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Biomedical subjects

M Ohtake

Publications and source records attributed to M Ohtake.

At least 37 records · Page 2Linked to original sources
PubMed1994

Enhanced hepatic portal blood flow induced by prostaglandin E1 following liver transplantation in pigs.

Portal venous blood flow (PVF), hepatic arterial blood flow (HAF), and systemic arterial pressure (SAP) were examined after prostaglandin E1 (PGE1) was injected into the vena cava superior (VCS) of liver-transplanted pigs. The injection of PGE1 at 0.2 micrograms/kg/min for 2 min on the day of transplantation and 3 days later produced an increase in PVF without causing any change in HAF or SAP, the response in PVF being dose-dependent. However, no reliable change in PVF, HAF, or SAP was seen when the same dose of PGE1 was administered 7 days after transplantation. Furthermore, no significant difference was noted among the values for PVF and total hepatic blood flow (THF) during the experimented days, although the HAF value had increased markedly 3 days after transplantation. These findings suggest that PGE1 is effective in increasing PVF in the liver transplanted condition; however, the hepatic circulatory improvement attributed to this agent would be limited to the first few days following transplantation.

Alprostadil↗
PubMed1994

Interaction of glucose signals between the nucleus of the vagus nerve and the portal vein area in the regulation of gastric motility in rats.

Intragastric pressures were examined after glucose injection into the nucleus of the vagus nerve (X) of the medulla oblongata or into the portal vein (PV) or both in bilaterally adrenalectomized rats. Ten mM glucose (500 nl) injected into the X or into the PV (25 microliters) decreased gastric pressure associated with insulin-hypoglycemia. Simultaneous injection of glucose into the X and PV produced a reduction in gastric pressure in an additive manner. In addition, a significant fall in gastric pressure was seen when an ineffective concentration of glucose was injected into the X and PV simultaneously. The results suggest that the X and PV signals interact with each other to inhibit gastric motility.

Adrenalectomy↗
PubMed1994

Efficacy of twice-daily cimetidine in pediatric peptic ulcer.

The clinical efficacy of twice-daily cimetidine (20 mg/kg/day) was retrospectively studied in 19 children with gastric ulcer (GU) and 23 with duodenal ulcer (DU) in the active stage. Endoscopically confirmed cumulative healing rates at 2, 4, and 8 weeks of treatment were 53.5, 73.7, and 94.7% in the GU group and 15.4, 50.0, and 87.0% in the DU group, respectively. There was no significant difference between the groups at each time point. The mean period of time until complete disappearance of symptoms in the GU and DU groups was 3.5 +/- 2.6 and 4.2 +/- 3.3 days, respectively (NS). With regard to symptoms, abdominal tenderness rather than spontaneous pain appeared to be a better indicator of ulcer healing. Ulcer recurrence was found endoscopically during follow-up in 2 of 13 GU patients (15.4%) and 11 of 19 DU patients (57.9%); thus, the cumulative recurrence rate of the DU group was higher than that of the GU group (p < 0.05). No adverse effects related to cimetidine were demonstrated during treatment or short-term follow-up. We conclude that twice-daily cimetidine at a dosage of 20 mg/kg/day is as effective for the symptomatic improvement and healing of peptic ulcer as the conventional three- or four-times-daily regimens. The optimal dosage of cimetidine requires further study.

Adolescent↗
PubMed1993

Hepatic glucose signals vagally modulate the cyclicity of gastric motility in rats.

The cyclicity and intensity of gastric motility were examined following glucose injection into the portal vein with an intragastric balloon in anesthetized rats. Enhanced gastric motility caused by insulin administration was influenced by 4 mM glucose (25 microliters) injected into the portal vein; glucose provoked a shift in the cyclicity power spectrum without any change in intensity. The peak power spectrum shifted from 4.0-5.0 cpm to 2.0-3.0 cpm. Hepatic branch vagotomy abolished the response. The results suggest that glucose signals in the hepatic vagal branch modulate the cyclicity of gastric motility.

Animals↗
PubMed1993

Orally administered prostaglandin E1 derivative can enhance liver regeneration in partially hepatectomized rats.

The effect of orally administered 17(S),20-dimethyl-6-oxo prostaglandin E1 (PGE1) methyl ester (OP) on liver regeneration was examined in 66% hepatectomized rats. Administration of OP increased the mitotic index of the hepatocyte 3 days after hepatectomy, and the mitotic index response due to OP was dose dependent. The OP administration had no effect on food intake, but reduced water intake. The serum scores relative to nutrition and hepatic function showed transient change after OP administration, whereas the serum blood urea nitrogen level indicated a slight renal dysfunction with OP. The fat store in the body was transiently reduced. These observations lead us to conclude that orally administered OP is capable of stimulating liver regeneration without serious systemic effects.

Administration, Oral↗
PubMed1993

A pharmacological analysis of prostaglandin E1 on portal blood flow after partial hepatectomy in rats.

Portal venous flow (PVF) and portal venous pressure (PVP) were examined after the jugular or portal injection of Prostaglandin E1 (PGE) in rats partially hepatectomized by either 40% or 66%. In the 66% hepatectomized animals, the jugular injection of PGE at 5.0 micrograms/kg/min produced an increase in PVF concomitant with a fall in systemic arterial pressure (SAP), while PVP remained unchanged. The portal injection of PGE at 0.5 micrograms/kg/min increased PVF to a level equivalent to that evoked by the jugular injection of 5.0 micrograms/kg/min PGE, without any change in SAP. PVP was reduced synchronistically with an increase in PVF. The PVF response to a portal injection of PGE at 0.5 micrograms/kg/min was not reproduced in liver intact rats. These results suggest that PGE is potent in increasing PVF in the partially resected condition of the liver and that the portal vascular bed is involved in this response.

Alprostadil↗
PubMed1993

Enhanced liver regeneration in rats treated with 15-deoxyspergualin alone and in combination with FK 506.

The effects of 15-deoxyspergualin (DSG) alone and in combination with FK 506 (FK) on liver regeneration after 2/3 hepatectomy was studied. The administration of 5 mg/kg DSG increased the liver weight as a percentage of the body weight (RLW) in the 5 days following the hepatectomy. This enhanced regeneration was not affected if interleukin(IL)-2 was also given. The combination of 1 mg/kg DSG and 0.05 mg/kg FK induced the highest values for RLW. The amounts of food and water intake increased in the DSG and FK combined group. Blood chemistry indicated that the combined administration of DSG and FK could reduce side-effects more effectively than separate administration. These observation led us to conclude that DSG has a stimulating potency in liver regeneration by means of direct suppression of T cell activation, and there is a synergistic effect on regeneration by DSG and FK.

Animals↗
PubMed1993

Hepatic branch vagotomy can suppress liver regeneration in partially hepatectomized rats.

The role of the vagus nerve in liver regeneration after partial hepatectomy was studied by comparing the effects of hepatic branch vagotomy with those of hepatic branch sympathectomy in rats. The liver weight as a percentage of body weight decreased significantly 7 days after vagotomy compared with the controls and this was associated with a reduction in food intake. There was no difference in the liver weights between the control rats and the pair-fed vagotomized rats. Hepatic sympathectomy had no significant effect on the liver weight. The serum scores indicating hepatic function showed no difference between the control and the vagotomized rats except alkaline phosphatase. The concentration of insulin was unchanged. The number of mitotic hepatocytes remained high at 7 days after vagotomy. These observations led us to conclude that the vagus nerve stimulates liver regeneration, and its effect depends on vagal factors directly and specifically.

Alanine Transaminase↗
PubMed1993

Changes in zinc and copper concentrations in breast milk and blood of Japanese women during lactation.

To evaluate the changes in zinc and copper concentrations in breast milk and maternal blood during lactation, milk and blood samples were obtained from 80 lactating women during the period between 2 and 201 days of lactation. Zinc and copper concentrations were measured by atomic absorption spectrophotometry. Breast milk zinc and copper concentrations markedly decreased during the first few weeks of lactation and gradually declined for the remaining period. Mean values of milk zinc and copper levels were 1.76 and 0.29 micrograms/ml, respectively, between 15 and 84 days after parturition and were 0.76 and 0.19 microgram/ml between 85 and 201 days of lactation. Calculated daily intakes of these minerals for infants from breast milk were markedly lower than those of US Recommended Dietary Allowances. Plasma zinc levels of lactating mothers increased as lactation progressed, whereas erythrocyte zinc and plasma copper concentrations decreased. Plasma zinc and copper and erythrocyte zinc values returned to normal approximately three months after parturition.

Adult↗
PubMed1992

Enhanced gastric acid secretion induced by gastrin can be suppressed partially by glucose injection into the medullary nuclei in rats.

Gastric acid outputs after glucose injection into the nucleus of the vagus nerve (X) or into the nucleus of the tractus solitarius (SOL) were examined in rats with tetragastrin. The enhanced acid output caused by gastrin was partially inhibited by glucose injection into the X or SOL. Glucose injection into the X depressed acid output in a dose-dependent fashion, but a non-dose-dependent response in acid output was seen when glucose was injected into the SOL. There was no interaction between the X and SOL in acid response due to glucose. These findings suggest that glucose modulates gastric acid secretion stimulated by gastrin at the medullary level, and that such a modulation is characterized by the medullary X or SOL, separately.

Animals↗
PubMed1992

The role of the abdominal sympathetic nervous system in regulating portal venous flow and its functional distribution.

The role of the abdominal sympathetic nervous system in regulating portal venous flow (PVF) was examined in anesthetized rats using an ultrasonic volume flowmeter. Electrical stimulation of the hepatic sympathetic branch, given at 10 Hz, 1 ms, 10 s and 12 V, caused approximately a 28 percent reduction in PVF, which was equivalent to that produced by occlusion of the bilateral carotid arteries for 30 s, without causing any change in the systemic arterial pressure. Stimulation of the major splanchnic nerve decreased PVF, the response being greater by stimulation of the right nerve than by stimulation of the left (p less than 0.05). Bilateral adrenalectomy shortened the recovery time without changing the magnitude or lateral predominancy. Neither proper hepatic arterial occlusion nor partial hepatectomy affected the response. In the partially hepatectomized animals, stimulation of the hepatic branch did not decrease the splenic flow but decreased the superior mesenteric venous flow (SMVF) and induced a similar response in PVF even when the SMVF was interrupted. An intraportal injection of noradrenaline decreased PVF dose-dependently. These findings indicate that the sympathetic nerve regulates PVF directly, and that there is functional laterality of the regulatory mechanism in the abdominal cavity, which suggests that adrenal factors work together with the nerve that supplies the portal vein.

Adrenalectomy↗
PubMed1991

Secretion of gastric acid inhibited by oxytocin injected into the hypothalamic paraventricular nucleus in the rat.

Gastric acid output was examined following oxytocin injection into the hypothalamic paraventricular nucleus (PVN) or into the vagus nucleus (X) of the medulla in rats with insulin-hypoglycemia. Gastric acid output was reduced following the injection of nanomolar quantities of oxytocin into these nuclei, and the response was dose-dependent. It was also noted that there was a synergistic action on the response by the peptide between PVN and X. The acid response was blocked by section of the vagus nerve at the subdiaphragmatic level or by prior administration of atropine sulfate. These observations suggest that oxytocin in the PVN is active in suppressing gastric acid secretion, and the vagal response is characteristic of activation of the PVN and X.

Animals↗
PubMed1990

Gastrin-17 injected into the hypothalamic paraventricular nucleus can induce gastric acid secretion in rats.

Injections of picomolar quantities of gastrin-17 into the hypothalamic paraventricular nucleus increased gastric acid output in anesthetized rats. The response was dose-dependent, and it was blocked by atropin and by vagotomy. The same doses, injected intravenously, intraventriculary or into sites far from the nucleus, did not increase the output. Cholecystokinin-8 injected into the nucleus had no effect on the acid output.

Animals↗
PubMed1990

Activation of quiescent ovaries by administration of PMSG after LH-RH analogue treatment in heifers.

The effect of pregnant mare serum gonadotrophin (PMSG) treatment on activation of quiescent ovaries was examined in heifers. Groups of thirteen, twenty and twelve heifers which showed ovulation within 2 d and corpus luteum (CL) development after injection with a luteinizing hormone releasing hormone analogue (LH-RH-A) were supplementally injected with 500 IU of PMSG (Group I); 500 IU of PMSG and 500 mug of Prostaglandin F(2alpha) analogue (PGF(2alpha)-A; Group II); and 500 mug of PGF(2alpha)-A (Group III) on Day 6 after the injection of 200 mug of LH-RH-A (Day 0), respectively. Estrus appeared in 33.3 to 45.0% of the heifers of the respective groups after the treatment. Ovulation occurred at a significantly (P<0.01) higher rate in Groups I (100%) and II (90.0%) than in Group III (41.7%). The ovarian cyclic activity was initiated in all the heifers that ovulated. Plasma progesterone levels decreased significantly (P<0.05) to about 1 ng/ml on Day 8 and Day 7 in Group I and Groups II and III, respectively. Plasma estradiol-17beta (E(z)) levels increased significantly (P<0.05), reaching a peak on Days 7 to 7.5 in Groups I and II but not in Group III. It is concluded that PMSG treatment stimulates maturation and E(z) secretion of a follicle, thus promoting ovulation and the onset of ovarian cyclic activity.

Journal Article↗
PubMed1987

Inhibition of gastric acid secretion evoked by activation of the hypothalamic paraventricular nucleus.

Electrical stimulation of the paraventricular nucleus depressed the gastric acid output of adrenalectomized male rats of which gastric acid output had been induced by insulin hypoglycemia. Electrical stimulation of the pituitary stalk produced a similar secretory response, but the response was abolished by bilateral lesion of the paraventricular nucleus. These findings allow us to speculate that the paraventricular nucleus is capable of modulating gastric acid secretion, and suggest that the nucleus has a neural connection between the neurohypophysis and the system relevant to gastric acid secretion.

Adrenalectomy↗
PubMed1987

Alterations in gastric acid secretion following hepatic vagotomy at a stage of development in rats.

The relation of gastric acid secretion to the hepatic vagal section was examined in consideration of developmental stages of a rat. Acid outputs in rats deprived of food for 22 hr before the experiment were estimated with or without insulin. The animals were classified into five groups according to their body weights at the experiments (50, 100, 200, 300 and 400 g). Hepatic vagotomy was effective in decreasing acid output in all of the groups treated with food deprivation and insulin, and it was found that there was a close relationship between the output and glucose concentration in the portal blood. In rats treated only with food deprivation, hepatic vagotomy produced different effects for the five groups; the vagotomy failed to cause acid response when the rats weighed about 300 and 400 g, while in the animals weighing about 50, 100 and 200 g acid outputs were reduced following the vagotomy. It was noted that the sensitivity to hypoglycemia in the acid output was greater in the young rats than the older ones. Results suggest that function of the hepatic vagal nerve may be prominent in modulating acid secretion in an earlier stage of development when the animals are most sensitive to hypoglycemia.

Aging↗
PubMed1986

Effect of long-term administration of anticonvulsants on copper, zinc, and ceruloplasmin levels.

Anticonvulsant therapy is known to be associated with elevated plasma copper and ceruloplasmin levels. To investigate the effect of long-term phenytoin and/or phenobarbital administration, plasma copper, zinc, and ceruloplasmin levels were measured in two groups of patients with developmental disorders who were either living at home (study 1) or institutionalized (study 2). Plasma copper and zinc levels were measured using an atomic absorption spectrophotometric method, and ceruloplasmin levels were determined using a method measuring oxidase activity (study 1) and an immunodiffusion plate method (study 2). In both studies, the mean plasma copper and ceruloplasmin levels of the anticonvulsant groups were significantly higher than those of control groups, while the mean plasma zinc levels for the anticonvulsant and control groups were similar. Possible change in the tissue zinc/copper ratio among the patients receiving long-term anticonvulsants is discussed.

Adolescent↗