Search PubMed⌕ Search

Biomedical subjects

H Enomoto

Publications and source records attributed to H Enomoto.

At least 163 records · Page 9Linked to original sources

Effects of a new dihydropyridine calcium antagonist on vascular smooth muscles, cardiac muscles and [3H]-nitrendipine binding.

The effects of methyl 2,6-dimethyl-4-(2-nitrophenyl)-5-(2-oxo-1,3,2-dioxaphosphorinan-2- yl)-1,4- dihydropyridine 3-carboxylate (DHP-218), a new dihydropyridine calcium antagonist, on vascular smooth muscles, cardiac muscles and [3H]-nitrendipine binding to the cardiac muscle and brain membranes were investigated in vitro. Vascular smooth muscles: Calcium-induced contraction of the rat aorta in high K+ solution was inhibited by DHP-218 with the pA2 value of 9.11. The IC50 value for the inhibitory effects of this compound in high K+-induced and phenylephrine-induced contraction was 6.3 nmol/l and 66 nmol/l, respectively. Vasodilatory effects of this drug on various blood vessels of rabbits contracted by high K+ appeared to a similar extent. The onset of the vasodilatory effect was very slow and the recovery rate of vasodilatory response after washout with the bathing solution containing high K+ or phenylephrine was also very slow. Cardiac muscles: Negative chronotropic and inotropic actions were observed at concentrations more than 30 and 100 nmol/l, respectively. Duration of the plateau phase of normal action potential was shortened and the amplitude and duration of slow action potential were reduced at concentrations more than 1 mumol/l. Very high vasculoselectivity was observed. Displacement of [3H]-nitrendipine binding: The pattern of displacement of [3H]-nitrendipine binding by DHP-218 was very similar to that of other 1,4-dihydropyridines but this compound was about 70 times less potent than nifedipine in [3H]-nitrendipine displacement capacity. These results indicate that DHP-218 has specific vasodilatory action due to calcium antagonism, but association and dissociation rates with tissue and receptors were different from those of nifedipine.

Action Potentials↗

Antihypertensive effects of a new dihydropyridine calcium antagonist.

Methyl 2,6-dimethyl-4-(2-nitrophenyl)-5-(2-oxo-1,3,2-dioxaphosphorinan-2 -yl)-1,4-dihydropyridine-3-carboxylate (DHP-218) is a new vasodilatory calcium antagonist with pronounced and long-lasting antihypertensive effects. It produced a significant decrease in blood pressure at doses more than 1 mg/kg in normotensive rats, 0.1 mg/kg in spontaneously hypertensive rats (SHR) and desoxycorticosterone acetate (DOCA)-salt hypertensive rats and 0.3 mg/kg in renal hypertensive rats. In SHR, the antihypertensive effect of DHP-218 was approximately 7 times more potent than nifedipine. The antihypertensive effect of DHP-218 appeared very slowly and persisted even after it was injected i.v. No tolerance to the antihypertensive effects of DHP-218 was observed for 5 weeks at daily doses of 0.3 and 1 mg/kg. The antihypertensive effects of DHP-218 in cats and dogs with normal blood pressure was more than 10 and 30 times more potent than those of nifedipine, respectively. At an equivalent antihypertensive dose, the effect of DHP-218 persisted longer than that of nifedipine in all the animal species used.

Animals↗

Cardiovascular effects of a new dihydropyridine calcium antagonist.

The effects of methyl 2,6-dimethyl-4-(2-nitrophenyl)-5-(2-oxo- 1,3,2-dioxaphosphorinan-2-yl)-1,4-dihydropyridine-3-carboxylate (DHP-218), a 1,4-dihydropyridine derivative, on the cardiovascular system and myocardial oxygen consumption were investigated. Effects on cardiovascular system: In urethane-alpha-chloralose anesthetized dogs, DHP-218 at a dose of 0.01 mg/kg i.v. decreased blood pressure (BP), and at 0.03 mg/kg i.v., long-lasting BP decrease was accompanied by an increase in heart rate (HR), and an increase in blood flow of the coronary, vertebral and internal carotid arteries. No significant changes in myocardial contractile force (MCF) and blood flow of the common carotid and renal arteries were observed. The duration of action was different for various effects. At doses more than 0.05 mg/kg i.d., blood pressure decreased and HR, MCF and the blood flow of coronary and vertebral arteries increased. The effects of nifedipine on the cardiac and regional blood flow were observed at doses more than 0.001 mg/kg i.v. and 1 mg/kg i.d., but the duration of its action was very short compared to those of DHP-218. Effects on cardiohemodynamics: In urethane-alpha-chloralose anesthetized dogs, DHP-218 at a dose of 0.01 mg/kg i.v. produced a decrease in BP and total peripheral resistance (TPR) and an increase in cardiac output (CO). At a dose of 0.03 mg/kg, a decrease in BP and TPR and increases in HR and CO were observed. The duration of action was different for various parameters. No significant changes in dp/dtmax, stroke volume and cardiac work were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

[Posttraumatic aneurysm-like shadow at the supraclinoid portion of the internal carotid artery--a case report].

Traumatic cerebral aneurysms occupy less than 1% in all cerebral aneurysms and the onset usually occurs two to three weeks after the head injury. The authors present a case revealing an aneurysm-like shadow at the supraclinoid portion of the internal carotid artery immediately after the head injury. A 45-year-old man was admitted in a semi-comatose state, with bleeding from the nose and the ear. He presented anisocoria, with the left pupil larger, and absence of light reflex of the pupil. Roentgenographic examinations revealed fractures of the skull, the left radius, and the pelvis. CT disclosed subarachnoid hemorrhage and intrasylvian and intracerebral hematoma, with midline shift to the right. Left carotid angiograms revealed an aneurysm-like shadow projecting medially at the supraclinoid portion of the left internal carotid artery, and an emergency operation was performed. A left fronto-temporo-parietal craniectomy was done. Incision of the dura disclosed a thin subdural hematoma and subarachnoid hemorrhage on the surface of the brain. Following removal of the intrasylvian and intracerebral hematoma and slight retraction of the left frontal lobe, a bone fracture and dural tear of the anterior cranial fossa were found. During exposure of the internal carotid artery, a heavy bleeding occurred from the supraclinoid internal carotid artery. Under control of the bleeding by temporary clipping of the internal carotid artery, the bleeding point was proved to be a longitudinal tear of the infero-medial wall of the internal carotid artery, and its length was about 5 mm. Because it was difficult to suture the tear, the internal carotid artery was doubly clipped.(ABSTRACT TRUNCATED AT 250 WORDS)

Aneurysm↗

Multiple hemangioblastomas accompanied by syringomyelia in the cerebellum and the spinal cord.

The present report covers an autopsied case of multiple hemangioblastomas in the cerebellum and the spinal cord, which did not involve the retinas and other organs. An intramedullary hemangioblastoma was found at the C3-4 level of the spinal cord and similar small tumors were present at the C-7 and Th-4 levels. Multiple cysts were located from the C1-2 to the lumbar level; some of these seemed to be longitudinally continuous, like syringomyelic cavities. These findings appear only rarely in published reports of autopsied cases of hemangioblastomas in the spinal cord.

Adult↗

Chronic anethole trithione treatment enhances the salivary secretion and increases the muscarinic acetylcholine receptors in the rat submaxillary gland.

Chronic treatment with trithio-p-methoxyphenylpropene (anethole trithione; ANTT) increased the salivary secretion from the rat submaxillary gland induced by electrical stimulation of the parasympathetic nerve and by injection of pilocarpine. In parallel with the enhancement of the salivary secretion, the number of the muscarinic acetylcholine receptors was significantly increased. The increased number of receptors may be involved in the enhancement of the salivary secretion by ANTT treatment.

Anethole Trithione↗

Effect of 2,4-diamino-6-(2,5-dichlorophenyl)-s-triazine maleate (MN-1695) on gastric ulcers and gastric secretion in experimental animals.

The effect of 2,4-diamino-6-(2,5-dichlorophenyl)-s-triazine maleate (MN-1695) on various experimental gastric ulcers and gastric secretion in experimental animals was compared with that of cimetidine and cetraxate. MN-1695 significantly inhibited the formation of Shay, stress-induced, indomethacin-induced, and histamine-induced ulcers and significantly accelerated the healing of acetic acid-induced gastric ulcers. MN-1695 was much more effective in suppressing stress- and acetic acid-induced ulcers than indomethacin-induced, histamine-induced or Shay ulcers. Cimetidine was effective in preventing stress- and acetic acid-induced ulcers but had no significant effect on Shay, indomethacin-induced and histamine-induced ulcers. Cetraxate was effective in preventing only stress-induced ulcers and had almost no effect on other experimental ulcers. MN-1695 inhibited secretion of gastric juice, acid and pepsin in Shay rats, but had no influence on basal and secretagogue-stimulated acid secretion in the perfused stomach of urethanized rats. These findings suggest that MN-1695 is a new type of anti-ulcer agent.

Acetates↗

Effect of 2,4-diamino-6-(2,5-dichlorophenyl)-s-triazine maleate (MN-1695) on gastric mucosal blood flow in dogs.

The effect of 2,4-diamino-6-(2,5-dichlorophenyl)-s-triazine maleate (MN-1695) on gastric mucosal blood flow ( GMBF ) and on the changes of GMBF induced by catecholamines, tetragastrin, histamine and indomethacin were investigated in anesthetized dogs. MN-1695 at doses up to 1 mumol/kg i.v. showed only a slight but prolonged increase of GMBF . MN-1695 tended to inhibit the decreases of GMBF induced by norepinephrine and the increase of GMBF induced by tetragastrin. The later phase of decreased GMBF induced by histamine was suppressed by MN-1695. However, MN-1695 had almost no effect on the increase of GMBF induced by epinephrine. MN-1695 produced a marked increase of antral mucosal blood flow which was reduced by pretreatment with indomethacin. Systemic blood pressure, respiration and the pressor responses induced by catecholamines and gastric secretagogues were not affected by MN-1695. These results suggest that MN-1695 may possess selective effects on the gastric mucosal microcirculation and that suppressive effects of MN-1695 on the GMBF decrease induced by ulcerogenic stimuli may be responsible for its anti-ulcer activities in various types of experimental gastric ulcers.

Animals↗

Effect of 2,4-diamino-6-(2,5-dichlorophenyl)-s-triazine maleate (MN-1695) on gastric mucosal damage induced by various necrotizing agents in rats.

The effect of 2,4-diamino-6-(2,5-dichlorophenyl)-s-triazine maleate (MN-1695) on the gastric mucosal damage induced in rats by various necrotizing agents was compared with those of cimetidine, cetraxate and prostaglandin (PG) E2. MN-1695 at doses of 0.37 mg (1 mumol) to 3.72 mg (10 mumol)/kg, significantly decreased in a dose-dependent manner the damage indices after the application of ethanol, HCl, NaOH, 25% NaCl or boiling water. Cimetidine in doses of 12.6 mg (50 mumol) to 126 mg (500 mumol)/kg was effective only against HCl-induced damage. Cetraxate in doses of 34.2 mg (100 mumol) to 342 mg (1 mmol)/kg was effective against damage due to ethanol, HCl, 25% NaCl or boiling water. However, cetraxate increased the damage index of NaOH-induced injury. PGE2 in a dose of 25 micrograms (70 nmol)/kg was effective against ethanol and 25% NaCl. The histological changes of gastric mucosal cells produced by ethanol were significantly decreased by MN-1695 and PGE2. These results suggest that MN-1695 has a cytoprotective action like that of PGE2 and that this cytoprotection inhibits the development of various kinds of experimental gastric ulcers.

Animals↗

Human alpha 1-microglobulin levels in neurological disorders.

The concentration of alpha 1-microglobulin (alpha 1-m) in sera and cerebrospinal fluids (CSF) was measured in 121 patients with various neurological disorders. Using single radial immunodiffusion, its serum level was determined. No significant difference was found between the patients (29.1 +/- 4.3 mg/l; mean +/- 1 SD) and normal control group (23.7 +/- 4.6 mg/l). The level of CSF alpha 1-m was determined by the radioimmunoassay of solid antibody system. Its CSF level in the control group was 34.8 +/- 16.0 micrograms/l, while it was significantly increased in the patients with viral meningitis (p less than 0.01) and cerebral infarct (p less than 0.05). The level was also elevated in some cases of brain tumor, bacterial meningitis, cerebral hemorrhage, cervical spondylosis, and acute lymphocytic leukemia. There was a positive correlation between alpha 1-m and albumin levels in CSF. The analysis by CSF/serum albumin ratio and alpha 1-m ratio suggested that the increase of alpha 1-m in CSF could be explained mainly by an increase in permeability of the serum alpha 1-m through damaged blood brain barrier under these pathological conditions. Its local production within the central nervous system, however, could not be ruled out in these disorders.

Adolescent↗