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Biomedical subjects

A Kitabatake

Publications and source records attributed to A Kitabatake.

At least 109 records · Page 6Linked to original sources
PubMed1996

A new approach for evaluation of left ventricular diastolic function: spatial and temporal analysis of left ventricular filling flow propagation by color M-mode Doppler echocardiography.

OBJECTIVES: To evaluate left ventricular diastolic function and differentiate the pseudonormalized transmitral flow pattern from the normal pattern, the propagation of left ventricular early filling flow was assessed quantitatively using color M-mode Doppler echocardiography. BACKGROUND: Because the propagation of left ventricular early filling flow is disturbed in the left ventricle with impaired relaxation, quantification of such alterations should provide useful indexes for the evaluation of left ventricular diastolic function. METHODS: Study subjects were classified into three groups according to the ratio of early to late transmitral flow velocity (E/A ratio) and left ventricular ejection fraction: 29 subjects with an ejection fraction > or = 60% (control group); 34 with an ejection fraction < 60% and E/A ratio < 1 (group I); and 25 with ejection fraction < 60% and E/A ratio > or = 1 (group II). The propagation of peak early filling flow was visualized by changing the first aliasing limit of the color Doppler signals. The rate of propagation of peak early filling flow velocity was defined as the distance/time ratio between two sampling points: the point of the maximal velocity around the mitral orifice and the point in the mid-left ventricle at which the velocity decreased to 70% of its initial value. High fidelity manometer-tipped measurement was performed in 40 randomly selected subjects. RESULTS: The rate of propagation decreased in groups I and II compared with that in the control group (33.8 +/- 13.8 [mean +/- SD] and 30.0 +/- 8.6 vs. 74.3 +/- 17.4 cm/s, p < 0.001, respectively) and correlated inversely with the time constant of left ventricular isovolumetric relaxation and the minimal first derivative of left ventricular pressure (peak negative dP/dt) (r = 0.82 and r = 0.72, respectively). CONCLUSIONS: Spatial and temporal analysis of filling flow propagation by color M-mode Doppler echocardiography was free of pseudonormalization and correlated well with the invasive variables of left ventricular relaxation.

Blood Flow Velocity↗
PubMed1996

Altered signal transduction system in hypertrophied myocardium: angiotensin II stimulates collagen synthesis in hypertrophied hearts.

Hypertensive cardiac hypertrophy is associated with the accumulation of collagen in the myocardial interstitium. Previous studies have demonstrated that this myocardial fibrosis accounts for impaired myocardial stiffness and ventricular dysfunction. Although cardiac fibroblasts are responsible for the synthesis of fibrillar collagen, the factors that regulate collagen synthesis in cardiac fibroblasts are not fully understood. We investigated the effects of angiotensin II on cardiac collagen synthesis in cardiac fibroblasts of 10-week-old spontaneously hypertensive rats and age-matched WKY rats. Basal collagen synthesis in cardiac fibroblasts from spontaneously hypertensive rats was 1.6-fold greater than that in the cell of WKY rats. Angiotensin II stimulated collagen synthesis in cardiac fibroblasts in a dose-dependent manner. The responsiveness of collagen production to angiotensin II was significantly enhanced in cardiac fibroblasts from spontaneously hypertensive rats (100 nM angiotensin II resulted in 185 +/- 18% increase above basal levels, 185 +/- 18 vs 128 +/- 19% in WKY rats, P < .01). This effect was receptor-specific, because it was blocked by the competitive inhibitors saralasin and MK 954. These results indicate that collagen production is enhanced in cardiac fibroblasts from spontaneously hypertensive rats, that angiotensin II has a stimulatory effect on collagen synthesis in cardiac fibroblasts, and that cardiac fibroblasts from spontaneously hypertensive rats are hyper-responsive to stimulation by angiotensin II. In the hearts of spontaneously hypertensive rats, mRNA of the renin-angiotensin system (renin, angiotensinogen, angiotensin converting enzyme) was expressed. Levels of angiotensinogen and renin mRNA expressed in ventricles, and angiotensinogen mRNA expressed in fibroblasts from SHR were higher than those from WKY. ACE mRNA was also more strongly expressed in the ventricles and fibroblasts from SHR compared with those of WKY. These findings suggest that the cardiac reninangiotensin system may play an important role in collagen accumulation in hypertensive cardiac hypertrophy (fig.4).

Angiotensin II↗
PubMed1996

Neurofibromatosis complicated with XXX syndrome and renovascular hypertension.

A 25-year-old woman with neurofibromatosis was admitted to our hospital for evaluation of hypertension. When she was 6 years old, she was diagnosed as having neurofibromatosis and XXX syndrome because of multiple café-au-lait spots, neurofibromas of the skin and mental retardation. Chromosome analysis revealed that her karyotype was 46, XX/47, XXX. Renal arteriography disclosed aneurysmal change and stenosis of the right renal artery. After right-side nephrectomy and aneurysmectomy, the kidney was autotransplanted in the left iliac fossa. Surgical procedure resulted in marked amelioration of the hypertension without medical treatment. Thus, aortorenal bypass and renal autotransplantation have emerged as the preferred revascularization operations. This is the first report of a chromosomal linkage between neurofibromatosis which is thought to be an autosomal dominant disease and the XXX syndrome.

Adult↗
PubMed1996

Inhibition of endothelium-dependent relaxation by hemoglobin in rabbit aortic strips: comparison between acellular hemoglobin derivatives and cellular hemoglobins.

Hemoglobin (Hb)-based artificial oxygen carriers are supposed to induce vasoconstriction through the inactivation of endothelium-derived relaxing factor (EDRF). We examined the vasoconstrictive activity of acellular Hb and cellular Hb solutions in rabbit aortic strips. Unmodified Hb, pyridoxalated Hb, bovine unmodified Hb, haptoglobin-Hb complex (Hp-Hb), and polyoxyethylene glycol-conjugated Hb (PEG-Hb) were used as acellular Hbs having different molecular masses. Cellular Hbs included liposome-encapsulated Hb and red blood cells (RBC). In the first experiment, Hb (10 ng/ml to 1 mg/ml) was cumulatively added to the tissues in which steady-state relaxation was evoked by acetylcholine (ACh) after precontraction induced by phenylephrine. Although all Hb solutions induced a dose-dependent reversal of ACh-induced relaxation, the most potent vasoconstrictive effect was noted with acellular Hbs, and their contractile activities were almost the same independent of molecular mass. On the other hand, liposome-Hb and RBC showed reduced potencies in this order. These results indicate the importance of cellularity as the major factor determining Hb-related EDRF inactivation. In another experiment, the tissues were exposed to Hb at 0.01, 0.1, or 1 mg/ml for 30 min and ACh-induced relaxation was recorded after the complete removal of Hb in an organ bath chamber. Exposure to unmodified Hb at > 0.1-mg/ml concentrations significantly reduced the ACh-induced relaxation, whereas the relaxation was not affected by PEG-Hb, Hp-Hb, liposome-Hb, or RBC. These results suggest that unmodified Hb might be persistently associated with tissues and thereby inhibit ACh-induced relaxation. From these findings, we propose two attributes of Hb-related inhibition of endothelium-dependent relaxation: Acellular Hbs inhibit EDRF more efficiently in the luminal space than cellular Hbs, and unmodified Hb can also inhibit it adluminally and/or adventitially.

Acetylcholine↗
PubMed1996

Alpha 1-adrenoceptor subtypes mediating inotropic and electrophysiological effects in mammalian myocardium.

Stimulation of alpha 1-adrenoceptors produces a positive inotropic effect in rat and rabbit ventricular myocardium via different mechanisms, the prolongation of action potential duration (APD) exclusively in the former and an increase in myofibrillar Ca2+ sensitivity in large part in the latter. This study was designed to determine whether the two inotropic mechanisms are mediated by different alpha 1-adrenoceptor subtypes. In rat papillary muscles, the positive inotropic effect and APD prolongation induced by phenylephrine (in the presence of propranolol) were inhibited by WB-4101, but not affected by chlorethylclonidine (CEC). WB-4101, but not CEC, blocked the phenylephrine-induced inhibition of the transient outward current (Ito) in rat ventricular cells. On the other hand, WB-4101 and CEC each antagonized the positive inotropic effect of phenylephrine in rabbit papillary muscles. However, the phenylephrine-induced APD prolongation observed in rabbit papillary muscles was blocked only by WB-4101. These results indicate that the WB-4101 sensitive alpha 1-adrenoceptor subtype mediates the positive inotropism that is correlated with the APD prolongation resulting from Ito reduction, whereas the CEC-sensitive subtype mediates the positive inotropism that is probably associated with increased myofibrillar Ca2+ sensitivity. Radioligand binding studies with [3H] prazosin showed a similar ratio of alpha 1A-to alpha 1B-adrenoceptor subtypes in rat and rabbit ventricular myocardium, implying that the different degree of contribution of each action mechanism to the overall inotropic effect in the two species cannot be explained by distribution of the alpha 1-adrenoceptor subtypes.

Adrenergic alpha-Agonists↗
PubMed1996

A case of adenosine-sensitive ventricular tachycardia in a very elderly male.

The best-known type of adenosine-sensitive ventricular tachycardia is idiopathic and of right ventricular outflow origin; however, there is little information about other types of adenosine-sensitive ventricular tachycardia. Idiopathic adenosine-sensitive ventricular tachycardia is common in the young. An 87-year-old man with ventricular tachycardia was admitted to our hospital. His ventricular tachycardia was sensitive to adenosine triphosphate, edrophonium, verapamil, and Valsalva's maneuver. He had experienced no anginal episodes. His ventricular tachycardia was thought to be idiopathic. We report this very rare case of adenosine-sensitive ventricular tachycardia, which was not derived from the right ventricular outflow tract, in a very elderly male.

Adenosine↗
PubMed1996

[Evaluation of valvular lesions by three-dimensional echocardiography].

A recently developed, on-line image processing system (Tomtec EchoScan) for three-dimensional (3D) echocardiography was compared with conventional two-dimensional examination and our own off-line 3D system. Transesophageal echocardiography was performed in 10 cardiac patients using an omniplane transducer which was automatically rotated under the control of the 3D system. At each angle of the transducer, the respiration-gated image of one cardiac cycle was acquired and transferred into the computer, where the dynamic 3D images of mitral and/or aortic valve were reconstructed. The EchoScan system enabled 3D recognition of the structural and dynamic abnormalities of the valves, such as mitral valve prolapse, although tissue information, which is expressed as a gray scale in the conventional echocardiography, cannot be evaluated from the 3D image. Average times were 5.4 min for the data acquisition, 11.8 min for the 3D processing and 5.7 min for the rendering. Although it seems necessary to improve the efficacy of data acquisition, to shorten the calculation time and to minimize the artifacts, this system enables assessment of 3D cardiac structures at the bedside and to fully recognize valvular lesions preoperatively in patients with valvular heart disease.

Aged↗
PubMed1995

Purification method for alpha-1-acid glycoprotein with subsequent high-performance liquid chromatographic determination of monosaccharides in plasma of healthy subjects and patients with renal insufficiency.

A simple purification method for human plasma alpha-1-acid glycoprotein (AAG) using an ion-exchange and hydroxyapatite column was developed. The recovery of the method was found to be high. We also improved a determination method for N-acetylneuraminic acid and monosaccharides in the carbohydrate moiety of AAG by using an ion-exchange column and pulse-amperometric detection. By this method, a composition analysis of the carbohydrate moiety of AAG (N-acetylneuraminic acid, fucose, N-acetyl glucosamine, galactose and mannose) was possible with 1.0 ml of plasma. We compared these carbohydrate concentrations in the AAG of patients with renal insufficiency with those of healthy subjects. In the AAG of the patients, the concentrations of N-acetylglucosamine, galactose and mannose were significantly higher than those in the AAG of the healthy subjects.

Acetylglucosamine↗
PubMed1995

Cytosolic localization of beta 3-subunit of heterotrimeric GTP binding protein in rat hearts.

The expression of three different subtypes of GTP binding protein beta-subunits (beta 1, beta 2 and beta 3) was examined in rat hearts at both mRNA and protein levels. Among three subtypes, beta 3 mRNA was more abundant in ventricles while beta 1 and beta 2 mRNAs were expressed ubiquitously among ventricles, atria and aortas. The immunodetectable beta 1- and beta 3-proteins were predominantly found in the cytosolic fraction of rat ventricles. In this study, we demonstrate ventricle-specific expression of beta 3-subunit and localization of G protein beta 3-subunit in the cytosol of rat hearts. This unusual cytosolic localization of G protein beta 3-subunit might indicate subtype-specific function of G protein beta (gamma)-subunits in rat hearts.

Animals↗