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Biomedical subjects

F Takeda

Publications and source records attributed to F Takeda.

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

[Anticholinergic properties of oxitropium bromide (Ba 253) and its metabolites].

Anticholinergic properties of oxitropium bromide (Ba 253) were compared with those of atropine and ipratropium bromide (Sch 1000). The metabolites of Ba 253 (Ba 941, BEA 1125), the decomposition product (Ba 250), and the impurity (Ad 187) were also studied. In rat salivary activity, gastric secretion and rabbit gastric-motility, the anticholinergic activities of parenterally administered Ba 253 were 2.3 to 11.8 times and 1 to 2 times stronger than that of atropine and Sch 1000, respectively. The mydriatic and antisecretory actions of Ba 253 (p.o. or i.d.) were 1/7 and 1/47 those of atropine, respectively. In isolated rat stomach, guinea pig gallbladder and ileum, the anticholinergic activity of Ba 253 is similar to that of atropine. Inhalation of Ba 253 aerosol prevented ACh- and histamine-induced cough in guinea pigs, and its potency was 1/5 that of atropine or as the same as that of Sch 1000. In the isolated guinea pig trachea and ileum, the potencies of the anticholinergic activities of Ba 250 and Ad 187 were the same as that of Ba 253, but those of the other metabolites were very weak. These results suggest that the anticholinergic activity of Ba 253 is stronger than that of atropine when parenterally administered, and it cannot distinguish between the subtypes of muscarinic receptors.

Animals↗
PubMed1989

Roles of gastric acid secretion and motility in gastric mucosal lesion formation induced by water-immersion stress in rats.

The roles of gastric acid and motility in gastric mucosal lesion formation induced by water-immersion stress were studied pharmacologically in rats. Gastric acid secretion and motility increased markedly during water-immersion, and mucosal lesions were formed. Cimetidine inhibited the increase in gastric acid secretion, but papaverine inhibited the increases in both acid secretion and motility. Both agents prevented the formation of mucosal lesions. In acid perfused rats, the increase in motility and lesion formation induced by water-immersion stress were prevented by papaverine, but not by cimetidine. These results suggest that the increases in both acid secretion and motility play important roles in the formation of mucosal lesions induced by water-immersion stress in rats.

Animals↗
PubMed1989

Gastric mucosal protective action of endothelium-derived relaxing factor.

The change in the endothelial function by the application of 0.6 N HCl and the effects of endothelium-derived relaxing factor (EDRF) inhibitors and nitrites on HCl-induced lesions were studied to clarify the effect of EDRF on gastric lesions in rats. The EDRF-induced increase in the gastric mucosal hemodynamics induced by vagal stimulation or intra-arterial administration of acetylcholine was inhibited by the EDRF inhibitors or removal of endothelial cells. Topical application of 0.6 N HCl on the exposed gastric mucosa abolished the response of the mucosal hemodynamics to acetylcholine or vagal stimulation. Gastric lesions induced by 0.45 N HCl were enhanced by EDRF inhibitors or removal of endothelial cells from gastric submucosal arterioles.

Animals↗
PubMed1989

[Quality of life in cancer patients].

Quality of life has a broad meaning. It should be measured based on subjective comfort and discomfort of the patient in terms of physical, psychological, social and spiritual well-being. Care for physical and psychological problems from which cancer patients are suffering has been surprisingly inappropriate, and the quality of life issue has been almost always neglected in cancer treatment and care. However, in recent years, clear practical guidelines on cancer care were proposed, which can be used through the existing health care system and, when put into practice, will help cancer patients in the far-advanced stages spend the final days of their lives with comfort. To assess the quality of life, several effective instruments have been developed by outstanding experts for easy, repeated patient self administration, and usually involve a 20-50 item questionnaire that has been validated on cancer patients. Further discussion on quality of life of cancer patients in this country should include 'informed consent', 'truth-telling', and rearrangement/provision of hospital facilities to meet the needs of dying patients.

Family↗
PubMed1989

[Cancer pain management].

Pain, the most frequent subjective symptom in cancer patients, can and must be treated. Satisfactory pain relief helps whatever patients achieve their remaining potential. This transforms his experience and the memories of his family. Management of pain becomes the physician's primary objective if there is no available treatment for the cause of pain. The use of analgesic drugs is the mainstay in cancer pain management. When used correctly, analgesics are effective in a high percentage of cancer patients. This approach can be implemented in all medical settings and serves to improve quality of life in far-advanced cancer patients. A three-step analgesic ladder indicating the sequential use of the drugs was proposed by the World Health Organization (WHO) in 1986. The three standard analgesics making up this ladder are aspirin (non-opioid), codeine (weak opioid) and morphine (strong opioid). In patients with mild pain, non-opioid drugs such as aspirin, acetaminophen, or any of the non-steroidal anti-inflammatory drugs will be adequate. In patients with moderate pain, if non-opioids do not provide adequate relief, codeine or an alternative weak opioid should be prescribed. In patients with severe pain, morphine, a strong opioid, is the drug of choice. A series of principles established on the basis of considerable clinical experience and of controlled studies of analgesics indicate that the dose of an analgesic should be determined on an individual basis, and administered on a regular basis by the clock.

Analgesics↗
PubMed1988

Effect of subcutaneous injection of a long-acting analogue of somatostatin (SMS 201-995) on plasma thyroid-stimulating hormone in normal human subjects.

SMS 201-995 (SMS), a synthetic analogue of somatostatin (SRIF) has been shown to be effective in the treatment of the hypersecretion of hormones such as in acromegaly. However, little is known about the effects of SMS on the secretion of thyroid-stimulating hormone (TSH) in normal subjects. In this study, plasma TSH was determined with a highly sensitive immunoradiometric assay, in addition to the concentration of SMS in plasma and urine with a radioimmunoassay, following subcutaneous injection of 25, 50, 100 micrograms of SMS (4 subjects/dose) or a placebo (6 subjects) to normal male subjects, at 0900 h after an overnight fast. The plasma concentrations of SMS were dose-responsive and the peak levels were 1.61 +/- 0.09, 4.91 +/- 0.30 and 8.52 +/- 1.18 ng/ml, which were observed at 30, 15 and 45 min after the injection of 25, 50 and 100 micrograms of SMS, respectively. Mean plasma disappearance half-time of SMS was estimated to be 110 +/- 3 min. Plasma TSH was suppressed in a dose dependent manner and the suppression lasted for at least 8 hours. At 8 hours after the injection of 25, 50 and 100 micrograms of SMS, the plasma TSH levels were 43.8 +/- 19.4, 33.9 +/- 9.4 and 24.9 +/- 3.2%, respectively, of the basal values. The results suggest that SMS suppresses secretion of TSH from the normal thyrotrophs in man and thus also that attention should be paid to possible hypothyroidism during the long-term treatment of patients such as those with acromegaly with this potent analogue of SRIF.

Adult↗
PubMed1988

Role of endogenous arginine vasopressin in potentiating corticotropin-releasing hormone-stimulated corticotropin secretion in man.

Exogenously administered vasopressin (VP) augments ACTH secretion stimulated by CRH. This study was performed to elucidate the role of endogenous VP in potentiating CRH-induced ACTH secretion in man. Synthetic human CRH (100 micrograms) was injected iv into seven normal men after they had been water loaded (20 mL/kg; 60 and 30 min before CRH injection; WL-CRH test) and water deprived (water restriction for 18 h before CRH injection; WD-CRH test). Blood samples were obtained before and 5, 15, 30, 60, 90, and 120 min after CRH injection at 0900 h for determination of plasma ACTH, cortisol, arginine vasopressin (AVP), CRH, and catecholamine levels and osmolality. Urine was obtained immediately before and 120 min after CRH injection for determination of osmolality. The mean plasma AVP levels were significantly higher during the WD-CRH test [1.8 +/- 0.4 (+/- SE) to 1.9 +/- 0.4 pmol/L] than during the WL-CRH test (0.6 +/- 0.1 to 0.9 +/- 0.1 pmol/L). The mean plasma ACTH and cortisol levels rose significantly from basal (4.5 +/- 0.6 pmol/L and 320 +/- 20 nmol/L, respectively) to peak values of 14.0 +/- 2.1 pmol/L at 30 min and 700 +/- 50 nmol/L at 60 min, respectively, during the WD-CRH test. During the WL-CRH test, mean basal plasma ACTH and cortisol levels were 3.5 +/- 0.7 pmol/L and 420 +/- 50 nmol/L, respectively, and reached peak values of 7.7 +/- 1.1 pmol/L at 60 min and 550 +/- 40 nmol/L at 30 min, respectively. Both the mean peak levels and integrated ACTH and cortisol responses were significantly higher during the WD-CRH than during the WL-CRH test. There was no significant difference between the plasma CRH and catecholamine concentrations in both tests. These results suggest that endogenous AVP potentiates CRH-stimulated ACTH secretion and, thus, plays a physiologically significant role in regulating CRH-stimulated ACTH and cortisol secretion in man.

Adrenocorticotropic Hormone↗
PubMed1988

[General pharmacological studies on a bronchodilator, oxitropium bromide (Ba 253)].

The effects of oxitropium bromide (Ba 253) on respiratory, cardiovascular, digestive and urogenital systems were studied. Ba 253 increased heart rate in anesthetized cats at low doses (0.1-0.3 mg/kg, i.v.) and decreased blood pressure in dogs and cats at high dose (3 mg/kg, i.v.). Aerosol inhalation of a high concentration of Ba 253, however, did not influence the heart rate. Ba 253 enhanced the isoproterenol-induced inotropic action and vasodilation. Intestinal transport of mice were inhibited by Ba 253 (s.c.), but not inhibited by oral administration. Ba 253 (1-30 mg/kg, i.v.) enhanced the motility of rat uterus in vivo, but inhalation of the Ba 253 aerosol did not have any affect. Ba 253 had no effects on vasoconstriction, spontaneous motility of the ileum, bile secretion, urinary excretion and spontaneous motility of the urinary bladder. These results indicate that intravenous or subcutaneous administration of Ba 253 decreased blood pressure, enhanced uterus motility and inhibited intestinal transport, but the inhalation or oral administration, even at high doses, has no effects on the cardiovascular system and uterine motility.

Animals↗
PubMed1987

Endothelium-dependent increases in rat gastric mucosal hemodynamics induced by acetylcholine and vagal stimulation.

The role of vascular endothelial cells in the vagal control of hemodynamics was studied in rat gastric mucosa. Vagal stimulation and intra-arterial administration of acetylcholine and of papaverine increased hemoglobin (Hb) and oxygen saturation of hemoglobin (SO2) in the gastric mucosa. The increases induced by vagal stimulation were reduced but not abolished by atropine. The responses to acetylcholine and vagal stimulation were reduced by quinacrine, p-bromophenacyl bromide and nordihydroguaiaretic acid, while indomethacin had no effect. Intra-arterial infusion of collagenase removed the endothelial cells from submucosal vasculatures and depressed the increase in mucosal hemodynamics in response to acetylcholine and vagal stimulation. The response to papaverine was not depressed in rats treated with quinacrine or collagenase. These results suggest that the increase in gastric mucosal blood flow induced by acetylcholine or vagal stimulation is mediated by the endothelium-derived relaxing factor.

Acetylcholine↗
PubMed1987

Hormonal responses to insulin-induced hypoglycemia in man.

Insulin-induced hypoglycemia is a potent stress stimulating ACTH release, but the factors responsible for this ACTH secretion are not known. In this study, several ACTH-stimulating factors, such as CRH, arginine vasopressin (AVP), epinephrine (E), norepinephrine (NE), and dopamine, in addition to ACTH, cortisol, and glucose, were simultaneously measured in plasma before and 15, 30, 60, 90, and 120 min after iv administration of 0.1 U/kg BW regular insulin to seven normal subjects. Insulin administration resulted in significant rises in the mean plasma ACTH level from 4.6 +/- 1.1 (+/- SEM) to 21.6 +/- 4.8 pmol/L at 30 min (P less than 0.01) and in plasma cortisol from 330 +/- 60 to 720 +/- 50 nmol/L at 60 min (P less than 0.01). These increases were preceded by a 41.0 +/- 1.9% (P less than 0.001) fall in blood glucose levels. The mean plasma CRH level rose significantly from 1.0 +/- 0.1 to 1.2 +/- 0.1 pmol/L (P less than 0.01) at 30 min and remained elevated until 120 min. In addition, concomitant and significant rises in plasma AVP levels (basal, 1.5 +/- 0.01; peak, 4.5 +/- 1.1 pmol/L at 30 min; P less than 0.01), E (basal, less than 50; peak, 640 +/- 130 pmol/L at 30 min; P less than 0.01), and NE (basal, 0.07 +/- 0.01; peak, 0.17 +/- 0.03 nmol/L at 60 min; P less than 0.05), but not dopamine, also occurred. These results suggest that multiple ACTH-releasing factors, such as CRH, AVP, E, and NE, are involved in ACTH secretion induced by insulin-induced hypoglycemia in man.

Adrenocorticotropic Hormone↗
PubMed1986

Simple management of cerebrospinal fluid rhinorrhea after pituitary surgery.

A simple procedure for managing postoperative cerebrospinal fluid rhinorrhea after pituitary surgery is described. Under local anesthesia, a needle is introduced manually through a nostril toward the sella turcica and EDH adhesive or fibrin glue is injected into the sellar cavity or sphenoid sinus, or both. This procedure is simple and safe to perform, acceptable to the patient, and can be done in a short hospital stay.

Aprotinin↗
PubMed1986

The pituitary as a target of antalgic treatment of chronic cancer pain: a possible mechanism of pain relief through pituitary neuroadenolysis.

Surgical hypophysectomy performed in 18 cases with hormone-dependent carcinoma resulted in tumour regression in 38.8% of the cases, and pain relief in 88%. Neuroadenolysis performed 170 times on 130 cases resulted in pain relief in 94% with hormone-dependent carcinoma, and 70% with non-dependent carcinoma. The clinical investigations, following performance of neuroadenolysis, indicate suppressed pituitary function, significant increase of ACTH, thyrotropin-releasing hormone and vasopressin in the cerebrospinal fluid (CSF), delay of long latencies in somatosensory evoked potential and increased pain threshold of C-fibres. Increase of beta-endorphin in CSF was very brief. Though the exact physiological activity in pain sensation of those peptides other than endorphins still remains obscure, increase of the peptides which are mainly synthesized in the hypothalamopituitary axis, along with suppressed pituitary function, is considered to exert a long-lasting suppressive effect on the mediation and perception of cancer pain through C-fibres and the central nervous system.

Endorphins↗
PubMed1986

Effects of antimuscarinic agents and prostaglandin E2 on the gastric mucosal lesions induced by necrotizing agents and water-immersion stress in rats.

The role of antimuscarinic action in gastric mucosal protection against necrotizing agents and the role of such mucosal protection in antiulcerogenic action were studied in rats with i.v. administered antimuscarinic agents. Pirenzepine, as well as PGE2, prevented the gastric mucosal lesions induced by all necrotizing agents (99.5% ethanol, 0.6 N HCI, 0.15 N NaOH, 0.4 N HCI-50 mM taurocholate), but atropine did not prevent the HCI-induced lesions. Cimetidine inhibited only the ethanol-induced lesions even at the antisecretory dose. Higher doses of pirenzepine (5-fold) and atropine (10-fold) were required to inhibit the gastric secretion in Shay rats than in vagally stimulated rats. There was no difference between the antisecretory doses of cimetidine in Shay rats and vagally stimulated rats. PGE2 (0.03-0.1 mg/kg) did not affect gastric secretion. The protective doses of pirenzepine and atropine against mucosal lesions induced by necrotizing agents were similar to the dose in inhibiting vagally stimulated acid secretion and water-immersion stress-induced lesions. PGE2 (100 micrograms/kg) did not prevent the water-immersion stress induced gastric lesions. These results suggested that antimuscarinic agents protect the gastric mucosa from necrotizing agents via a blocking action on the activation of the intrinsic cholinergic nerve. However, antiulcerogenic action is more deeply concerned with antisecretory action than cytoprotection.

Animals↗