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Biomedical subjects

Y Asakura

Publications and source records attributed to Y Asakura.

At least 73 records · Page 4Linked to original sources
PubMed1996

Effect of brief hypoxia on reperfusion arrhythmias and release of Ca2+ by rat heart homogenate blocked by ryanodine.

OBJECTIVES: We previously reported that a brief period of hypoxic perfusion (BHP) prior to ischemia in rat hearts improved functional recovery upon reperfusion with reduced Ca2+ overload. The present study was designed to determine whether the effect of BHP would be associated with a reduction in reperfusion arrhythmias and a preservation of function of the sarcoplasmic reticulum (SR). METHODS: Hearts were subjected to 40 min of global ischemia and 30 min of reperfusion after a 20 min period of oxygenated perfusion (oxygenated group: OG), or a 10 min period of oxygenation and 10 min of hypoxic perfusion (hypoxic group: HG). We evaluated the release of Ca2+ by SR blocked by ryanodine, the recovery of left ventricular function, and the reperfusion induced ventricular tachycardia/fibrillation (VT/VF). RESULTS: Functional recovery improved and the incidence and duration of reperfusion VT/VF were reduced in HG. In HG the uptake of Ca2+ in SR decreased during ischemia, but this decrease was less than that in OG. However, recovery of Ca2+ uptake after reperfusion did not differ between groups. The release of Ca2+ by SR blocked by ryanodine was inhibited in HG throughout the ischemia-reperfusion sequence. CONCLUSIONS: Observations suggest that the benefits of BHP on recovery of function and reperfusion arrhythmias were associated with a decrease in release of Ca2+ by SR blocked by ryanodine.

Animals↗
PubMed1996

[Carney syndrome].

Explore the source record for details and available documents.

Adrenal Hyperplasia, Congenital↗
PubMed1995

Improvement of insulin sensitivity for glucose metabolism with the long-acting Ca-channel blocker amlodipine in essential hypertensive subjects.

To clarify whether the long-acting calcium-channel blocker amlodipine restores insulin insensitivity in essential hypertension, insulin sensitivity tests were performed at the physiological steady-state insulin level (45 to 55 microU/mL) before and after amlodipine (2.5 to 7.5 mg/d) administration for 2 to 4 months in borderline and mild essential hypertensive subjects. Instead of somatostatin, Sandostatin (Sandoz, Basel, Switzerland) was used for the determination of steady-state plasma glucose (SSPG) in the same way as previously described. SSPG, which was initially high (212.9 +/- 18.0 mg/dL, mean +/- SE), was significantly reduced to 169.8 +/- 14.7 after amlodipine treatment. Responses of ketone bodies during the test at 30 minutes, which reflect the insulin effect on lipolysis in adipose tissue and hepatic fatty acid oxidation, also improved after amlodipine treatment. Norepinephrine, noted to be mildly elevated after amlodipine treatment, decreased during the sensitivity test at 2 hours probably due to the sedative effect, without any change in the fractional extraction of Na. This indicates that the physiological level of insulin does not activate sympathetic nerve activity or stimulate Na reabsorption. The long-acting calcium-channel blocker amlodipine has significantly improved the initially decreased insulin sensitivity for glucose metabolism at least partially in borderline or mild essential hypertension.

Amlodipine↗
PubMed1995

Preinfarction angina as a major predictor of left ventricular function and long-term prognosis after a first Q wave myocardial infarction.

OBJECTIVES: The purpose of this study was to assess the prognostic significance of preinfarction angina after a first Q wave myocardial infarction. Patients with anterior or inferior myocardial infarction were compared. BACKGROUND: The effect of preinfarction angina on prognosis after anterior and inferior myocardial infarction remains unclear. METHODS: A total of 291 patients with a first Q wave anterior (n = 171) or inferior (n = 120) myocardial infarction were examined to assess the effect of preinfarction angina on short- and long-term prognosis. The relation between predischarge left ventriculographic findings and preinfarction angina was also examined. RESULTS: The presence of preinfarction angina was associated with lower peak creatine kinase activity, a lower in-hospital incidence of sustained ventricular tachycardia and fibrillation and a lower incidence of pump failure and cardiac mortality in patients with either anterior or inferior infarction. Among patients with anterior infarction, preinfarction angina was associated with a lower incidence of cardiac rupture and less need for readmission for heart failure within 1 year after the onset of infarction. In this subgroup it was also associated with a higher ejection fraction, a smaller end-diastolic volume and a lower incidence of aneurysm formation noted on ventriculography during convalescence. In patients with inferior infarction, these variables did not differ significantly in the presence or absence of preinfarction angina. Multivariate analysis confirmed that the presence of preinfarction angina was an independent predictor of development of ventricular aneurysm, late phase heart failure and 1-year cardiac mortality. CONCLUSIONS: The presence of preinfarction angina has a favorable effect on infarct expansion and late phase left ventricular function, especially in patients with anterior myocardial infarction. The mechanisms responsible for this phenomenon are not known but may be secondary to limitations of infarct size through unidentified mechanisms other than collateralization (e.g., ischemic preconditioning).

Adult↗
PubMed1995

Case report: inhalation therapy of paromomycin is effective for respiratory infection and hypoxia by cryptosporidium with AIDS.

A 24-year-old man with AIDS and hemophilia A had intractable diarrhea and fever. Upon examination of stool and of a sigmoidal biopsy specimen, cryptosporidium was revealed. Approximately 2 months after admission, respiratory infection with hypoxia due to cryptosporidium developed. Paromomycin inhalation was effective therapy. To the authors' knowledge, this is the first case of respiratory cryptosporidiosis treated successfully by paromomycin inhalation.

AIDS-Related Opportunistic Infections↗
PubMed1995

Efficacy of Ibudilast on lower limb circulation of diabetic patients with minimally impaired baseline flow: a study using color Doppler ultrasonography and laser Doppler flowmetry.

Ibudilast is a prostacyclin-mediated vasodilator and antiplatelet agent. The hemodynamic effects of ibudilast were evaluated in 41 patients with non-insulin-dependent diabetes mellitus by means of two-dimensional Doppler ultrasonography and laser Doppler blood flowmetry. Before and one hour after oral administration of ibudilast (10 mg), or elastase (1800 U) as a control, the cross-sectional area (CSA) of the dorsal pedis artery, its blood flow index (BFI), and dermal microcirculatory blood volume (MBV) were measured. In the ibudilast group, all of the parameters (CSA, BFI, and MBV) significantly increased as compared with the elastase group. These data suggest that ibudilast is effective in ameliorating diabetic macroangiopathy and microangiopathy of the lower limbs.

Administration, Oral↗
PubMed1995

Study of the de novo synthesis of cholesterol in the rat liver: a newly developed radiotracer technique, "TLC-autoradioluminography".

A possible evaluation technique was devised for examing timely cholesterol synthetic activity in the rat liver. The principle of the technique is to measure the incorporation rate of 14C atoms into a few target metabolites excreted in bile with time after an intraportal injection of [1,2-14C] acetate to the conscious rats. The measuring technique, TLC-autoradioluminography (TLC-ARLG), was devised for much more accurate, quantitative, simple and quick ultramicroanalysis of radioactive metabolites than ever before. Practically, a few microliters of the bile samples were analyzed by TLC before recording of a 2-dimensional radioactive image on the TLC plate. The incorporation ratio of 14C into cholesterol to succinic acid (C/S ratio) varied such that the value found in a 24-h fasting group was less than one-tenth of that in a sufficiently fed control group. For use as an antihyperglycemic drug, the bile C/S ratio in the nicotinic-acid-dosed group was approximately one-fifth of that in the control group.

Acetates↗
PubMed1994

Effect on short-term prognosis and left ventricular function of angina pectoris prior to first Q-wave anterior wall acute myocardial infarction.

The prognostic significance of angina pectoris before the development of first Q-wave anterior wall acute myocardial infarction (AMI) was assessed in 153 patients. A total of 100 patients in this study had angina before Q-wave AMI, whereas 53 patients had no antecedent symptoms of angina. The presence of angina before AMI was associated with a lower incidence of complications including sustained ventricular tachycardia or fibrillation (7% vs 25%, p = 0.0022), pump failure (24% vs 47%, p = 0.0035), cardiac rupture (1% vs 17%, p = 0.0001), and a lower in-hospital mortality rate (11% vs 28%, p = 0.0067). The peak creatine phosphokinase activity was lower in patients with than without antecedent angina (1,727 +/- 1,238 vs 2,675 +/- 2,569 IU/liter, respectively, p = 0.023). There was no difference in the prevalence of multivessel coronary artery disease or the presence of collateral circulation between the 2 groups. Left ventriculography revealed a higher left ventricular ejection fraction (54 +/- 13% vs 46 +/- 11%, p = 0.034) and smaller left ventricular end-diastolic volumes (75 +/- 15 vs 86 +/- 18 ml/m2, p = 0.017) in patients with than without antecedent angina. These findings suggest that the presence of angina before AMI may be associated with a protective effect on left ventricular function during anterior wall AMI. Although the precise mechanisms underlying the beneficial effects are unknown, they may be related to the development of collateral channels or ischemic preconditioning.

Adult↗
PubMed1994

[A case of Shy-Drager syndrome complicated with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and incomplete paralysis of bilateral vocal cords].

A 67-year-old man with SIADH complicated by slowly progressing autonomic failure was described. The patient noticed constipation at the age of 57. In the following years, he suffered from urinary incontinence, depletion of sweating, impotence, sleeplessness with snore, and dizziness while walking. Physical examination revealed a masked oily face with slight cerebellar disturbance. Abnormality of autonomic function tests was recognized and he was diagnosed as Shy-Drager syndrome with gradually progressing, diffuse autonomic failure accompanied by slight cerebellar ataxia and Parkinsonism. Both serum sodium level and plasma osmotic pressure were reduced, whereas daily sodium excretion was more than 100mEq and urinary osmolality was about 500mOsm/kgH2O. His renal function was intact, and the adrenocortical and thyroid hormone levels were normal, then criteria of SIADH was fulfilled. SIADH was thought to have occurred on the basis of Shy-Drager syndrome. Water load test showed failure of adequate water diuresis, but intravenous phenytoin administration following the water load test ameliorated the diuresis to normal. The relationship between plasma osmolality and the ADH response indicates that ADH was adequately secreted in response to the increase in plasma osmolality but not suppressed in response to the decrease in plasma osmolality below 280mOsm/kgH2O. These results suggest that ADH synthesis in the hypothalamus and its secretion from the pituitary gland were both intact. The response of ADH secretion to the orthostatic hypotension induced by head-up tilt was quite blunted, being compatible with Shy-Drager Syndrome. Sleep disturbance was studied by polysomnography and laryngoscopy, and was revealed to be based upon severe sleep apnea due to incomplete paralysis of the bilateral vocal cords. Sleep apnea due to vocal cord paralysis is sometimes found to be complicated in patients with multiple system atrophy (MSA) including Shy-Drager syndrome, and is known as Gerhardt syndrome. This is the first report on a case of Shy-Drager syndrome complicated with SIADH and bilateral vocal cord paralysis. In this case, SIADH is caused by impaired afferent pathways from baroreceptors to the hypothalamus, which transfer inhibitory stimuli on ADH secretion. It is suggested that Shy-Drager syndrome should be considered one of the causes of SIADH.

Aged↗
PubMed1994

Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and Gerhardt syndrome associated with Shy-Drager syndrome.

This is the first report on a case of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with Gerhardt syndrome (paralysis of bilateral vocal cords). A 67-year-old Japanese man suffering from progressive autonomic failure was diagnosed as having Shy-Drager syndrome (SDS) with hyponatremia due to SIADH and severe sleep apnea caused by a bilateral recurrent nerve palsy. Water load test showed alteration in diuresis which was corrected by phenytoin. Arginine vasopressin secretion was not suppressed by plasma osmolality below 280 mOsm/kgH2O. Impairment of the afferent pathways of baroreceptors, or impairment of the osmoreceptors could be speculated as the etiological factor of the SIADH observed in this case.

Aged↗
PubMed1993

[Quantitative and qualitative alterations of plasma lipoproteins in obesity].

In order to clarify lipoprotein abnormality in mild to moderate obesity (BMI > or = 25), plasma was separated by table top ultracentrifugation into VLDL (chylomicron), IDL, LDL and HDL. Chol, TG and ApoB were determined in each fraction by enzymatic and sensitive Latex method. The data were analysed according to glucose intolerance and hyperinsulinemia (HI). In obese subjects, irrespective of glucose intolerance, Chol, TG & ApoB levels were high in plasma, and an increase in VLDL (Chol, TG & ApoB), IDL (Chol & ApoB), LDL (Chol & ApoB), and a decrease in HDL-Chol were observed. These levels were also abnormal in nonDM particularly with HI. In DM, HI did not seem to affect hyperlipidemia. Correlation between Chol, TG and ApoB in three ApoB containing lipoprotein subfractions was noted in obesity. The ratio of Chol/ApoB and TG/ApoB in LDL was significantly lower in obesity implying that LDL particles were smaller in size. Half of nonDM patients had HI, and only 29% of DM patients had HI, and both groups had almost the same lipoprotein abnormality. Hyperlipidemia was severe in nonDMHI(+) compared to nonDMHI(-). Therefore, in hyperlipidemia of obesity, hyperinsulinemia plays a role in nonDM and hyperglycemia in DM. Insulin resistance seems to be an important factor in DM. Although the mechanism may be different, the consequence of hyperlipidemia is similar. Increased numbers of ApoB containing lipoproteins and smaller size of LDL are the characteristic features of hyperlipidemia in mild to moderate obesity. Because these quantitative and qualitative changes appear to be linked to an increased risk for premature arteriosclerosis, intensive therapy should be recommended even in mild to moderate obesity.

Apolipoproteins B↗
PubMed1993

Inhibition of glycolysis or increased perfusate H+ buffering capacity, but not their combination, attenuates myocardial stunning.

OBJECTIVE: Both inhibition of glycolysis and enhancement of the H+ buffering capacity of the perfusate during ischaemia reduce myocardial reperfusion injury. The aim of the study was to investigate whether these manoeuvres, performed separately or together, could reduce myocardial stunning after brief global ischaemia. METHODS: The hearts of male Sprague-Dawley rats were preperfused for 10 min with oxygenated or hypoxic buffer (pH 7.4) containing 100 mM sucrose, 100 mM HEPES, or 5 mM 2-deoxyglucose plus 100 mM sucrose, followed by 15 min of total ischaemia and 30 min of reperfusion. In some hearts, 5 mM 2-deoxyglucose was combined with 100 mM HEPES during the 10 min preperfusion period. RESULTS: Brief hypoxic preperfusion, 2-deoxyglucose, or HEPES reduced myocardial stunning as well as improving the metabolic recovery and reducing Ca2+ overload after reperfusion. These changes were associated with a smaller increase in intracellular Na+ and a smaller decrease of coronary effluent pH at the end of ischaemia. In contrast, the combination of HEPES with hypoxic preperfusion or 2-deoxyglucose depressed functional recovery and increased the intracellular Na+ level at the end of ischaemia as well as increasing Ca2+ overload after reperfusion. This happened even though the decrease in coronary effluent pH was attenuated to the same extent as before. CONCLUSIONS: Both inhibition of glycolysis and enhancement of the perfusate H+ buffering capacity before ischaemia attenuated myocardial stunning, but the protective effect of each manoeuvre was lost when they were combined.

Animals↗
PubMed1993

Rapid growth of left ventricular thrombus leading to fatal heart failure in six hours.

A left ventricular (LV) thrombus grew rapidly over chronic endocarditis 2 months after anterior myocardial infarction. Echocardiograms demonstrated a rapidly growing LV thrombus an eventual obstruction. Despite anticoagulant/thrombolytic therapy, the patient died of acute LV failure. Histopathologically, a fresh thrombus overlay thickened endocardium with massive T lymphocyte infiltration over healed infarction.

Chronic Disease↗
PubMed1993

Attenuation of myocardial stunning by an increase in the H+ buffering capacity of the perfusate and that by hypoxic preperfusion are affected differently by the free [Ca2+] of the perfusate.

OBJECTIVES: Protons produced during ischemia may increase intracellular Na+ (Na+i) through Na+/H+ exchange, and may lead to Ca2+ overload through Na+/Ca2+ exchange to cause myocardial stunning. This study investigated whether an increase in the H+ buffering capacity of the perfusate or a reduction of H+ production by a brief hypoxic preperfusion before ischemia would reduce myocardial stunning. We also investigated whether the protective effect of these maneuvers depends on the free [Ca2+] of the perfusate. METHODS: Isolated rat hearts were preperfused with oxygenated or hypoxic buffer (pH 7.4) containing 100 mM of either sucrose or HEPES for 10 min, followed by 15 min of total ischemia and 30 min of reperfusion. To investigate the dependence of the effects of HEPES or a brief hypoxic preperfusion, the free Ca2+ concentration in the buffer was changed from 1.25 mM to 2.5 mM in some hearts. RESULTS: Oxygenated preperfusion with buffer containing HEPES and 1.25 or 2.5 mM Ca2+ improved the metabolic and functional recovery with a decrease in the accumulation of Na+i during ischemia and in 45Ca2+ uptake during reperfusion. A brief hypoxic preperfusion with 1.25 mM Ca2+ provided a similar protective effect whereas no protective effect was observed when the [Ca2+] was raised to 2.5 mM. CONCLUSIONS: An increase in the H+ buffering capacity or a brief hypoxic preperfusion reduced myocardial stunning with improved metabolic recovery, and reduced Ca2+ uptake. However, the effects of these interventions were affected differently by the free [Ca2+] of the perfusate, which suggests that they work, at least in part, through some different mechanism(s).

Animals↗
PubMed1993

[Coronary flow dynamics in the right coronary artery providing collateral circulation: comparison before and after successful angioplasty with a Doppler catheter].

Coronary blood flow dynamics were investigated in 9 patients with isolated coronary artery disease of the left anterior descending artery (LAD) with good collateral flow (grade 2 or 3 of Rentrop's classification) from the right coronary artery (RCA) and 20 patients with normal coronary arteries as controls. The coronary flow velocity (Vs: systolic peak, Vd: diastolic peak, Vm: mean) was measured with a Doppler catheter and the diameter (D) by the edge detection method in the proximal portion of the RCA. Vs/Vd was calculated. The areas under the velocity curve during systole (integral of s) and diastole (integral of d) were measured to obtain the ratio (integral of s/integral of d). Peak to resting velocity ratio (PRVR) was obtained as an index of coronary flow reserve, using intracoronary injections of 6 ml contrast medium or 8-12 mg papaverine. These parameters before percutaneous transluminal coronary angioplasty (PTCA), after PTCA, and in control subjects were compared. The collaterals disappeared angiographically immediately after successful PTCA. D (before PTCA: 3.2 +/- 0.1 mm, after PTCA: 3.3 +/- 0.1 mm, controls: 3.2 +/- 0.1 mm) and Vs did not vary between before and after PTCA and in control subjects (NS). The values of Vd, Vm decreased and Vs/Vd and integral of s/integral of d increased after PTCA to the values in the controls. PRVR obtained with contrast medium and papaverine also increased.

Aged↗
PubMed1993

Hemodynamic effects of lipo-PGE1 on peripheral artery in patients with diabetic neuropathy: evaluated by two-dimensional color Doppler echography.

Twenty non-insulin-dependent diabetic patients were studied to evaluate the hemodynamic effects of lipo-PGE1 (prostaglandin E1 incorporated in lipid microspheres). Improvement of diabetic neuropathy was assessed on the basis of subjective symptoms such as pain, coldness, numbness and dysethesia (subjective) after intravenous administration of lipo-PGE1. After lipo-PGE1 treatment, the subjective symptoms were markedly improved. Hemodynamic effects of this drug on the dorsalis pedis artery were examined using new real-time two-dimensional color Doppler echography. After administration of lipo-PGE1, the cross-sectional area of the dorsalis pedis artery significantly increased from 2.6 +/- 0.2 mm2 to 3.5 +/- 0.2 mm2 (P < 0.01). Moreover, the blood flow index significantly increased from 40 +/- 7 to 61 +/- 11 (P < 0.05). The results of this study suggest that lipo-PGE1 may serve as a useful drug in improving diabetic neuropathy.

Adult↗
PubMed1992

Insulin insensitivity in nonobese, nondiabetic essential hypertension and its improvement by an alpha 1-blocker (bunazosin).

To investigate insulin insensitivity and its reversibility, we performed an insulin sensitivity test using the steady state plasma glucose (SSPG) method in 10 lean hypertensive subjects with normal glucose tolerance before and after treatment with alpha 1-blocker bunazosin, and 14 age body mass index-adjusted healthy control subjects. Steady state plasma glucose was significantly higher in the hypertensive subjects compared with the control group (182 +/- 10 mg/dL v 104 +/- 7, P < .01, mean +/- standard error of the mean (SEM). Steady state plasma glucose significantly decreased to 136 +/- 12 mg/dL (P < .01) after the treatment with alpha 1-blocker bunazosin, with a decrease of blood pressure. Hypertensive subjects had shown an increased area under the curve of glucose and insulin during the oral glucose tolerance test compared with normal controls. The glucose area decreased significantly, but the insulin area did not change after the treatment. There was no difference in plasma epinephrine, norepinephrine, and fractional excretion of Na between normal and hypertensive subjects both before and after treatment with bunazosin at basal and during insulin sensitivity tests (2 h). Serum total cholesterol level decreased and HDL cholesterol increased significantly after treatment with bunazosin. A significant correlation was observed between SSPG and blood pressure, but not between insulin level and blood pressure. The results indicate that insulin sensitivity is better related than hyperinsulinemia to hypertension and that this insensitivity is partially reversible by alpha 1-blocker, bunazosin.

Adrenergic alpha-Antagonists↗