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Biomedical subjects

H Ohkawa

Publications and source records attributed to H Ohkawa.

At least 163 records · Page 9Linked to original sources

Effects of ATP, its related nucleotides and VIP on the inhibitory potentials in the smooth muscle cells of the guinea-pig duodenum.

Non-adrenergic inhibitory potentials (i.p.'s) were recorded from the smooth muscle cells of the guinea-pig duodenum following field stimulation. ATP, ADP and AMP increased the membrane potential of the cell and decreased the amplitude and the rate of hyperpolarization of the i.p. The amplitudes of the maximum hyperpolarization due to a repeated stimulation and the post-stimulus depolarization were reduced by ATP and AMP. Methylxanthine could not inhibit the i.p. while apamin reversibly decreased the amplitudes of the i.p. and the post-stimulus depolarization. The latency and the time to peak were prolonged by apamin. Biphasic effect of quinidine on the i.p. was obtained. The amplitude and the rate of hyperpolarization of the i.p. were decreased at 10-4 g/ml of quinidine. The amplitudes of the maximum hyperpolarization by repetitive stimulation and the post-stimulus depolarization were decreased by quinidine. The membrane potential of the cell was not affected by VIP. The amplitude and the other parameters of the i.p. were not changed in the used concentration of VIP. Trypsin reduced the membrane potential of the cell but not changed the parameters of the i.p. The membrane was slightly depolarized by the treatment with papain while no significant changes on the i.p. were observed in papain. The obtained results suggest that ATP, its related substances and VIP do not contribute to the non-adrenergic inhibitory neurotransmission.

Adenosine Diphosphate↗

Effects of divalent cations on the inhibitory potentials in the duodenal smooth muscle cells of the guinea-pig.

The effects of divalent cations and some Ca2+ antagonists on the non-adrenergic inhibitory potential (i.p.) in the duodenal smooth muscle cells of the guinea-pig were investigated intracellularly. The membrane potential was a function of the external Ca2+ (0.25-7.5 mM) and Mg2+ (1.2-24 mM) concentrations. The latency and the time to peak of the i.p. were prolonged by low Ca2+ and excess Mg2+. The amplitude and the rate of hyperpolarization of the i.p. were reduced by low Ca2+ and excess Mg2+. The effects of Mn2+ (5-10 mM) on the i.p. were similar to those by excess Mg2+ except for the small depolarization. The i.p. evoked in the Ca2+-free solution was considerably restored by the addition of Ba2+ (1.25 mM) and Sr2+ (2 mM). The actions of Ba2+ and Sr2+ on the i.p. were inhibited by verapamil (10(-4)g/ml). Verapamil (2 X 10(-5)-2 X 10(-4)g/ml) and gentamicin (10(-3)g/ml) reduced the amplitude and the rate of hyperpolarization of the i.p. The latency and the time to peak of the i.p. were prolonged by verapamil but not by gentamicin. In nifedipine (10(-4)g/ml), the two-peaked i.p. was evoked by a single stimulus. This potential was similar to that evoked by a paired pulse in normal solution. The results obtained suggest that the released of the non-adrenergic inhibitory substance requires Ca2+ which moves into the non-adrenergic inhibitory neurons through the Ca2+ conductance pathway.

Animals↗

Effects of enkephalin and endorphin on the inhibitory junction potentials in the duodenal smooth muscle cells of the guinea-pig.

Inhibitory junction potentials (i.j.p.s) evoked by field stimulation were recorded from the smooth muscle cells of the guinea-pig duodenum intracellularly. The membrane potential was -54.3 mV. The parameters of the i.j.p. were as follows: latency, 71 msec; time to peak, 146 msec; amplitude, 15.5 mV; rate of hyperpolarization, 107 mV/sec; and half decay time of the i.j.p., 193 msec. Met-enkephalin (10(-7)-10(-6) M) had no effect on the membrane potential and the i.j.p. The membrane potential was decreased by beta-endorphin (1.7 X 10(-7)-6.8 X 10(-7) M). Increase in the latency and the time to peak and decrease in the amplitude and the rate of hyperpolarization of the i.j.p. were observed for beta-endorphin. "Spontaneous" excitatory junction potentials (e.j.p.s) were generated by beta-endorphin. Naloxone (3.1 X 10(-6)-3.1 X 10(-4) M) hyperpolarized the membrane of the muscle cells. At high concentrations of naloxone (3.1 X 10(-4) and 3.1 X 10(-3) M), inhibition of the i.j.p. was observed. Levallorphan (2.3 X 10(-4) M) prolonged the latency and the time to peak and reduced the amplitude of the i.j.p. The membrane potential was slightly decreased by levallorphan. "Spontaneous" e.j.p.s were generated by levallorphan in a certain population of the cells. It is concluded that Met-enkephalin does not contribute to the non-adrenergic inhibitory transmission and that beta-endorphin acts as a modulator in the control mechanism of the intestinal motility. The effects of naloxone and levallorphan on the i.j.p. are discussed.

Animals↗

Effects of 4-aminopyridine on the non-adrenergic inhibitory neurotransmission in the guinea-pig duodenum.

The effects of 4-aminopyridine (4-AP) on the non-adrenergic inhibitory potential (i.p.) in the longitudinal and circular smooth muscle cells of the guinea-pig duodenum were investigated using intracellular microelectrodes. The membrane potential of both smooth muscles was decreased by 4-AP and the amplitude of the evoked i.p.s. was increased. In a low-calcium solution (0.25 mM), the amplitude of the i.p.s. was reduced but the additional application of 4-AP increased the amplitude. In the 4-AP containing low-calcium solution, the i.p. was inhibited by verapamil and EGTA. The inhibitory effect of verapamil on the i.p. evoked in a low-calcium solution was less in the presence of 4-AP than that in its absence. In a high-calcium solution (5 mM), the amplitude of the i.p. increased and the additional application of 4-AP enhanced the i.p. further. The amplitude of the i.p. elicited in high-potassium solutions was not changed by 4-AP. The i.p. was not potentiated by 2-aminopyridine or 2,5-diaminopyridine. Tetraethylammonium ions enhanced the amplitude of the i.p. at low concentration but decreased it in high concentration. In a few longitudinal smooth muscle cells, the evoked excitatory potential (e.p.) was observed. Potentiation of the e.p. by 4-AP was completely blocked by atropine. From the results obtained, it is suggested that the release of the non-adrenergic inhibitory neurotransmitter is increased by 4-AP due to increase calcium influx in the nerve terminals. The release of the cholinergic excitatory neurotransmitter seems to be increased by 4-AP.

4-Aminopyridine↗

[Carcinoma of the colon associated with diffuse metastatic leptomeningeal carcinomatosis (DMLC) presenting as disturbance of consciousness--a case report].

A 58-year-old man was admitted to Saiseikai Hospital complaining of vertigo and visual acuity disturbance. His admission physical examination was unremarkable; his spinal fluid contained 69 large mononuclear cells/mm3. Cytological examination was not done. His disturbance of consciousness rapidly progressed to coma and he died on the 10 th hospital day. At autopsy, Borrmann Type II carcinoma (3 cm in diameter) was found in the cecum. Microscopical examination revealed that the tumor was a poorly differentiated adenocarcinoma. Diffuse metastasis was found in the leptomeningium , but there was no evidence of metastasis to other organ.

Adenocarcinoma↗

New metabolites of riboflavin appear in human urine.

By surveying compounds having isoalloxazine derived from flavins on a high performance liquid chromatogram with fluorescence detection, two new flavin derivatives were found in human urine. These two compounds were purified by partition chromatography on a cellulose column and by paper chromatography with several solvent systems, and their structures were determined to be 7 alpha-hydroxyriboflavin and 8 alpha-hydroxyriboflavin. The relative distributions, measured by high performance liquid chromatography, of 7 alpha- and 8 alpha-hydroxyriboflavin, riboflavin, and hydroxyethylflavin and its derivative were calculated to be 31.1, 5.0, 25.6, 4.9, and 21.9%, respectively, to total flavins in normal human urine obtained in early morning. The excretion of 7 alpha- and 8 alpha-hydroxyriboflavin in human urine indicates the occurrence of a metabolic pathway of the isoalloxazine ring of flavin at its 7 alpha and 8 alpha positions.

Adult↗

Sarcomatous Wilms tumor associated with consumption coagulopathy.

This is a case report of a sarcomatous Wilms tumor complicating disseminated intravascular coagulation with gastrointestinal bleeding, ascites, pleural effusion, and hepatitis after the second course of actinomycin D. A sarcomatous Wilms tumor is believed to have an unfavorable prognosis even if multimodal therapy is given. Arteriovenous fistulae which we created for purposes of chemotherapy and hyperalimentation by microvascular-sleeve anastomosis functioned well for three years in spite of repeated punctures.

Arteriovenous Shunt, Surgical↗

The determination of urinary oxalate by gas chromatography.

A new quantitative determination method for urinary oxalate by gas chromatography has been established. This method consists of concentration of urine to dryness followed by methylation of the oxalic acid with 7 per cent hydrochloric acid-methanol, subsequent extraction with chloroform and gas chromatographic analysis. The advantages of the technique are smaller sample sizes (only 5 ml.), rapidity (within 2 to 3 hours) and accuracy (99.14 plus or minus 1.34 per cent recovery). In addition, the treatment of the sample is simple and no specialized equipment is required. Therefore, this method is recommended to clinicians for routine determination of oxalic acid in urine. Urinary oxalate content was analyzed with this method in 62 male patients with calcium oxalate stones. Urinary oxalate concentration and excretion in 33 patients with recurrent stones were significantly higher than in the 22 controls using Welch's test.

Adult↗

Properties of the inhibitory junction potentials recorded from smooth muscle cells of the guinea-pig duodenum.

Inhibitory junction potentials (IJPs) in response to single or repetitive stimulation were recorded intracellularly from smooth muscles of the guinea-pig duodenum. The amplitude of the IJP was dependent on the stimulus intensity and duration. The hyperpolarization of up to 30 mV was evoked by a single pulse. The mean values of the latency, the fall time, the rate of hyperpolarization, the half decay time and the time constant for decay of the IJPs evoked by 0.3 msec stimulation were 67 msec, 130 msec, 86 mV/sec, 156 msec and 194 msec, respectively. The latency and the half decay time were slightly decreased by changes in the stimulus intensity and duration. When repetitive stimulation was applied at low frequencies, successive IJPs were evoked but their amplitudes were decreased gradually. The maximum amplitude of the hyperpolarization was increased with increasing the frequency of stimulation over than 10 Hz. The spike activity due to rebound excitation was potentiated at high frequency. Over 90% of the cells exhibited only the IJP without atropinization. The excitatory junction potentials and the complex type in response to a brief pulse were recorded from a few cells. These results suggest the predominant nonadrenergic inhibition on the duodenal smooth muscles.

Action Potentials↗

Inhibitory junction potentials of the guinea-pig duodenum in the treatment with catecholamines.

The inhibitory junction potentials (IJPs) in response to single and repetitive stimulation were recorded from the smooth muscle cells of the guinea-pig duodenum intracellularly. In adrenaline and noradrenaline (10(-8)-10(-5) g/ml), the IJP could be evoked in spite of a hyperpolarization of the cell membrane. The amplitude of the IJP was slightly changed in these agents but not abolished. Similar results were obtained in isoprenaline (10(-5) g/ml) and phenylephrine (10(-5) g/ml). The IJPs evoked by single and repetitive stimulation were not blocked by phentolamine (10(-7) g/ml) and propranolol (10(-5) g/ml). In propranolol (10(-7)-10(-5)/g/ml), the membrane was depolarized and the amplitude and the rate of hyperpolarization in the IJP were decreased. The membrane potential was decreased and the amplitude of the IJP was slightly increased in the presence of guanethidine (10(-5) g/ml). The amplitude of the IJP was increased with increasing the concentration of tyramine (10(-6)-10(-5) g/ml). These results suggest that the transmitter released from the intramural inhibitory nerve in the duodenum is nonadrenergic and this type of inhibition seems to be independent from adrenergic inhibition.

Action Potentials↗

Occurrence of riboflavinyl glucoside in rat urine.

To investigate the metabolism of riboflavin, [2-14 C]-riboflavin was administered orally to a rat. The urine pooled for 24h after administration was fractionated by paper and silica gel thin layer chromatographies using various solvent systems. Among the radioactive metabolites, riboflavinyl glucoside was found along with 7-carboxy lumichrome and 8-carboxy lumichrome. The radioactivity of riboflavinyl glucoside comprised about 6% of the total radioactivity excreted in the urine during 24h.

Animals↗

Sympathetic neuromuscular transmission in the smooth muscle of guinea-pig prostate gland.

The electrical and mechanical activity of the smooth muscle of the guinea-pig prostate gland was studied. The electrical activity of the cells was recorded intracellularly. The resting membrane potential was about -50-60 mV. The majority of cells was electrically quiescent but some cells generated action potentials spontaneously in the normal solution. The repetitive stimulation evoked the excitatory junction potentials and an action potential in some cells. The repetitive stimulation produced the phasic contraction and the response was frequency-dependent. Adrenaline, noradrenaline, and phenylephrine (5 X 10(-7) - 5 X 10(-6) g/ml) exhibited an excitatory effect on the mechanical activity. The frequency of the spontaneous action potential was increased by these agents. The spike number and the duration of the action potential were increased by these drugs. The excitatatory action of adrenaline on the mechanical activity was antagonized by phentolamine. The mechanical responses produced by repetitive stimulation were inhibited by tetrodotoxin and phentolamine but not by propranolol. Atropine and d-tubocurarine did not inhibit the mechanical responses. Tetraethylammonium ions (TEA), at low concentrations, potentiated the mechanical responses. The excitatory action of TEA on the mechanical response was dose-dependent. The frequency of the action potential was increased by TEA. The potentiated mechanical responses obtained in TEA were inhibited by phentolamine but not by propranolol. These findings indicate that the smooth muscle cell of the prostate gland has alpha-excitatory receptors on the cell membrane and the sympathetic neuromuscular transmission is potentiated by TEA.

Action Potentials↗

Association of hypercalcemia with tumors producing colony-stimulating factor(s).

Two human malignant tumors, which we previously reported to produce colony-stimulating factors (CSFs), were found to be accompanied by remarkable hypercalcemia. A patient with a CSF-producing lower jaw cancer (squamous cell carcinoma) developed a marked granulocytosis (150,000/microliters) and hypercalcemia (more than 215 mg/dl). The tumor was successfully transplanted into nude mice, which developed marked granulocytosis (300,000/microliters) and hypercalcemia (20 mg/dl). White blood cell and serum calcium concentrations of these mice decreased promptly to normal levels when the tumor was excised. Treatment with prednisolone (1.5 mg/kg) or indomethacin (5 mg/kg) had no effect on the serum calcium level of these mice. Parathyroid hormone or prostaglandin E was not increased in the serum of the mice or in the tumor tissue. However, the mice bearing the tumor excreted extremely large amounts of calcium in their urine, and their bony tissues contained less calcium and phosphorus than controls. Moreover, histology of bony tissues of these nude mice clearly demonstrated the decrease in trabecular tissues and cortical thickness as well as remarkable activation of osteoclasts. Another patient with a CSF-producing bronchogenic squamous cell carcinoma showed mild granulocytosis and hypercalcemia. The biopsied tumor tissue was transplanted into nude mice, which developed marked granulocytosis (300,000/microliters) and also severe hypercalcemia (18 mg/dl). These results suggest the presence of a new syndrome of granulocytosis and hypercalcemia associated with CSF-producing tumors. The causal mechanism of the hypercalcemia was shown to be some humoral factor which activates osteoclasts other than parathyroid hormone. Neither prostaglandins nor osteoclast-activating factor seemed to be the cause of the hypercalcemia.

Adult↗