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Biomedical subjects

T Ogihara

Publications and source records attributed to T Ogihara.

At least 757 records · Page 42Linked to original sources
PubMed1988

Distribution of tocopherol among human plasma lipoproteins.

A study of the distribution of alpha-tocopherol among the plasma lipoproteins of 19 healthy adults, 20 pregnant women at delivery, and the umbilical cord blood of their fetuses has shown the following. 1. In healthy adults, LDL in males contained slightly more tocopherol than did HDL, while non-pregnant females showed the opposite tendency. 2. In the pregnant women, the percent distribution of tocopherol was much higher in VLDL fractions, and lower in HDL fractions, as compared with non-pregnant women. 3. In cord blood, the percent distribution of tocopherol was extremely low in LDL fractions, but it was high in HDL fractions. 4. The distribution of tocopherol among lipoproteins was directly related to the total lipid contents of the lipoprotein fractions in all groups examined. After the oral administration of tocopherol to healthy adults, the changes in RBC tocopherol concentrations correlated most closely with those in HDL tocopherol.

Adult↗
PubMed1988

Changes in the levels of plasma atrial natriuretic peptide, hemodynamic measurements, and the levels of vasoactive hormones during the clinical course of congestive heart failure.

To investigate the mechanism for the release of human atrial natriuretic peptide (hANP) and the pathophysiological role of hANP in patients with congestive heart failure (CHF), plasma hANP levels in patients with dilated cardiomyopathy (DCM) or acute myocardial infarction (AMI) were determined serially, and the relationship between plasma ANP levels and hemodynamic measurements or various vasoactive hormones was analyzed during the clinical course of congestive heart failure. In 63 patients with either AMI or DCM, plasma hANP, plasma renin activity, aldosterone concentration, and catecholamines were measured over 4 weeks, during the course of CHF. Cardiac catheterization with a Swan-Ganz catheter was also performed. Plasma hANP in patients with DCM was elevated continuously during the clinical course. Plasma hANP levels in patients with AMI of Groups II and IV of Forrester's class decreased on days 7 and 14 and those in patients with AMI of Group I changed within normal limits. Plasma hANP levels were correlated positively with pulmonary artery pressure and pulmonary capillary wedge pressure in patients with AMI or DCM. Plasma renin activity, noradrenaline, and adrenaline levels were elevated in the acute phase of myocardial infarction and had a tendency to decrease upon improvement in clinical status. Plasma renin activity and noradrenaline level correlated positively with plasma hANP levels. These data indicate that plasma hANP levels are regulated by atrial distension and severity of cardiac impairment, and that plasma hANP and plasma renin activity or catecholamines correlated closely during the clinical course of CHF, indicating that these hormones may be involved in the volume and electrolytes status in CHF.

Adult↗
PubMed1988

Endogenous platelet-activating factor and anti-platelet-activating factor in patients with renovascular hypertension.

Renovascular hypertension is relieved by percutaneous transluminal renal angioplasty. In four patients with renovascular hypertension, platelet-activating factor (PAF) was found to be released into the ipsilateral renal venous blood after percutaneous transluminal renal angioplasty, but was not found in the contralateral renal venous blood following this procedure. Anti-platelet-activating factor with a lipid-like property was also found, and its polarity was slightly lower than that of PAF judging by its behavior on thin layer chromatography. Anti-platelet-activating factor completely blocked the aggregation of rabbit platelets induced by PAF, ADP or arachidonic acid. These results indicate that PAF and anti-platelet-activating factor are released into renal venous blood following percutaneous transluminal renal angioplasty in patients with renovascular hypertension.

Adenosine Diphosphate↗
PubMed1988

Effect of vasodilator prostaglandins on the vascular renin-angiotensin system.

The interaction of prostaglandin (PG) with the vascular renin-angiotensin (R-A) system was examined by studies on the effects of PGI2, PGE2 and the inhibitor of PG synthesis, indomethacin, on the release of angiotensin II (Ang II) from isolated rat mesenteric arteries. The Ang II released from the vasculature was measured after its concentration in a Sep-Pak C18 cartridge connected to the perfusion system. After perfusion with drugs, the specific vascular renin activity inhibited by anti-renin antibody was determined. The basal perfusion pressure was constant (19.6 +/- 1.1 mmHg) at a flow rate of 4.5 ml/min, and was not changed by any of these drugs. The basal levels of Ang II release and vascular renin activity were 44 +/- 5 pg/30 min and 113 +/- 8 pg Ang I/mg protein/hr, respectively. Infusion of PGI2 (10(-6) M) significantly decreased both Ang II release (p less than 0.01) and vascular renin activity (p less than 0.05) as compared with the control levels. Infusion of PGE2 (10(-6) M) decreased Ang II release significantly (p less than 0.05) and vascular renin activity slightly. Infusion of indomethacin (10(-6)M) increased vascular renin activity significantly (p less than 0.01). Pretreatment with indomethacin (10 mg/kg, ip) for 2 days also increased vascular renin activity (p less than 0.01). These results indicate that in contrast to their effects on the renal R-A system, PGs suppress the vascular R-A system and that these two local vasoactive factors interact to regulate vascular tone.

Angiotensin II↗
PubMed1988

Effects of frusemide and captopril on the relationship between biologically and immunologically active renin in human plasma.

1. The plasma renin concentration (PRC) and active renin concentration determined by radioimmunometric assay (ARC) were measured before and after administration of frusemide or captopril to normal volunteers. 2. Injection of 40 mg of frusemide followed by 1 h in the upright position significantly increased both PRC (P less than 0.001) and ARC (P less than 0.001). Oral administration of 50 mg of captopril also increased PRC (P less than 0.05) and ARC (P less than 0.05). 3. ARC and PRC were linearly correlated in the basal supine position [y = 0.635x - 0.048 (y = PRC, x = ARC), r = 0.958, P less than 0.001], after frusemide injection and standing (y = 0.800x + 0.359, r = 0.793, P less than 0.02) and after captopril administration in the supine position (y = 0.938x - 0.555, r = 0.998, P less than 0.001). 4. A cross-calibration study in which pure human renin was added to pooled plasma and PRC and ARC were measured showed linearity between the values obtained by the two methods. 5. The regression line for values of PRC and ARC in the supine position after captopril administration had a significantly greater slope (P less than 0.001) and that for values after frusemide injection and standing was significantly elevated (P less than 0.001) compared with the regression line for basal values in the supine position. 6. These results show that the biological activity of renin may be increased by various acute stimulations of renin to inappropriately high levels compared with the immunological activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Potentiation of the pressor effect of angiotensin II by intraventricular infusion of hypertonic saline.

The effect of selective NaCl loading to the brain on the blood pressure regulation was examined in male Wistar rats. Hypertonic NaCl (0.8M, 1 microL/h) was infused for 7 days into the lateral ventricle (ICV) along with intravenous (IV) infusion of angiotensin II (AII) at a dose of 5.4 pmol/kg per minute. Although neither ICV hypertonic NaCl or IV AII infusion alone had any substantial pressor effect, concomitant administration of these resulted in a consistent and significant increase in the blood pressure on day 7 over the baseline value, amounting to 29 +/- 5 mm Hg (n = 9; P less than 0.001). Inasmuch as the increase in the BP was totally prevented by intraperitoneal injection of guanethidine (40 mg/day), hyperactivity of the sympathetic nervous system appears, at least in part, responsible for the BP elevation caused by the combination of ICV hypertonic NaCl and IV subpressor AII infusion.

Angiotensin II↗
PubMed1988

Partial purification and properties of a plasma ouabain-like inhibitor of Na+, K+-ATPase in patients with essential hypertension.

Plasma levels of an ouabain-like inhibitor of Na+,K+-ATPase were higher in patients with essential hypertension compared with normal levels. The ouabain-like inhibitor was correlated significantly with blood pressure and was increased by a high-salt diet. The substance was partially purified by high performance liquid chromatography which revealed lipid-like properties, but the elution time was different from that of free unsaturated fatty acid on silica-gel high performance liquid chromatography. Its molecular weight was 600 or less, as estimated by high performance liquid chromatography with an HSG-15H column. The ouabain-like substance inhibited Na+, K+-ATPase in competition with KCl and showed positive ouabain-like immunoreactivity, whereas lysophosphatidylcholine was a non-competitive inhibitor. The ouabain-like substance was unstable at room temperature and decomposed to smaller molecular compounds which did not inhibit Na+, K+-ATPase. The inhibitory fraction gave a positive thiobarbituric acid reaction test. The mobility of the ouabain-like inhibitor on silica-gel thin-layer chromatography was different from that of prostaglandins and arachidonic acid. These results indicate that the plasma ouabain-like inhibitor of patients with essential hypertension is a lipid which is different from free fatty acid or lysophosphatidylcholine, and may be an unstable peroxide.

Cardenolides↗
PubMed1988

Interaction between the vascular renin-angiotensin system and prostaglandins.

The effects of nephrectomy, prostacyclin (PGI2), prostaglandin E2 (PGE2) and indomethacin on the vascular renin-angiotensin system were examined using isolated perfused mesenteric arteries. Angiotensin II (Ang II) released from the vasculature was measured using a Sep-Pak C18 cartridge which was placed in the perfusion system. After perfusion with drugs, the specific vascular renin activity inhibited by antirenin antibody was determined. Plasma renin activity was markedly decreased 48 h after nephrectomy, whereas vascular renin activity was increased. Released Ang II from mesenteric arteries of nephrectomized rats was not significantly different from that in control rats. Infusion of PGI2 (10(-6) mol/l) and PGE2 (10(-6) mol/l) for 1 h caused significant decreases in Ang II release (P less than 0.01 and P less than 0.05, respectively) and also decreased vascular renin activity. In contrast, infusion of indomethacin (10(-6) mol/l) for 1 h resulted in an increase (P less than 0.01) in vascular renin activity. These findings suggest that the vascular renin-angiotensin system exists independently of the circulating renin-angiotensin system. In contrast with their effects on renal renin, prostaglandins suppress the vascular renin-angiotensin system. The interaction between two vasoactive hormones in the vascular wall may be important for local regulation of vascular tone and regional blood flow.

Angiotensin II↗
PubMed1988

Vasoconstriction and hypersensitivity to vasoactive substances after acute volume expansion in dogs.

In a search for factors contributing to the sustained blood pressure (BP) elevation in acutely volume-loaded animals, dextran dissolved in lactated Ringer's solution (20 ml/kg) was infused into 34 mongrel dogs over a period of 1 hour under pentobarbital anesthesia and changes in hemodynamic and humoral variables were monitored during its infusion and for 3 hours after its infusion. BP elevation during volume loading (from 114 +/- 3 to 128 +/- 3 [SEM] mm Hg) was attributed to an increase in cardiac output. After volume loading, some dogs maintained BP elevation whereas others did not. The former group showed an increase in total peripheral resistance, demonstrating a transformation of cardiac output to total peripheral resistance as a responsible factor in maintenance of the elevated BP. The plasma levels of norepinephrine, vasopressin, and plasma renin activity were not elevated, indicating that these vasoactive factors were not responsible for elevation of the BP or total peripheral resistance. The changes in the hematocrit, atrial natriuretic factor, urine volume, and urinary sodium excretion were identical in the two groups, and natriuresis was not prominent when total peripheral resistance was high. Pressor responses to norepinephrine and angiotensin II were potentiated 3 hours after stopping infusion in both groups, but this potentiation was not correlated with the increase in total peripheral resistance or mean BP. Thus, acute volume expansion produced resistance-dependent hypertension following the initial volume-dependent hypertension. It is unlikely that a vascular sensitizing natriuretic factor plays a role in the resistance-dependent BP elevation. The mechanism and physiological importance of hypersensitivity to vasoactive substances remain to be elucidated.

Aldosterone↗
PubMed1988

Metabolic disposition of ethyl eicosapentaenoate and its metabolites in rats and dogs.

When orally administered to rats, 14C-labelled ethyl eicosapentaenoate (14C-EPA-E) was hydrolyzed and, in the lymph, incorporated mainly into triglycerides (TG) in chylomicrons. In plasma and other tissues, eicosapentaenoic acid (EPA) and its metabolites, such as docosapentaenoic acid (DPA) and docosahexaenoic acid (DHA), were detected in TG and phospholipid fractions. In plasma, EPA and its metabolites were found to be integrated into lipoproteins. Tissue distribution of these metabolites showed characteristic patterns from one tissue to another, as did their compositional distribution in lipids. EPA, DPA and DHA were found to be metabolized via beta-oxidation in in vitro experiments with mitochondrial fraction.

Acyl Coenzyme A↗
PubMed1988

Dose-effect relationship of carvedilol in essential hypertension. An open study.

This study was performed to find the optimal dose of carvedilol, in terms of efficacy and safety, in Japanese patients with mild to moderate essential hypertension. 134 patients with blood pressure greater than 160/95 mm Hg after a 4-week placebo run-in period were initially given carvedilol 5mg once daily. The dose was increased to 10 and 20mg at 4-weekly intervals if the target blood pressure was not achieved. The duration of treatment was 12 weeks. After 12 weeks' administration, the average blood pressure was significantly (p less than 0.001) reduced from 170/101 to 150/91 mm Hg. The hypotensive activity of carvedilol 5mg was mild, but sufficient hypotensive effect was observed in 65% of patients receiving up to 20 mg/day. No significant postural changes in blood pressure were observed. Although heart rate was significantly decreased (77 to 66 beats/min, p less than 0.001), no patient was judged to have bradycardia. Side effects occurred in 5.2% of patients. Carvedilol 10 to 20mg once daily is considered to be an effective and safe treatment for essential hypertension.

Adrenergic beta-Antagonists↗
PubMed1988

Postpartum toxic shock syndrome: a report of a case.

We describe a case of a 29-year-old Japanese woman with toxic shock syndrome which occurred 6 days after a normal vaginal delivery. This is the second case of postpartum toxic shock syndrome in Japan, so far as we know. Staphylococcus aureus was isolated from the uterine cavity. The isolate was coagulase type II and it produced both enterotoxin C and toxic shock syndrome toxin-1. The clinical course and laboratory data for this patient were in conformance with previously reported typical postpartum toxic shock syndrome, except for the onset time after delivery, because the previously reported postpartum TSS cases were clearly divided into two groups, early onset within 3 days of delivery and late onset 2 or more weeks after delivery.

Adult↗
PubMed1988

Plasma levels and renal clearance of two isomers of dopamine sulfate in patients with essential hypertension.

Two isomers of dopamine sulfate, dopamine 3-O-sulfate(3-O-S) and dopamine 4-O-sulfate(4-O-S), in the plasma and urine of patients with essential hypertension and normotensive controls were measured by HPLC-fluorometry. The plasma level of 3-O-S was significantly higher in patients with essential hypertension than in normotensive controls (20.9 +/- 2.2 pmol/ml and 16.3 +/- 1.4 pmol/ml respectively, p less than 0.05) and the plasma levels of 4-O-S were slightly increased in hypertensive patients. The plasma level of 3-O-S was correlated with the serum level of creatinine in both normotensives and hypertensives. In hypertensives, the plasma level of 3-O-S was also correlated with that of noradrenaline. However the creatinine clearances were similar in the two groups, the urinary clearance of 3-O-S was slightly lower in patients with essential hypertension than in normotensive controls. These data indicate that the plasma level of 3-O-S is elevated in essential hypertension because of the abnormality in dopaminergic metabolism and renal disturbance in its excretion.

Creatinine↗
PubMed1988

Changes in the plasma hANP level during long-term salt loading in patient with essential hypertension.

Serial changes in the plasma hANP (human atrial natriuretic peptide) level in patients with essential hypertension were determined during high salt intake for two weeks after salt restriction for 5 days. The mean plasma hANP level decreased during salt depletion for 5 days from 60 +/- 10 pg/ml to 39 +/- 8 pg/ml. During high salt intake (20 g NaCl/day) for two weeks, the plasma hANP level increased gradually to a maximum of 71 +/- 16 pg/ml on day 7 and then decreased to 54 +/- 9 pg/ml on day 14. The plasma levels of renin activity, aldosterone and noradrenaline decreased during salt repletion. Changes in the plasma hANP level were correlated positively with those of urinary sodium excretion and negatively with those of plasma renin activity on days 7 and 14 of salt repletion. Change in the plasma hANP level correlated with that in the mean blood pressure on day 14, but not day 7 of salt repletion. These findings indicate that the plasma hANP level is closely related to sodium intake in patients with essential hypertension.

Aged↗
PubMed1988

Central sodium loading modifies norepinephrine content in the ventrolateral medulla and blood pressure in rats.

We evaluated the effects of intracerebroventricular (ICV) infusion of hypertonic NaCl on blood pressure (BP) control as well as on NE content in the ventrolateral medulla (VLM). Nine groups of Wistar rats received 10 day's ICV infusion of NaCl solutions containing either norepinephrine (NE, 1.3 micrograms/min) or a synthetic NE precursor, 1-threo-3,4-dihydroxyphenylserine (1-DOPS, 17 micrograms/min) for 3 concentrations (0.15M, 0.8M or 1.5M) of NaCl. On day 9, only the group on ICV infusion of 1.5M NaCl alone had a significant rise in BP (133 +/- 3 mmHg, P less than 0.05 vs control) while other groups remained normotensive. The ICV infusion of 1.5M NaCl reduced NE content, determined by a microdialysis method, in the VLM while the concomitant ICV infusion of NE or 1-DOPS restored it suggesting that the decrease in NE content in the VLM may be a contributing factor in the BP elevation by the central salt loading.

Animals↗