either condition of saline infusion than during water immersion. These results indicate that i) acute central hypervolemia caused by WI increases hANP secretion, and this increase may participate in natriuresis during WI, and ii) saline infusion causes an increase in plasma hANP of variable magnitude, the increase being more rapid for a more rapid infusion of saline. This suggests that hANP is released into the circulation by acute volume expansion and plays a physiologically important role in maintaining blood volume homeostasis in man.

Adult↗

Hyperthyroidism associated with autoimmune hemolytic anemia and periodic paralysis: a report of a case in which antihyperthyroid therapy alone was effective against hemolysis.

We describe a case of a 29-year-old man with hyperthyroidism associated with autoimmune hemolytic anemia and periodic paralysis. Euthyroidism, which was achieved by propylthiouracil, brought inhibition of hemolysis and amelioration of anemia in spite of continuously positive direct and indirect Coombs' tests. Neither adrenocortical steroid nor blood transfusion was administered. Since indirect monospecific Coombs' test was negative against anti-human complements serum, the membrane of red blood cells may be less fragile. This is one reason why hemolysis was inhibited by anti-hyperthyroid therapy only. This may indicate that the hyperdynamic circulatory state secondary to hyperthyroidism plays an important role in the destruction of red blood cells which were coated by anti-red blood cell antibody.

Adult↗

Contribution of elevated peripheral resistance to acute volume loaded hypertension in dogs.

The role of peripheral resistance in volume loaded hypertension was examined by measuring changes in hemodynamic and humoral factors during dextran infusion for one hour, and for three hours after stopping the infusion in 30 anesthetized dogs. The mean blood pressure was elevated significantly (118%, p less than 0.01), accompanied by increased cardiac output (170%, p less than 0.01) during volume loading. In the recovery period, cardiac output returned to the basal level while the total peripheral resistance gradually increased (118%, p less than 0.01) contributing to the maintenance of high blood pressure (108%, p less than 0.01). There was no significant correlation between the hematocrit change and the increase in peripheral resistance in the recovery period. The levels of plasma norepinephrine, epinephrine, renin activity and vasopressin were suppressed by volume loading. These results demonstrated the importance of increase in peripheral resistance for maintaining high blood pressure in this acute volume excess model. The participation of the renin-angiotensin system, the sympathetic nervous system and vasopressin were all excluded and vascular structural changes were most unlikely to be involved in this acute experiment. It remains unknown whether this conversion is attributable to the summation of local autoregulation or to some other factors.

Animals↗

Ouabain-like and non-ouabain-like factors in plasma of patients with essential hypertension.

Circulating inhibitor of Na+,K+-ATPase and ouabain-like immunoreactivity were studied in patients with essential hypertension. In the plasma of patients, two types of Na+,K+-ATPase inhibitors (ouabain-like and non-ouabain-like inhibitors) and ouabain-like immunoreactivity were detected. Ouabain-like inhibitor was clearly detected at a low KCl concentration (0.1 mM) in the assay buffer, and non-ouabain-like inhibitor was detected at a high KCl concentration (10 mM). The plasma level of ouabain-like inhibitor correlated significantly with that of ouabain-like immunoreactivity (p less than 0.001) and with a mean blood pressure (p less than 0.01). The plasma level of non-ouabain-like inhibitor was not correlated with the levels of either ouabain-like immunoreactivity or mean blood pressure. The level of plasma ouabain-like inhibitor did not correlate with that of plasma non-ouabain like inhibitor. Both ouabain-like inhibitor and ouabain-like immunoreactivity in the plasma of patients with essential hypertension were significantly higher than those in normotensive subjects, but the plasma level of non-ouabain-like inhibitor in patients with essential hypertension was not higher than that in normotensive subjects. These results suggest that the plasma from patients with essential hypertension contains ouabain-like factor(s) which is important to maintain the high blood pressure.

Adult↗

The hypotensive effect of captopril is not mediated by renal medullary lipids.

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.

Animals↗

Effect of captopril on angiotensin II release from vascular tissues in rats.

Isolated rat hindlegs were perfused with Krebs-Ringer solution and released angiotensin I (ANG I) and ANG II were determined. The release of ANG I and ANG II in nephrectomized rats did not differ from those in control group. Pretreatment with captopril (50 mg/kg/day) for 3 days or addition of captopril (2 X 10(-6) M) to the perfusate induced increase in ANG I release and decrease in ANG II release. These findings suggest that ANG II is locally generated and release from the vascular tissues. Captopril may inhibit the conversion of vascular ANG I into ANG II.

Angiotensin I↗