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Biomedical subjects

R Yamazaki

Publications and source records attributed to R Yamazaki.

At least 55 records · Page 3Linked to original sources
PubMed1991

[The urodynamic effects of an alpha 1-adrenoceptor agonist on the bladder and urethra of female dogs].

It has been known that alpha 1-adrenoceptors play an important role in urethral contraction. The incompetence of the urethral contraction is a cause of stress incontinence. We studied the urodynamic effects of a selective alpha 1-adrenoceptor agonist (midodrine hydrochloride) on the bladder and urethra of female dogs. Under anesthesia with intravenous chloralose, four doses (0.03, 0.1, 0.3 and 1.0 mg/kg) of midodrine were administered intravenously and urodynamic studies including cystometry, urethral pressure profilometry and electromyography (EMG) of the external urethral sphincter were performed. The administration of midodrine induced a significant increase of the maximum closing pressure in the proximal portion of the urethra (p less than 0.05 at 0.03 mg/kg and p less than 0.01 at 0.1, 0.3, 1.0 mg/kg). There were no significant changes in the functional profile length, the closing pressure at the external sphincters, the maximum bladder pressure, bladder capacity and bladder compliance. The administration of 0.3 mg/kg or more of midodrine produced a significant increase in the mean arterial blood pressure. After midodrine administration, transient increases in the external sphincter EMG activities were recognized. The activities showed the synergistic pattern during the bladder contractions. In conclusion, lower dose administration of a selective alpha 1-adrenoceptor agonist (midodrine) specifically produced an increase of the closing pressure in the proximal portion of the urethra without affecting blood pressure. These results suggest that midodrine is useful for the treatment of stress incontinence in humans.

Animals↗
PubMed1990

Effects of dihydroergotamine and etilefrine on experimentally-induced postural hypotension in dogs.

The effects of dihydroergotamine and etilefrine on experimentally-induced postural hypotension were examined. Although dihydroergotamine at 3 and 10 micrograms/kg (i.v.) increased blood pressure (BP), it did not affect cardiac output (CO). However, dihydroergotamine at 10 micrograms/kg reduced the decrease in CO induced by the tilt. Therefore, it is suggested that the increase in BP is induced by the contraction of resistance vessels, and that the inhibition of the decrease in CO due to tilt is induced by the contraction of capacitance vessels. Etilefrine at 0.1 mg/kg (i.v.) increased BP and heart rate (HR), however, it did not attenuate the decrease in BP induced by the tilt. Although it tended to increase CO, it did not attenuate the decrease in CO. It is suggested that the increase in BP is due to the contraction of resistance vessels, and to the increase in cardiac contractile force and HR. In this study, dihydroergotamine and etilefrine did not attenuate the decrease in BP due to tilt, though dihydroergotamine inhibited the decrease in CO due to tilt. As an explanation, it is suggested that dihydroergotamine induces contraction of resistance vessels as well as capacitance vessels, however the effects of the drug on resistance vessels is weak, and that etilefrine has little or no effect on capacitance vessels. In our previous study, midodrine, an alpha-1 agonist, attenuated the decreases in BP and CO due to tilt, and it has been suggested that the inhibition was induced by the contraction of capacitance vessels. Therefore, dihydroergotamine, etilefrine and midodrine show different pahrmacological profiles in experimentally-induced postural hypotension.

Anesthesia↗
PubMed1990

Hemodynamic effects of a potassium ionophore, lonomycin A.

Lonomycin A, an ionophorous antibiotic, exhibits a high transport rate for monovalent cations, especially potassium. The cardiovascular actions of lonomycin A were studied in anesthetized dogs. Lonomycin A administered intravenously at 30 micrograms/kg increased coronary blood flow slightly with relatively small alterations in other hemodynamic parameters. After 100 micrograms/kg, a slight and transient fall followed by an increase in blood pressure was observed. Coronary blood flow, cardiac output, left ventricular pressure, max dP/dt, and isometric ventricular segmental tension increased. Arterial venous O2 difference and total peripheral vescular resistance decreased. Above 300 micrograms/kg, dramatic alterations were produced in almost all hemodynamic parameters, and total peripheral vascular resistance was increased. Lonomycin A-induced positive inotropic action was partly inhibited by pretreatment with pindolol, however gradual shortening of the ventricular wall length was still observed. A positive chronotropic action induced by lonomycin A was inhibited by pindolol pretreatment in vivo. On the other hand, lonomycin A elicited a negative chronotropic effects in the isolated guinea-pig right atrium, concomitantly increasing resting tension. These results suggest that lonomycin A alone produces peripheral vascular dilation and effects cardiac functions, which are in turn modified by lonomycin A-induced cathecholamine release from nerve terminals.

Animals↗
PubMed1989

The deconjugation ability of bacteria isolated from the jejunal fluids in the blind loop syndrome with high 14CO2 excretion--using the breath analysis technique and thin-layer chromatography.

Five patients with blind loop syndrome (Billroth II) were examined by measuring 14CO2 specific activity of expired breath samples taken at intervals after a meal containing glycine-1-14C cholate. The 5 patients tested showed a marked increase of 14CO2 specific activity. Furthermore, the ability of deconjugation of bacteria isolated from the jejunal fluids in the efferent loop of these patients was tested by thin layer chromatography. The bacterial species identified from the samples were as follows: enterococcus, Lactobacillus (L) buchneri, L. bifidus, L. brevis, Eubacterium (E) lentum, Bacteroides (B) vulgaricus, B. filamentosum, Corynebacterium (C) granulosum, Escherichia (E) coli, Staphylococcus (S) epidermidis, and Aerobacter (A) aerogenes. These species of bacteria, except E. coli and A. aerogenes, showed the deconjugation ability by which conjugated bile acids in ox gall was hydrolyzed. Administration of chloramphenicol (1g per day for 14 days orally divided doses) to the 5 patients reduced 14CO2 specific activity significantly. On the other hand, 9 healthy men (control subjects) who were tested showed a flat curve, and 8 of the 9 had no growth of bacteria isolated from the jejunal fluids. The remaining healthy man showed an overgrowth of E. coli and Pseudomonas (P) aeruginosa, but the species did not have the ability of deconjugation. Thus, we concluded that the patients with blind loop syndrome(Billroth II) had the bacterial overgrowth in the efferent loop that contained species with deconjugation ability, and, as a result the bacterial overgrowth contributed to causing abnormalities (increased deconjugation) in the metabolism of bile acids in the small intestine. When the concentration of conjugated bile acids in the small intestine was reduced to levels below the critical micellar concentration by several factors, fat malabsorption and subsequent steatorrhea were induced (1,-4). Furthermore, H. Fromm and A. F. Hofmann presented in vivo that the patients with blind loop syndrome had fat malabsorption and the patients who had a high 14CO2 output after oral administration of glycine-1-14C cholate showed a low 14CO2 output after oral administration of antibiotic drug (5,6). However, there has been no report on the deconjugation ability of bile acids of bacteria isolated from the jejunal fluids in the efferent loop of patients with Billroth II who had positive breath tests.(ABSTRACT TRUNCATED AT 400 WORDS)

Bacteria↗
PubMed1987

Effects of midodrine on experimentally induced postural hypotension and venous pooling in dogs.

Effects of (+/-)-2-amino-N-2,5-(dimethoxyphenyl-beta-hydroxyphenyl) acetamide hydrochloride (midodrine) on experimental postural hypotension and venous pooling were examined in the anesthetized dog treated with hexamethonium (20 mg/kg s.c.). A 30 degree-tilt caused a significant decrease in blood pressure. Midodrine, at 0.1 mg/kg, significantly attenuated the decrease in blood pressure induced by the tilt 10, 20 and 30 min after its administration. The heart rate was not affected by the tilt. Cardiac output decreased significantly following the tilt. Midodrine significantly increased the basal rate of cardiac output and attenuated the decrease in cardiac output induced by the tilt. Venous pooling was produced by the occlusion of the circulation of the dog foot, and the increase of limb girth by the cuff inflating was measured as an indicator of venous pooling. Midodrine, at 0.1 mg/kg, significantly attenuated the increase of limb girth, indicating that the drug reduced venous pooling. These results suggest that midodrine (0.1 mg/kg i.v.) constricts the venous bed, resulting in the increase in cardiac output in the anesthetized dog with experimental postural hypotension.

Animals↗
PubMed1987

Effects of the new calcium antagonist 2-nitratopropyl-3-nitratopropyl-2,6-dimethyl-4-(3-nitrophe nyl)- 1,4-dihydropyridine-3,5-dicarboxylate on cerebral circulation in dogs.

2-Nitratopropyl-3-nitratopropyl-2,6-dimethyl-4-(3-nitropheny l)- 1,4-dihydropyridine-3,5-dicarboxylate (CD-349), nimodipine and nicardipine (0.3-3 micrograms/kg i.v.) increased vertebral blood flow (VBF) in the anesthetized dog, the effect of CD-349 being the strongest, and they also decreased blood pressure. All these drugs slightly increased femoral blood flow. CD-349, nimodipine and nicardipine (1-10 micrograms/kg i.v.) increased cerebral tissue blood flow (CBF) in the anesthetized dog, CD-349 producing the most sustained and pronounced effect. CD-349 (3 micrograms/kg i.v.) restored the decrease of CBF induced by the application of 0.5 ml of serotonin (5-HT, 10(-5) mol/l), KCl (30 mmol/l) and prostaglandin F2 alpha (PGF2 alpha, 10(-4) mol/l) to the surface of the cerebrum of the anesthetized dog. In isolated canine basilar arteries. K-contraction was completely inhibited, but the relaxation of 5-HT- and PGF2 alpha-contractions by these drugs was incomplete. CD-349 had a more potent effect than nicardipine and nimodipine on basilar arteries. These results indicate that CD-349 is a potent cerebrovasodilator.

Animals↗
PubMed1987

[A case of ruptured aneurysm of the thoraco-abdominal aorta associated with Behçet's disease].

A 41-year-old male with incomplete type of Behçet's disease was operated on because of ruptured aneurysm of the thoraco-abdominal aorta. A saccular pseudoaneurysm developed by rupture of the aortic wall involved the left postero-lateral portion of the supra-renal abdominal aorta. The defect in the aneurysm was closed using Dacron patch. The post-operative course was uneventful. However, seven months after discharge, the patient developed severe back pain at midnight, and was referred to our institution. On physical examination, a pulsatile mass was found in the right epigastric area. CT and DSA showed saccular pseudoaneurysm at the patch anastomotic site. Extra-anatomic long bypass grafting was performed from the ascending aorta to the infra-renal abdominal aorta. The abdominal aorta was occluded just below the diaphragm and the supra-renal portion of the aorta. Reconstruction of coeliac artery and superior mesenteric artery was made using branch grafts attached to the long graft. Surgical treatment of the complicated Behçet's disease should include extra-anatomic bypass, especially in the re-operative cases of ruptured aneurysm of the aorta.

Adult↗
PubMed1986

Effects of propranolol on tissue necrosis in experimental myocardial infarction in dogs.

We studied the effects of propranolol on degradation of cardiac structural proteins resulting from ischemia induced by 24 h ligation of the coronary artery in dogs. Degradation of myocardial myosin heavy chain, alpha-actinin and troponin-I was used as an indicator of degradation of cardiac structural proteins. In dogs with left circumflex coronary artery ligation, propranolol, given orally in the dose of 10 or 30 mg/kg, significantly reduced degradation of cardiac structural proteins. This can be supported by the facts that treatment with propranolol, 10 or 30 mg/kg, reduced release of cathepsins B, L and D from lysosome to cytosol in the ischemic tissue and that the reduced acidity of the ischemic tissue was improved by treatment with propranolol, 30 mg/kg. In conclusion, propranlol delays the necrotic development of the severely ischemic myocardial tissue as shown by reduced protein degradation.

Animals↗
PubMed1986

Effects of midodrine on blood flow in dog vascular beds.

Effects of alpha-(2,5-dimethoxyphenyl)-beta-glycinamide-ethanol hydrochloride (midodrine, ST-1085) on blood flow in different vascular beds were examined in anesthetized dogs. Intravenously administered midodrine at doses of 0.3 and 0.6 mg/kg induced a transient increase followed by a long-lasting decrease in femoral arterial blood flow. Renal arterial blood flow exhibited an initial decrease followed by returning toward the control level, and thereafter decreased again. Vertebral, common carotid, superior mesenteric and coronary arterial blood flow, and cardiac output gradually decreased. Midodrine did not have any effects on cerebral tissue blood flow. The changes were more remarkable at a dose of 0.6 mg/kg than at 0.3 mg/kg. Each arterial blood flow change was statistically analyzed 20, 30 and 60 min after the administration of 0.6 mg/kg of midodrine. The decrease of coronary arterial blood flow by the treatment with midodrine was significantly smaller than those of superior mesenteric and femoral arterial blood flow at 20 and 30 min after midodrine administration. The decrease of renal arterial blood flow was significantly smaller than those of superior mesenteric arterial blood flow at 20 and 30 min, and femoral arterial blood flow at 20, 30 and 60 min after the administration. The decrease of vertebral arterial blood flow was also smaller than that of femoral arterial blood flow at 20, 30 and 60 min after the administration.

Adrenergic alpha-Agonists↗
PubMed1986

Effects of midodrine on experimentally-induced postural hypotension in dogs.

Effects of alpha-(2,5-dimethoxyphenyl)-beta-glycinamide-ethanol hydrochloride (midodrine, ST-1085) on experimental postural hypotension was examined in hexamethonium (20 mg/kg s.c.)-treated anesthetized dogs. The dogs were tilted 30 degrees to a head-up position. A 30 degree-tilt caused a significant decrease in blood pressure. Midodrine, 0.3 mg/kg, attenuated the decrease in blood pressure induced by the tilt significantly at 10 and 30 min after administration of the drug. The heart rate increased following the tilt, but the degree of the increase was rather small. Cerebral tissue blood flow significantly decreased by the tilt. Midodrine, 0.3 mg/kg, significantly attenuated the decrease in cerebral tissue blood flow induced by the tilt at 10 and 30 min. Vertebral arterial blood flow significantly decreased by the tilt. Midodrine reduced the decrease in vertebral arterial blood flow induced by the tilt significantly at 10 and 30 min. Cardiac output also decreased significantly by the tilt. Midodrine attenuated the decrease in cardiac output significantly at 10 min. Femoral arterial blood flow decreased significantly by the tilt. Midodrine tended to reduce the decrease in femoral arterial blood flow induced by the tilt at 30 min. Therefore, midodrine via vasoconstriction seems to be useful for the decrease in blood flows due to the postural hypotension.

Adrenergic alpha-Agonists↗
PubMed1985

Effects of propranolol on infarct size and the impaired hemodynamics in experimental myocardial infarcted dogs.

We studied the effects of propranolol on infarct size and hemodynamic impairment induced by 24 h-coronary ligation. The myocardial infarction produced by the left circumflex coronary artery ligation was more consistent than that induced by the left anterior descending coronary artery ligation, suggesting that the former is a more appropriate experimental model for pharmacological evaluations. Oral treatment with propranolol, 3-30 mg/kg, reduced infarct size and reduced the elevated left ventricular end-diastolic pressure, which was shown to be most closely related with infarct size, in dogs with circumflex coronary artery ligation extending over 24 h. In conclusion, our results indicate that propranolol protects against the enlargement of infarct size and improves the impaired hemodynamics observed in myocardial infarcted dogs with occlusions extending over 24 h, as well as in dogs with less than 24 h-occlusions reported by numerous investigators.

Administration, Oral↗