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Biomedical subjects

R Takeda

Publications and source records attributed to R Takeda.

At least 181 records · Page 10Linked to original sources
PubMed1992

[Response of coronary arteries to intracoronary acetylcholine infusion in patients with familial hypercholesterolemia].

Loss of the vasodilator response to acetylcholine (Ach), an endothelium-dependent vasodilator, has been demonstrated in animal models of atherosclerosis and in atherosclerotic coronary arteries of humans studied in vitro. The response of normal coronary arteries on angiograms to the intracoronary injection of Ach in patients with familial hypercholesterolemia (FH) was studied. Ten patients with FH (mean age, 53.6 +/- 6.5 years) with a mean serum total cholesterol of 334.8 mg/dl and 12 controls (mean age, 55.8 +/- 14.5 years) with a total cholesterol level of 183.6 mg/dl, and with normal coronary arteries on angiograms were studied. Patients with clinical histories suggestive of coronary spastic angina were excluded from this study. A bolus of 20, 50 micrograms Ach and 2 mg isosorbide dinitrate (ISDN) were infused into the left coronary artery in each subject. Changes in coronary diameters were measured after each injection with a videodensitometric analysis system. In the control group, the diameter at the middle segments of the left anterior descending artery (LAD) and at the proximal and middle segments of the left circumflex artery (LCX) increased significantly in response to Ach; whereas, in the FH group the diameter at the proximal segments of the LAD decreased significantly. There were significant differences in the coronary diameter changes in response to 50 micrograms Ach at the proximal and middle segments of the LAD and the LCX between the 2 groups. In contrast, between these 2 groups, there were no significant differences in the vasodilator responses to ISDN, a direct vascular smooth muscle dilator. The vasodilator response of coronary artery to Ach was diminished in patients with FH.

Acetylcholine↗
PubMed1992

[The functional significance of coronary collateral circulation during sudden coronary occlusion].

The functional significance of the coronary collateral circulation remains controversial. It has been suggested that collateral circulation possibly helps prevent myocardial ischemia. Seventeen target lesions in 15 patients were studied to determine the relationship between the extent of the coronary collateral circulation and the degree of ventricular dysfunction during percutaneous transluminal coronary angioplasty (PTCA). During the first balloon inflation, diastolic indices such as left ventricular end-diastolic pressure, max negative dP/dt and the time constant of early relaxation were measured immediately before and at 60 sec following balloon inflation. During the second inflation, the contralateral and ipsilateral collateral circulations were evaluated. The latter was graded as follows: 0 = none; I = filling of side branches only; II = partial filling of the epicardial segment; and III = complete filling of the epicardial segment. Following balloon inflation, a significant increase was noted in the time constant of early relaxation in patients with grade 0 collateral circulation (40 +/- 7 to 47 +/- 7 msec: p < 0.01) and grade II collateral circulation (52 +/- 12 to 56 +/- 13 msec: p < 0.05). The percent increase in the time constant of early relaxation of patients with grade 0 and I collateral circulations exceeded that of patients with grade II (p < 0.05) or grade III collateral circulation (p < 0.05). Left ventricular end-diastolic pressure was elevated in all groups during PTCA. There was no significant difference in the percent increase of left ventricular end-diastolic pressure (LVEDP) between the 4 groups. However, LVEDP before PTCA was higher in patients with grade III collateral circulation than in patients in the other groups. Max negative dP/dt did not change significantly in any group. In conclusion, collateral circulation helps prevent myocardial ischemia during acute coronary occlusion, which is most precisely shown by the time constant of early relaxation. The degree of this protective function of collateral circulation seems to vary.

Aged↗
PubMed1992

[Distribution of myocardial damage in patients with hypertrophic cardiomyopathy: evaluation by exercise thallium-201 scintigraphy].

The characteristic of myocardial damage in hypertrophic cardiomyopathy (HCM) was evaluated as to whether the damage is limited to the hypertrophied wall or extends throughout the entire wall. The myocardial damage was detected by exercise thallium-201 (Tl-201) scintigraphy and was evaluated using circumferential profile analysis, calculation of initial uptake and washout rate. Eleven patients with asymmetrical hypertrophy (ASH), whose septal and posterior wall thickness ratio exceeded 1.3 on left ventriculography and biventriculography, and 13 age-matched control subjects without heart disease were studied. The mean values of initial uptake in both groups did not differ significantly, but the washout rate for the entire heart was significantly decreased only in the HCM group (p < 0.05). All of the regional washout rates (antero-septal, apical and postero-lateral) were significantly decreased in the HCM group (p < 0.05), without any difference between the hypertrophied wall and the non-thickened free wall being noted. These results demonstrated that the analysis of myocardial damage by exercise Tl-201 scintigraphy using calculation of the washout rate is a very sensitive means of detecting myocardial damage in HCM, and that such myocardial damage is not restricted to the hypertrophied wall, but rather extends to the entire wall, including the free wall which is not thickened.

Aged↗
PubMed1992

[Acid-base disturbance in adrenal and parathyroid diseases].

Aldosterone stimulates sodium absorption in the collecting tubule, which makes the potential more lumen-negative, and secondarily stimulates proton and potassium secretion. Potassium depletion stimulates ammonia synthesis, which increases distal buffer delivery, increases luminal pH in the collecting tubule, and secondarily stimulates proton secretion. This stimulation of the distal nephron acidification by aldosterone can result in metabolic alkalosis. Inversely, aldosterone deficiency can produce characteristic metabolic acidosis with hyperkalemia (type IV renal tubular acidosis). Acute administration of parathyroidhormone (PTH) decreases renal bicarbonate reabsorption in the proximal tubule. Since the effect of PTH is overridden by other factors, such as PTH-induced base release from bone, hyperparathyroidism does not uniformly cause metabolic acidosis.

Acidosis↗
PubMed1991

Left atrial afterload mismatch in hypertrophic cardiomyopathy.

To investigate left atrial (LA) booster pump function in hypertrophic cardiomyopathy (HC), LA and left ventricular pressure-volume loops were estimated in 5 control subjects, 6 patients with essential hypertension and 11 patients with HC. Investigation of LA preload revealed that LA pressure and volume immediately before LA contraction were both increased in patients with hypertension (10 +/- 5 mm Hg, 71 +/- 19 ml/m2) compared with control subjects (7 +/- 1 mm Hg, 59 +/- 6 ml/m2), and even more increased in patients with HC (16 +/- 7 mm Hg, 81 +/- 25 ml/m2). Investigation of LA afterload revealed that the left ventricular chamber stiffness constant was higher in patients with hypertension (0.035 +/- 0.015) than in control subjects (0.028 +/- 0.009), and even more increased in patients with HC (0.056 +/- 0.017). LA stroke work index was higher in patients with hypertension (116 +/- 34 mm Hg.ml) and HC (115 +/- 19 mm Hg.ml) than in control subjects (87 +/- 23 mm Hg.ml). Investigation of LA ejection revealed that LA stroke index was higher in patients with hypertension (24 +/- 5 ml/m2) than in control subjects (18 +/- 4 ml/m2) and patients with HC (18 +/- 2 ml/m2), and LA ejection fraction was lower in patients with HC (23 +/- 6%) than in control subjects (32 +/- 7%) and patients with hypertension (34 +/- 8%). In patients with HC, LA function curve showed a shift to the lower right, and LA stroke index was inversely correlated (r = -0.76) with LA afterload. This study suggests that LA booster pump failure due to LA afterload mismatch exists in HC.

Adult↗
PubMed1991

Synaptic response of bulbar respiratory neurons to hypercapnic stimulation in peripherally chemodenervated cats.

Effects of hypercapnia on the membrane potential and synaptic activity of bulbar respiratory neurons were studied in decerebrate, vagotomized, glomectomized and artificially ventilated cats. Coaxial multibarrelled electrodes were used for intracellular recording and extracellular iontophoresis of drugs. Hypoventilation with oxygen-enriched air (hyperoxic hypercapnia) produced an increase of depolarization together with an increase of spiking during the active phase and an increase of hyperpolarization during the inactive phase of each respiratory cycle in the inspiratory, postinspiratory and expiratory neurons of the ventral respiratory group. Both depolarizing and hyperpolarizing effects were associated with a decrease in input resistance. Intracellular injection of Cl- reversed the polarity of the hyperpolarizing synaptic wave to depolarization during the inactive phase, and hypercapnia increased the depolarization at that phase. Iontophoresis of tetrodotoxin eliminated the CO2-induced changes in membrane potential and input resistance. In 20 out of 58 neurons examined, iontophoretically applied atropine partly or totally suppressed the depolarizing response to hypercapnia. For these neurons, iontophoresed acetylcholine produced a sustained depolarization that was antagonized by atropine, but not by hexamethonium. The present study shows that both depolarizing and hyperpolarizing responses of medullary respiratory neurons to hyperoxic hypercapnia are synaptically mediated. A muscarinic mechanism is involved in part of the respiratory neuronal excitation evoked by hypercapnia.

Acetylcholine↗
PubMed1991

Stimulation of atrial natriuretic peptide secretion and synthesis by Na-K-ATPase inhibitors.

Ouabain has been reported to increase the secretion of ANP in vitro. In this study, we focused on whether this action is common in Na-K-ATPase inhibitors (ATPI) and whether ATPI simply increase the release of ANP or stimulate both its biosynthesis and release. The effects of ouabain and digoxin on secretion of ANP and accumulation of ANP mRNA were investigated in the rat cardiocyte superfusion system. Ouabain and digoxin increased the immunoreactive ANP (iANP) output into perfusate and accumulation of ANP mRNA significantly. These results suggest that ATPI may stimulate both ANP biosynthesis and release in vitro.

Animals↗
PubMed1991

Elevated endogenous digitalis-like substance in hypertensive diabetic patients with a family history of hypertension.

Endogenous digital-like substance (DLS) is increased in patients with essential hypertension and is hypothesized to play a role in the pathogenesis of high blood pressure. Whether an increase in DLS in diabetic patients with hypertension is associated with a family history of hypertension or diabetic nephropathy was investigated. Plasma DLS was measured as Na(+)-K(+)-ATPase inhibitory activity (ATPI) in 100 Type 2 diabetic patients. Ouabain was used as a standard of Na-K-ATPase inhibition. Diabetic patients with hypertension demonstrated a greater ATPI level than normotensive diabetic patients (p less than 0.05). In patients with hypertension groups, the positive family history group had a higher ATPI level than the negative family history group (p less than 0.01). Microalbuminuria was not correlated with the ATPI level in diabetic patients. These results suggest that ATPI might play a role in the pathogenesis of hereditary hypertension associated with diabetes mellitus, but not have etiologic significance in diabetic nephropathy.

Aged↗
PubMed1991

Interleukin-2 enhances the release of endothelin-1 from the rat mesenteric artery.

We measured the ET-1 concentration in plasma and in the perfusate of the mesenteric arteries of rats treated with a therapeutic dose of IL-2 for 7 days (100000 U/Kg, iv.). The plasma ET-1 concentration in rats given IL-2 was 14.2 +/- 3.2 pg/ml which was significantly greater than that in the controls (2.5 +/- 0.4 pg/ml, P less than 0.05). The mesenteric arteries also released a significantly greater amount of ET-1 (29.5 +/- 1.6 pg/h) than that in controls (16.8 +/- 2.3 pg/h, P less than 0.01). The arterial blood pressure was significantly lower after IL-2 treatment than the pre-dosing level (P less than 0.05). It is concluded that IL-2 induces ET-1 release from the vascular wall, possibly as a result of reversible endothelial dysfunction caused by IL-2.

Animals↗
PubMed1991

Production of endothelin-1 from the mesenteric arteries of streptozotocin-induced diabetic rats.

Release of endothelin-1 (ET-1) from the mesenteric arteries of Wistar rats with streptozotocin-induced diabetes (STZ-DM) rats and nondiabetic rats was measured by a specific enzyme immunoassay following purification using an immunoaffinity column. The mesenteric arteries from STZ-DM rats released a significantly higher amount of ET-1 as compared to control rats (35.8 +/- 2.8 vs 14.9 +/- 2.0 pg/1hr, p less than 0.05). The plasma level of ET-1 in STZ-DM rats was also elevated to a significant extent as compared to controls (5.1 +/- 0.4 vs 3.0 +/- 0.4 pg/ml, p less than 0.05). The systolic blood pressure of STZ-DM rats was significantly higher than of the controls (p less than 0.05). The increased level of plasma ET-1 as well as its release from the mesenteric artery of STZ-DM rats may suggest its release following damage to the endothelium caused by diabetes and/or by associated changes in blood pressure.

Animals↗
PubMed1991

Effect of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor pravastatin on urinary 6 beta-hydroxycortisol excretion: a preliminary study.

In this preliminary study, the levels of urinary 6 beta-hydroxycortisol and urinary free cortisol and the 6 beta-hydroxycortisol/free cortisol ratio were determined in normal volunteers and in patients with heterozygous familial hypercholesterolemia before and after Pravastatin administration (10 mg/d for 2 weeks). Urinary 6 beta-hydroxycortisol and 6 beta-hydroxycortisol/free cortisol ratio increased significantly in both groups after Pravastatin administration (P less than 0.05). The percent increase of 6 beta-hydroxycortisol/free cortisol did not differ significantly when the two groups were compared. Our preliminary results suggest that Pravastatin induces hepatic microsomal 6 beta-hydroxylase both in normal volunteers and in patients with heterozygous familial hypercholesterolemia.

Adult↗
PubMed1991

Mitochondrial P-450 activities in aldosteronoma tissues.

Adrenal P-450 activities were measured by an in vitro reconstitution system from tissues obtained from human aldosteronomata, and the results compared with those of the normal adrenal tissues from patients with Grawitz's tumor. The P-45011 beta activity was significantly increased in adenoma tissue (55.6 +/- 5.3 vs 9.0 +/- 6.2 nmol corticosterone/mg of protein/min in the control tissues, P less than 0.01). P-450scc activity in adrenal adenomata was 13.4 +/- 2.0 nmol pregnenolone/mg of protein/min, significantly higher than control (P less than 0.05). The present results suggest that increased mitochondrial P-450(11 beta) activities may be characteristic of aldosterone-producing adenomata.

Adenoma↗
PubMed1991

Correlation between histopathological changes and mechanical dysfunction in diabetic rat hearts.

Recent clinical and experimental studies have suggested that diabetic patients may develop myocardial dysfunction in the absence of coronary heart disease and hypertension. In this study, the correlation between histopathological changes and myocardial dysfunction was studied in experimental diabetic rat hearts. Male Wistar rats were made diabetic at 9 weeks of age with a single intravenous injection of streptozotocin 50 mg/kg. The diabetic rats were studied along with age-matched control and insulin-treated rats at 4, 8, 12 and 24 weeks after the induction of diabetes to investigate isolated papillary muscle contraction and the histopathological picture simultaneously. In the isometric contractions, resting and developed tensions were similar. Time to peak tension and time to 1/2 relaxation were prolonged and the peak rate of tension rise and tension fall was depressed. On histological examination of left ventricular walls, diameters of myocytes were similar at all disease durations. Interstitial fibrosis and disarrangement of myocytes after 12 weeks were slightly increased in the diabetic hearts. Mechanical parameters did not worsen in parallel with the duration of diabetes and histological changes, but correlated with the blood glucose level. These data suggest that short-term mechanical defects in the experimental diabetic rat heart result from the metabolic disorder itself, with histopathological changes occurring later.

Animals↗