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Biomedical subjects

M Hongo

Publications and source records attributed to M Hongo.

162 records · Page 9Linked to original sources

[Clinical effect of nifedipine in patients with achalasia].

The effect of nifedipine, one of calcium antagonists, was studied on esophageal function of 10 patients with achalasia. Lower esophageal sphincter pressure (LESP) was measured with constantly perfused catheter before and after sublingual administration of 10 mg nifedipine. Nifedipine decreased LESP both in achalasia patients and normal controls except one patient. The fall of LESP by nifedipine seems to correlate with initial resting LESP. A clinical trial of nifedipine on patients with achalasia was carried out taking nifedipine sublingually in a daily dosage of 30 to 60 mg before meal. Nifedipine therapy gave good results in 8 patients, and poor response in one and no effects in one patient. Nifedipine improved symptoms of achalasia, but did not improve the degree of esophageal dilatation. Side effect was observed in only one patient, which was flushing of extremities caused by vasodilation, and it is not hazardous to continue nifedipine therapy. Sublingual administration of nifedipine in patients with achalasia is very useful way of medical treatment in two respects, 1) nifedipine decreases LESP, and 2) sublingual administration does not need to pass through the drug through esophagogastric junction which pressure is abnormally high in achalasia patients.

Adult↗

[Effect of nifedipine on canine LESP (author's transl)].

Nifedipine acts on smooth muscle cells to prevent the influx of calcium ions. The present study was undertaken to see whether a relaxatory effect of nifedipine is present on esophageal smooth muscle as well as on vascular smooth muscle. The experiment was performed on anesthetized dog's lower esophageal sphincter pressure (LESP). Nifedipine (0.5 mg/kg) administered sublingually caused rapid and marked depression of LESP. LESP response to either ACO-tetragastrin (0.5 microgram/kg) or bethanechol (5 microgram/kg) was inhibited partially but markedly. This inhibition might be caused by prevention of calcium-ion influx. This depressant effect of nifedipine on LESP both in resting state and in stimulated state is able to apply to therapy of hypermotile disorders of the esophagus.

Animals↗

Morphological changes during conversion of Clostridium saccharoperbutylacetonicum to protoplasts by sucrose-induced autolysis.

When exponentially growing cells of Clostridium saccharoperbutylacetonicum (ATCC 13564) were exposed to hypertonic concentrations of sucrose (0.3--0.5 M), rapid degradation of the cell wall occurred (sucrose-induced autolysis). The morphological changes from the original rod-shaped cells to protoplasts during the sucrose-induced autolysis were investigated by phase contrast and electron microscopy. When the cells were autolysed in the sucrose solution (0.35 M), each cell began to swell at the middle or at one pole and then formed a small bulb at the swollen part. The bulk consisted of the cytoplasm which was enveloped by the plasma membrane and extruded from the small gap produced by the degradation of the cell wall. The bulb gradually enlarged as lysis progressed, and finally became a protoplast which had no cell wall. The large pre-division cell frequently formed the bulb at the middle (septal site), while the small post-division cell formed the bulb at the pole.

Autolysis↗

Effect of duodenal acidification on the lower esophageal sphincter pressure in the dog with special reference to related gastrointestinal hormones.

The role of the duodenum in the regulation of the lower esophageal sphincter pressure was studied in 3 anesthetized dogs with a duodenal fistula by relating the lower esophageal sphincter pressure with plasma gastrin and secretin level during intraduodenal acid infusion test. Instillation of hydrochloric acid into the duodenum produced an initial fall followed by a significant and sustained increase of the lower esophageal sphincter pressure. The initial fall of the lower esophageal sphincter pressure was found to correspond to a prompt but transient rise of plasma secretin concentration, while plasma gastrin did not change significantly throughout the experimental period. It is concluded that duodenum may be an important regulator of the lower esophageal sphincter pressure in the dog through secretin and other unknown factors.

Animals↗

Korean haemorrhagic fever in staff in an animal laboratory.

In March, 1975, and January, 1978, there were outbreaks of Korean haemorrhagic fever (K.H.F.) among staff in the animal laboratory of the clinical research building of Tohoku University hospital. 13 doctors and 1 veterinarian had K.H.F., and all except 1 had a mild but typical clinical course. K.H.F. antibody titres were significantly raised in all 14 patients. 12 other doctors working in the same room had no symptoms and no K.H.F. antibody. K.H.F. antibody was also detected in 3 animal technicians who had not been ill, but who had worked in the same room. Antibody was not detected in any of the 4 technicians who worked in different animal rooms in another building. Epidemiological studies suggest that laboratory rats were the source of the infection. High titres of K.H.F. antibody were most common in rats reared in the animal laboratory associated with the outbreak.

Adult↗

Histopathological findings in proliferative membrane from a patient with sarcoid uveitis.

BACKGROUND: Sarcoid uveitis is occasionally accompanied by proliferative changes, such as retinal neovascularization and vitreous hemorrhage. Steroid administration, retinal photocoagulation, and vitrectomy may be indicated in such proliferative cases. CASE: A 19-year-old woman presented with proliferative sarcoid uveitis accompanied by recurrent vitreous hemorrhage. OBSERVATIONS: At the initial examination, bilateral vitreous opacity, retinal exudates, mild vitreous hemorrhage, retinal vasculitis, and neovascularization of the retina and optic disc were observed. Although prednisolone was administered and panretinal photocoagulation was performed several times, recurrent vitreous hemorrhage continued. Since the vitreous hemorrhage was not absorbed, pars plana vitrectomy and lensectomy were performed. After surgery, neovascularization and intraocular inflammation decreased, and the corrected visual acuity in the right eye improved to 20/50. Histopathologic analysis of the proliferative membrane removed during surgery revealed substantial neovascularization and numerous neutrophils in the vessels. CONCLUSIONS: Based on these findings, an inflammatory reaction as well as retinal ischemia were thought to be involved in the proliferative changes in this patient.

Adult↗

Effects of intravenous disopyramide on coronary hemodynamics and vasodilator reserve in hypertrophic obstructive cardiomyopathy.

Disopyramide reduces the subaortic pressure gradients and improves the clinical symptoms of patients with hypertrophic obstructive cardiomyopathy. Changes in coronary hemodynamics and vasodilator reserve in response to this agent have not been evaluated in such patients. To assess the acute effects of intravenous administration of disopyramide on coronary hemodynamics, microvascular dilatory capacity, and balance between myocardial oxygen supply and demand in hypertrophic obstructive cardiomyopathy, we examined 12 patients using an intravascular Doppler catheter and spectral analysis. Intravenous disopyramide 100 mg over 10 min caused mild increases in heart rate and aortic systolic pressure and a significant fall in left ventricular systolic pressure, resulting in a 13% decrease in the product of heart rate and left ventricular systolic pressure (from 1.13 +/- 0.18 x 10(4) before disopyramide to 0.98 +/- 0.17 x 10(4) beats/min x mm Hg 10 min afterwards; p < 0.05) and a reduction in the resting peak systolic pressure gradients of the left ventricular outflow tract. There was a 14% reduction in coronary blood flow (from 93.5 +/- 13.2 to 80.3 +/- 11.6 ml/min; p < 0.05) with an increase in coronary resistance (from 0.94 +/- 0.16 to 1.23 +/- 0.21 mm Hg/ml/min; p < 0.001). The index of coronary vasodilator reserve remained unchanged. These findings suggest that intravenous disopyramide causes a coronary vasoconstrictive effect without significantly changing the coronary microvascular dilatory capacity, but this effect may not be harmful to the balance between myocardial oxygen supply and demand in patients with hypertrophic obstructive cardiomyopathy.

Adult↗

Germanium poisoning: clinical symptoms and renal damage caused by long-term intake of germanium.

We report five patients who have taken inorganic germanium preparations over a prolonged period. In all cases, the renal function deteriorated with no proteinuria or hematuria. Histological examination of the kidneys showed widespread tubular degeneration and interstitial fibrosis with minor glomerular abnormalities. Most patients had gastrointestinal symptoms such as vomiting, anorexia and weight loss; one patient had peripheral neuropathy and myopathy. A considerable amount of germanium was detected in the hair or nails of these patients. These cases clearly show that abuse of inorganic germanium compounds can induce renal damage with various extrarenal manifestations.

Aged↗