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Biomedical subjects

A Otsuka

Publications and source records attributed to A Otsuka.

At least 73 records · Page 4Linked to original sources
PubMed1989

Synergism of intraventricular NaCl infusion and subpressor angiotensins in rats.

The effect of selective salt infusion to the central nervous system on the blood pressure (BP) regulation was examined in male Wistar rats. Hypertonic NaCl (0.8 M, 1 microliter/h) was infused into the lateral ventricle concomitantly with intravenous infusion of a subpressor dose (5.4 pmol.kg-1.min-1) of angiotensin II (ANG II) or its analogues for 7 days using osmotic minipumps. The BP was not increased by intracerebroventricular infusion of NaCl alone at this dose but was significantly and consistently increased by concomitant intravenous infusion of ANG II or its analogues. The increases in the BP over the base-line values on day 7 in groups on infusions of ANG II, ANG III, and pentasarcosyl-ANG II [(Sar)5ANG II] were 29 +/- 5 mmHg (n = 9, P less than 0.05), 8 +/- 2 mmHg (n = 8, P less than 0.05), and 19 +/- 3 mmHg (n = 6, P less than 0.05), respectively. The responses to hexamethonium, prazosin, and antagonists of arginine vasopressin and ANG II were examined in separate sets of conscious and unrestrained animals that had received intracerebroventricular infusion of NaCl and intravenous infusion of ANG II for the preceding 6 days. These animals showed significantly greater depressor responses only to hexamethonium and prazosin than control. These results indicate that the pressor effect of continuous and concomitant administration of intracerebroventricular NaCl and intravenous ANG II is mainly due to activation of the sympathetic nerve function. Synergism of the effects of selective central sodium administration and a subpressor dose of ANG II in the central nervous system is suggested.

Angiotensins↗
PubMed1989

Contribution of the baroreflex afferent nerves to the production of vasoconstricted hypertension in volume-expanded dogs.

Dextran in lactated Ringer's solution (20 ml/kg) was infused for 1 hour into anesthetized dogs with sinoaortic denervation and vagotomy (deafferentation; n = 10) and dogs treated with hexamethonium (de-efferentation; n = 13) to compare with our previous observation in dogs with an intact autonomic nervous system (control, n = 34). During the infusion, increase in blood pressure associated with increase in cardiac output was observed in all three groups. The increases in blood pressure were larger in the two groups with an impaired autonomic nervous system. In the recovery period, the control dogs and the hexamethonium-treated dogs showed gradual increases in total peripheral resistance and in vasoconstricted hypertension 3 hours after stopping the infusion. In contrast, the dogs with sinoaortic denervation and vagotomy did not show any increase in total peripheral resistance. The vasoconstricted groups showed peaks of natriuresis soon after the infusion, not 3 hours after the infusion when vasoconstriction was observed, although the dogs with deafferentation did not show a significant increase in natriuresis. Norepinephrine (0.5 micrograms/kg) was administered intravenously before and after volume expansion, and the pressor responses in the three groups after volume expansion were enhanced similarly (143%, 128%, and 136%, respectively). These results indicate that the afferent signals from peripheral vessels to the brain contribute to the production of vasoconstricted hypertension after acute volume expansion and that the vasoconstriction is independent of pressor hypersensitivity and is dissociated in time from the natriuresis.

Afferent Pathways↗
PubMed1989

Changes in plasma renin activity and aldosterone concentration in response to endothelin injection in dogs.

The effects of endothelin on the renin-aldosterone system were examined by injecting it intravenously at low (40 pmol/kg) and high (400 pmol/kg) doses into pentobarbital-anesthetized dogs. Plasma renin activity and aldosterone concentration together with hemodynamic parameters were measured before and 60 min after endothelin injection. The lower dose of endothelin induced no significant increase in mean blood pressure or total peripheral resistance. It caused a slight decrease of plasma renin activity from 10.3 +/- 1.6 to 5.9 +/- 1.3 micrograms.l-1.h-1 (p less than 0.1) and a decrease of aldosterone concentration from 364 +/- 68 to 231 +/- 58 ng/l (p less than 0.05) with an increase in total peripheral resistance (p less than 0.05), but it did not cause any clear change in the plasma renin activity or aldosterone concentration. Thus, endothelin increases the blood pressure mainly by vasoconstriction. The finding of a slight decrease in the plasma renin activity after the lower dose of endothelin, together with our previous finding that endothelin inhibits renin release from isolated rat glomeruli, suggests that endothelin inhibits renin release in vivo. With the higher dose of endothelin, stimulation of renin release secondary to renal vasoconstriction might have counteracted the direct inhibitory action of endothelin. The decrease in aldosterone concentration may have been due to the direct inhibitory action of endothelin on aldosterone release or it may be a secondary effect induced by suppression of plasma renin activity.

Aldosterone↗
PubMed1989

High plasma levels of cortisol in patients with senile dementia of the Alzheimer's type.

Plasma cortisol levels and other factors including thyroid hormone in patients with Alzheimer's type (n = 10), vascular type (n = 10) or mixed type (n = 10) senile dementia were compared with those in non-demented senile controls (n = 10). Plasma cortisol levels at 8:00 a.m. in Alzheimer's type dementia and mixed type dementia were 17.3 +/- 4.3 micrograms/dl (mean +/- SD) and 15.6 +/- 2.3 micrograms/dl, respectively. These values were significantly higher (p less than 0.005 and p less than 0.01) than those found in the control subjects (12.0 +/- 3.1 micrograms/dl). Plasma cortisol levels in vascular-type dementia (14.4 +/- 6.3 micrograms/dl) did not differ significantly from those in the controls. Plasma ACTH in senile dementia of the Alzheimer's type was lower, but not significant as compared with that in normal controls. In three subgroups of senile dementia and normal controls, plasma cortisol levels inversely correlated significantly with the degree of cognitive function. Plasma levels in TSH-thyroid system and blood pressure did not show any significant change in three types of senile dementia. These data suggest that senile dementia of the Alzheimer's type accompanies relatively and primarily high plasma cortisol levels and this may associate with cognitive dysfunction in Alzheimer's type senile dementia.

Adrenocorticotropic Hormone↗
PubMed1989

[Contribution of the spleen to the lipid metabolism in plasma and red cells. On hereditary spherocytosis and hereditary high red cell membrane phosphatidylcholine hemolytic anemia].

Clinical and experimental studies on hereditary spherocytosis (HS) and high red cell membrane phosphatidylcholine hemolytic anemia (HPCHA) were performed in relation to lipid metabolism in plasma and in red cells of these patients. In HS, red cell (RBC) membrane lipids (free cholesterol (FC) and phospholipids (PL) such as phosphatidylethanolamine, phosphatidylcholine (PC), sphingomyelin (SM) and lysophosphatidylcholine (LPC] were markedly decreased in unsplenectomized HS. Plasma lipids (total cholesterol, FC, HDL-cholesterol, PL) were also decreased in these patients. After splenectomy, substantial normalization of plasma and RBC lipids were observed. Concerning lipid kinetics, the extents of 14C-PC synthesis in RBC from 14C-LPC in medium and of 14C-PC exchange between RBC and the medium were almost identical to those in normal control in the in vitro incubation conditions. These observations indicate that the decreased RBC lipids may be induced by the shortage of lipid materials in plasma in the presence of the spleen. In unsplenectomized HPCHA, plasma lipids were also decreased same as in HS. In contrast, membrane lipids (FC and PC) were markedly increased. Even after splenectomy, increased PC contents were rather enhanced in their membranes concomitant to developing of hemolytic anemia, although plasma lipids were almost normalized. Thus RBC membrane lipids in HPCHA appeared not to be affected by plasma lipids. In experimental studies on HPCHA, 14C-PC synthesis from 14C-LPC and 14C-PC uptake in these RBC were increased, in spite that large amounts of PC were already accumulated in these RBC.(ABSTRACT TRUNCATED AT 250 WORDS)

Anemia, Hemolytic, Congenital↗
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

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

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↗
PubMed1987

Acute promyelocytic leukemia with an intracerebral mass and meningeal involvement after treatment of non-Hodgkin's lymphoma.

After a 3-month leukopenic phase, a patient developed hematologic pictures of acute promyelocytic leukemia (APL). Treatment with chemotherapy and radiotherapy had been given 10 months previously for a non-Hodgkin's lymphoma (NHL) of diffuse large cell type arising in the Waldeyer's ring. A computed tomographic scan demonstrated a high density mass in the left frontal cerebrum, which was enhanced uniformly by the contrast material. Cytocentrifuge examination of cerebrospinal fluid also showed an excess of promyelocytes. From these observations, the mass was considered to be an infiltration of leukemic cells. The intracerebral mass and meningeal involvement were resolved concomitantly with a hematologic remission of APL after intrathecal injection of cytosine arabinoside and systemic combination chemotherapy. This is a particular case of APL previously undescribed, representing an unusual presentation with intracerebral APL mass as well as a rare posttherapeutic APL following NHL.

Adult↗
PubMed1987

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↗
PubMed1986

Contribution of area postrema to pressor actions of angiotensin II in dog.

To generate quantitative data on the contribution of the area postrema (AP) to the pressor activity of angiotensin II (ANG II), the peptide (7 ng X kg-1 X min-1) was infused intravenously in 10 conscious dogs for 6 h before, and several weeks after, AP lesion. Mean arterial pressure (MAP) and heart rate (HR) were recorded continuously, and plasma renin activity (PRA), ANG II immunoreactivity (ANG II-IR), aldosterone (ALDO), arginine vasopressin (AVP), norepinephrine (NE), epinephrine (EPI), and serum Na+ and K+ were measured at 3 and 6 h. Three hours into the infusion, MAP averaged 123 +/- 2 compared with 96 +/- 2 mmHg for controls (P less than 0.01). The increases in pressure were associated with unchanged HR, but increased lability of MAP and HR. PRA fell, whereas plasma levels of ANG II-IR and ALDO rose. Plasma levels of AVP, NE, serum Na+ and K+ did not change, but plasma EPI was significantly elevated at 6 h. Removal of the AP produced mild hypotension and decreased lability. Within 8 to 21 days after AP ablation, a significant decrease in the plateau phase (3-6 h) of the ANG II pressor response was recorded in all dogs. The attenuation of the pressor effects was not sustained, since 4-7 wk after AP lesion, the increases in pressure were equivalent to those obtained during the control period. These data indicate that the AP participates in the production of the pressor response to intravenous infusion of ANG II in conscious dogs. However, in the absence of this structure, alternative mechanisms are brought into play to restore the loss of its function.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1986

The polymorphism linked to the human insulin gene: its lack of association with either IDDM or NIDDM in Japanese.

Polymorphism of 5' portion of the human insulin gene was examined in 188 unrelated Japanese subjects (49 normal, 71 with IDDM, and 68 with NIDDM) using restriction endonuclease analysis. Restriction fragments were classified according to the insertion size: Class 1 (600 base pairs), Class 2 (1300 base pairs), and Class 3 (2000 base pairs). We found a very high frequency of Class 1 alleles (96.8%) and a low frequency of both Class 2 (0.8%) and Class 3 alleles (2.4%) and that approximately 94% of the genotypes were Class 1/Class 1 homozygote. In addition, there was no correlation of allelic or genotypic frequency with NIDDM or IDDM. We conclude that length polymorphism of the human insulin gene cannot be a useful marker for diabetes in Japanese.

Diabetes Mellitus, Type 1↗
PubMed1986

[Clinical effect of prostaglandin F2 alpha on postoperative bowel movement in transurethral and transretroperitoneal urologic surgery].

The clinical effectiveness of prostaglandin F2 alpha (PGF2 alpha) injection on postoperative bowel movement was studied in 455 patients who underwent transurethral and transretroperitoneal operation. The patients were divided into two groups, 417 patients with PGF2 alpha injection and 38 without injection. 1,000 micrograms of PGF2 alpha were infused twice a day postoperatively until the onset of active flatus. The onset of flatus was recorded in each group. The onset of flatus after operation was 15 hours and 47 minutes for the injection group of 194 patients operated transurethrally, which was shorter than the 21 hours and 50 minutes for the uninjected group (p less than 0.01), but the onset of flatus was not significantly affected by the injection in the patients operated transretroperitoneally. Postoperative PGF2 alpha infusion facilitated flatus in the patients undergoing transretroperitoneal urologic surgery which took 1 and a half hours or more in doing so (p less than 0.05). Generally, postoperative paralytic ileus was milder after urological surgery than after bowel surgery, but PGF2 alpha injection was effective clinically both in transurethral surgery and transretroperitoneal surgery.

Adult↗
PubMed1985

Effects of 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (platelet activating factor) on cardiac function in perfused guinea-pig heart.

The direct cardiac action of 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (PAF) was studied in isolated perfused guinea-pig heart preparations. PAF produced a fall in left ventricular pressure, decreases in the rate of rise of the left ventricular pressure (dp/dt) and coronary flow, but had no effect on heart rate. These results indicate that PAF is a cardiodepressant with inotropic selectivity and this effect on heart is blocked by CV-3988, a specific PAF antagonist.

Animals↗
PubMed1985

Hypotensive mechanism of acetyl glyceryl ether phosphorylcholine (AGEPC) in dogs. Effects on hemodynamics and humoral factors.

One-O-hexadecyl-2-O-acetyl-sn-glycero-3-phosphorylcholine (AGEPC) was intravenously administered to anesthetized dogs to study the effects on hemodynamics and several endocrine factors. The effect of AGEPC on local blood flow was also studied by direct intra-arterial injection. Following intravenous injection, blood pressure and cardiac output decreased significantly (p less than 0.001). Changes in total peripheral resistance (TPR) and heart rate were biphasic. TPR increased significantly (p less than 0.01) after an initial slight reduction. Heart rate decreased significantly (p less than 0.01) with only a transient slight elevation. Femoral blood flow was increased (p less than 0.001) by intraarterial injection and decreased (p less than 0.05) by intravenous administration. Plasma norepinephrine (p less than 0.001), epinephrine (p less than 0.01), thromboxane B2 (p less than 0.001), 6-0-PGF1 alpha (p less than 0.01), aldosterone (p less than 0.001) and cortisol (p less than 0.001) were elevated, but plasma renin activity did not change. These results suggest that the hypotensive mechanism of AGEPC is due to both cardiosuppression and vasodilation. AGEPC increased plasma catecholamines, thromboxane A2, PGI2, aldosterone and cortisol which, in turn, may modify hemodynamics.

Aldosterone↗