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Biomedical subjects

T Ogihara

Publications and source records attributed to T Ogihara.

At least 649 records · Page 36Linked to original sources
PubMed1991

Adverse reactions to lipiodol ultra fluid: report of an accidental case.

A 25-year-old Japanese woman experienced pulmonary edema, shock, encephalopathy and silent pancreatitis after hysterosalpingography using lipiodol ultra fluid, because the contrast media flowed directly into the blood stream from endometrium injured by several curettages for termination of pregnancy. Total iodine concentrations in plasma and urine decreased exponentially and their half-life was 16.12 and 13.04 days, respectively. Clear correlations were observed between the iodine concentration in plasma and the amelioration of both electroencephalogram and neuropsychic abnormalities. Adverse reactions of oil-soluble contrast media are also discussed.

Adult↗
PubMed1991

Vitamin E and the peroxidizability of erythrocyte membranes in neonates.

We showed the increased susceptibility of neonatal biomembranes to oxidation by a kinetic analysis using an azo compound as a free-radical initiator and red blood cell (RBC) ghosts as a model membrane. When the RBC ghosts were oxidized, oxygen consumption was suppressed during the induction period in which membrane tocopherol was consumed at a constant rate, while increased oxygen uptake was observed after the tocopherol was exhausted. The total tocopherol content was similar in cord, maternal, and adult RBC ghosts, and there were no differences in the induction period (tinh) among the three types of ghosts. While the oxygen uptake rate during the induction period (Rinh) was similar in cord and adult ghosts, the rate in the subsequent phase (Rp) was considerably faster in the cord ghosts. Fatty acid analysis in the membrane lipids showed that the active bisallylic hydrogen (active H) content was greater in cord ghosts than in adult ghosts. The active H content closely correlated with the Rp, but did not with the Rinh. The kinetic chain length (KCL), i.e., the ratio of the rate of propagation to that of initiation, was calculated from Rp and tocopherol consumption rate and KCL values were higher in cord ghosts than in adult ghosts. The faster Rp and the higher KCL of the cord ghosts were attributable to a greater active H content rather than to the tocopherol content.

Adult↗
PubMed1991

[Presence of circulating suppressive factor for muscarinic acetylcholine receptor in senile dementia].

Alzheimer's disease is one of the main causes of senile dementia. Although its pathogenesis is not clear, some evidence has revealed that the activity of acetylcholine receptor in the brains of these patients is decreased. In the present study, possible circulating factors, affecting the muscarinic acetylcholine receptor of the synaptic vesicle from the rat brain, were evaluated in the serum of 95 senile subjects (34 males and 61 females, mean +/- SD age of 77.5 +/- 8.6 years). The cognitive function of these subjects was assessed by their Mini-Mental State scores, and they subjects were divided into non-dementic-subjects with a score of 21 or more, or subjects with dementia with a score of 20 or less. The latter were further divided into senile dementia with Alzheimer type (SDAT) and vascular type dementia (VS) using Hatchinski's ischemic score. The mean suppression rate by the serum from the SDAT patients on the binding of tritiated quinuclidinyl benzilate (3H-QNB), an antagonist for muscarinic acetylcholine receptor, to the rat synaptic membrane, was 18.1 +/- 7.2% of the control value, which was significantly greater than that of the non-dementic subjects, (4.7 +/- 3.8%). However, that in the VD group (8.4 +/- 6.8%), was not significantly different from the control value. Moreover the suppression rate of the serum on 3H-QNB binding showed significant positive correlated with score for the Mini-Mental State (r = 0.480, p less than 0.01) in the SDAT group. These data support the hypothesis that circulating suppression factors may participate in the pathogenesis of SDAT.

Aged↗
PubMed1991

Initial appearance of an ill-defined shadow on a chest roentgenogram in a patient with aortitis syndrome.

A 20-years-old woman with fever and an abnormal shadow on a chest roentgenogram was admitted to our hospital. High grade fever continued even after gradual disappearance of the ill-defined shadow on the right upper lobe (S3) with minor fissure deviation upward, while neck pain and bruit gradually developed. She was diagnosed as aortitis syndrome from a digital subtraction angiography. The initial appearance of an ill-defined shadow on a chest roentgenogram, considered as pulmonary infarction, is rare in the aortitis syndrome and this kind of onset is interesting in relation to the pathogenesis and diagnosis of this syndrome.

Angiography, Digital Subtraction↗
PubMed1991

Bradykinin suppresses endothelin-induced contraction of coronary artery through its B2-receptor on the endothelium.

Bradykinin (BK), a powerful vasodilating peptide, has been known to be one of the factors regulating vascular contractility mainly through its action on the endothelium. The effects of BK on vascular contraction induced by endothelin-1 (ET-1), a potent vasoconstrictor peptide produced in endothelium, were investigated in vitro using the canine coronary ringed artery. ET-1 at concentrations of 10(-10) to 10(-7) M induced strong and persistent contraction dose-dependently. The ET-1-induced contraction was inhibited by BK at concentrations of 10(-7) and 10(-6) M only in the presence of endothelium. A B1-receptor agonist (des-Arg9-BK) and a B1-receptor antagonist (des-Arg9-[Leu8]-BK) did not affect these effects of BK, whereas a B2-receptor antagonist ([D-Arg0,Hyp3,Thi5,8,D-Phe7]-BK) inhibited the effect of BK on the ET-1-induced contraction. These results indicate that BK may be a potent counter-factor for the ET-1-induced coronary vasoconstriction through its B2-receptors on the endothelium.

Animals↗
PubMed1991

Clinical efficacy of carvedilol in severe hypertension.

In an open clinical study, the efficacy and safety of carvedilol was investigated in 26 severely hypertensive patients controlled inadequately on a diuretic [diastolic blood pressure (DBP) greater than 120 mm Hg at first visit and greater than 110 mm Hg following more than 1 week administration of a diuretic]. Following diuretic treatment all patients were initially administered 5 mg of carvedilol once daily. The dose was gradually increased to 10 mg and 20 mg until DBP was reduced below 100 mm Hg or until it was reduced by at least 10 mm Hg. Antihypertensive activity of carvedilol (5 mg) was sufficient in only three cases, but after 4 weeks (inpatients) or 8 weeks (outpatients) administration of carvedilol (10 mg or 20 mg), DBP/systolic blood pressure was significantly reduced from 176 +/- 6/117 +/- 3 to 145 +/- 3/94 +/- 2 mm Hg (p less than 0.001) in all patients. Overall, a sufficient antihypertensive effect was observed in 80% of the patients. Heart rate was significantly decreased from 76 +/- 2 to 67 +/- 2 beats/min, but no patient experienced bradycardia. Carvedilol was generally well tolerated. These findings suggest that 10-20 mg of carvedilol once daily, in combination with a diuretic, is an effective and safe treatment for patients with severe hypertension.

Adrenergic beta-Antagonists↗
PubMed1991

Importance of the sympathetic nervous system in blood pressure elevation by subpressor intraventricular NaCl and angiotensin II in the rat.

The present study was performed to examine the effect of chemical sympathectomy with guanethidine on the BP change and humoral factors in rats which received continuous and concomitant infusion of i.c.v. hypertonic NaCl with i.v. Ang II, both at subpressor doses for 7 days. Male rats were divided into 3 groups which received the following infusions using an osmotic minipump at a rate of 1 microliter/min: Group 1 (n = 11), 0.15 M NaCl i.c.v. and Ang II (5.4 pmol/kg/min) i.v.; Group 2 (n = 9), 0.8 M NaCl i.c.v. and Ang II i.v.; Group 3 (n = 5), 0.8 M NaCl i.c.v. and Ang II i.v. with daily i.p. injection of guanethidine (40 mg/kg). Significant increase in BP was observed only in Group 2 (from 103 +/- 3 mmHg to 132 +/- 5 mmHg on day 7, p less than 0.001). Addition of i.p. guanethidine to i.c.v. infusion of 0.8 M NaCl and the subpressor dose of Ang II completely prevented increase in the BP, suggesting that the presence of the intact sympathetic nervous system is necessary for the development of BP elevation in response to i.c.v. hypertonic NaCl plus i.v. Ang II. Thus, the sodium status in the central nervous system is important in the regulation of BP and is closely related to the activity of the sympathetic nervous system.

Angiotensin II↗
PubMed1991

Role of blood ethanol on gastric mucosal injury and gastric hemodynamics.

The present series of studies were performed to test the hypothesis that ethanol in the blood may play a role in the pathogenesis of gastric mucosal injury. Another hypothesis to be examined was that endothelin may be involved in ethanol-induced gastric mucosal injury. Elevated levels of blood ethanol induced by intraperitoneal infusion of ethanol increased vulnerability of the stomach to hydrochloric acid in a dose-dependent manner in rats. This may be due to impaired gastric mucosal hemodynamics and oxygenation as demonstrated by the results obtained by organ reflectance spectrophotometry (decreases in indices of mucosal hemoglobin contents and hemoglobin oxygen saturation). Ethanol infusion caused a dose-dependent increase in gastric vascular resistance in perfused rabbit stomach, which was accompanied by an increased production of endothelin-1. The results suggest that endothelin may be involved in the pathogenesis of ethanol-induced gastric mucosal injury.

Animals↗
PubMed1991

[Physiological and pathological aging and electrolyte metabolism].

The extracellular and intracellular concentrations of electrolyte were maintained by various systems including kidney and endocrine system. Although concentrations of electrolyte in the extracellular fluid were maintained in normal ranges in healthy elderly subjects, the reserve ability for the maintenance of electrolyte balance decreases with physiological aging. Occurrence of abnormality in electrolyte concentrations in extracellular fluid is thought to be related to pathological aging. The frequency of subjects with abnormal circulating concentrations of electrolytes, as well as abnormal rates of severe such abnormalities increase with age. Clinical characterization and differentiation of physiological and pathological aging are not always easy. On the other hand, the kidney is the central organ for maintenance of electrolyte homeostasis. Decrease in renal ability to retain electrolytes sometimes affect the features of disorders such as hypertension and osteoporosis of elderly subjects. Intravenous infusion of physiological saline at a dose of 20 ml/kg over 2 hr evoked excessive excretion of sodium, calcium and inorganic phosphate in the urine in hypertensive elderly patients and in some patients with senile osteoporosis. These subjects showed decreased levels of plasma renin activity and increased serum levels of parathyroid hormone and 1,25-dihydroxyvitamin D. These features indicate that abnormal renal metabolization of electrolytes involving abnormality of endocrine system may be a cause of, and modulate the clinical features of, some disorders of elderly subjects.

Aged↗
PubMed1991

[Intracellular calcium level, lipid peroxidation, and development of gastric mucosal injury in rat hemorrhagic shock].

Although acute gastric mucosal lesions (AGMLs) develop after the mucosal ischemia and reperfusion, precise intracellular mechanism for the development of AGMLs remains unclear. In the present paper, we investigated intracellular calcium level, lipid peroxidation, and gastric mucosal lesion in rat hemorrhagic shock model. We estimated intracellular calcium by measuring phosphorylase a activity in the gastric mucosa. The mucosal phosphorylase a increased during hemorrhagic shock, while it returned to be normal after the reinfusion of shed blood. Although mucosal lipid peroxide and area of AGMLs did not increase significantly during hemorrhagic shock, they increased significantly after the reinfusion. Diltiazem, a calcium antagonist, prohibited both of the increase in mucosal phosphorylase a activity during hemorrhagic shock and the increase in lipid peroxide content and area of AGMLs after the reinfusion of the shed blood. Organ reflectance spectrophotometry revealed that the gastric corpus suffered mucosal ischemia and hypoxia during the hemorrhagic shock. The are of AGMLs had a good correlation with a level of lipid peroxidation in the gastric mucosa. These results suggest 1) that intracellular free calcium in gastric mucosa increases during the mucosal ischemia; 2) that a calcium antagonist prohibits the increased intracellular free calcium during mucosal ischemia; and 3) that a calcium antagonist prohibits the increased mucosal lipid peroxide and the development of AGMLs after the mucosal reperfusion. Thus it is concluded that the increased intracellular free calcium during ischemia plays a key role in the mucosal tissue injury in the ischemia-reperfusion state.

Animals↗
PubMed1990

[Case report of a patient with pseudohypoparathyroidism associated with slight increase in serum level of unconjugated bilirubin].

We treated a 29-year-old male patient with pseudohypoparathyroidism type I, who showed a slight increase in serum indirect bilirubin without any signs of liver dysfunction. Serum levels of total, direct and indirect bilirubins were 2.4, 0.7 and 1.7mg/dl, respectively (normal ranges: 0.2-0.8, 0-0.2 and 0.2-0.6mg/dl, respectively). The cause of the increases in serum bilirubin levels was not clear; however, hemolytic anemia, hereditary unconjugated hyperbilirubinemia or ineffective erythropoiesis were ruled out as causes for the increase, since 1) his serum level of haptoglobin was normal, 2) increase in serum level of indirect bilirubin 120 minutes after the infusion of 50mg nicotinic acid was within the normal range, and 3) severe anemia was not observed. Osmotic fragility of his circulating red blood cells was also within normal range. Three other patients with pseudohypoparathyroidism visiting our clinic also showed slightly high levels of serum indirect bilirubin, although four outpatients with idiopathic hypoparathyroidism showed no such abnormality. Abnormality in the responsiveness to parathyroid hormone and/or to that in the cyclic AMP productivity in this disease may cause the increase in the circulating unconjugated bilirubin.

Adult↗
PubMed1990

Role of protein kinase C in the regulation of glucagon gene expression by arginine.

The cellular mechanism of glucagon gene expression in intact rat islets and their synthesis and release of glucagon were investigated. Arginine significantly increased the amounts of preproglucagon mRNA and glucagon in the islets and glucagon release. H-7, a specific inhibitor of protein kinase C (PKC), significantly inhibited these effects of arginine. However, H-8, a potent inhibitor of cyclic nucleotide-dependent protein kinases, did not affect the arginine-induced biosynthesis of glucagon or glucagon release. These results suggest that the regulation of glucagon gene expression by arginine is mediated by PKC, not by cyclic nucleotide-dependent protein kinases.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Evidence for endothelin-1 release from resistance vessels of rats in response to hypoxia.

To elucidate further the contribution of endothelin into endothelium-dependent vasoconstriction evoked by hypoxia, we observed endothelin release during hypoxia. Endothelin was detectable in perfusate from mesenteric artery. Immunoreactive endothelin was confirmed as endothelin-1 by a reverse phase-HPLC. Endothelin release increased 4.1 +/- 1.3 to 12.4 +/- 2.0 pg/30 min without changing perfusion pressure. Thirty minutes of hypoxia stimulated endothelin release by 71 +/- 11% (P less than 0.05) and was associated with an elevation of perfusion pressure. These results suggest that endothelin contributes to endothelium-dependent vasoconstriction by hypoxia in mesenteric artery and may play an important role in the local peripheral vascular tone.

Animals↗
PubMed1990

Participation of both intracellular free Ca2+ and protein kinase C in tonic vasoconstriction induced by prostaglandin F2 alpha.

The roles of intracellular free Ca2+ and protein kinase C in the tonic contraction induced by prostaglandin were studied. Prostaglandin F2 alpha induced tonic contraction of rat thoracic aorta in both control and Ca2(+)-free solution. Close correlations were observed between the contractile response of aortic strips and the changes in intracellular free Ca2+ concentration in vascular smooth muscle cells assessed with the fluorescent Ca2+ indicator fura 2, both in control and Ca2(+)-free solutions. Prostaglandin F2 alpha also enhanced the production of inositol 1,4,5-trisphosphate in vascular smooth muscle cells before the rise of the intracellular free Ca2+ concentration. Moreover, 1-(5-isoquinoline-sulfonyl)-2-methylpiperazine, an inhibitor of protein kinase C, inhibited the tonic contractions induced by PGF2 alpha and 12-O-tetradecanoyl phorbol-13-acetate, a direct activator of protein kinase C, at similar concentrations. These results suggest that both intracellular free Ca2+ and protein kinase C participate in prostaglandin F2 alpha-induced tonic contraction.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗