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Biomedical subjects

K Kanmatsuse

Publications and source records attributed to K Kanmatsuse.

At least 163 records · Page 9Linked to original sources

Effects of chemical stimulation of the rostral and caudal ventrolateral medulla on cerebral and renal microcirculation in rats.

We investigated the effects of neurons in the rostral and caudal ventrolateral medulla (RVL and CVL) on cerebral and renal microcirculation in rats. Rats were anesthetized with chloralose, paralyzed with tubocurarine, and artificially ventilated. Cerebral and renal blood flows (CBF and RBF) were measured simultaneously using laser-Doppler flowmetry. Chemical stimulation of the RVL neurons by microinjection of the excitatory amino acid L-glutamate increased arterial pressure (AP), whereas that of the CVL neurons decreased AP. Stimulation of the RVL neurons also elicited a stimulus-locked increase in CBF and a decrease in RBF. The percent change in CBF and RBF was dose-dependent as stimulus intensity was increased. Cerebral and renal vascular resistance (CVR and RVR) levels were calculated from changes in CBF or RBF and changes in mean AP. The percent reduction in CVR and percent elevation in RVR were also dose-dependent. Chemical stimulation of the CVL neurons elicited a stimulus-locked decrease in CBF and an increase in RBF. The percent reduction in CBF and percent elevation in CVR were dose-dependent. The percent reduction in RVR was also dose-dependent, while the percent elevation in RBF was not significant. Blood withdrawal reduced AP by a similar degree to CVL stimulation, but did not significantly decrease CBF. The results suggest that RVL and CVL neurons integrate cerebral and systemic microcirculation.

Animals↗

Transesophageal echocardiographically detected atherosclerotic aortic debris in a patient with systemic embolism following coronary angiography.

Transesophageal echocardiography (TEE) has enabled detection of the cardiac source of systemic emboli. We report the case of a patient who manifested systemic, multiple embolization in the kidney, skin, and upper gastrointestinal tract following coronary angiography. TEE allowed visualization of the atherosclerotic debris in the thoracic aorta. The clinical picture of the patient was consistent with that of cholesterol embolism. We recommend that patients with extensive atherosclerotic disease should undergo TEE before cardiac catheterization or other invasive procedures involving the aorta are carried out.

Aorta, Thoracic↗

Magnetic resonance imaging of cardiac hemangiopericytoma.

We report a patient with hemangiopericytoma, a rare soft tissue sarcoma, involving the left ventricle. T1- and T2-weighted magnetic resonance imaging (MRI) revealed a high signal mass invading the left ventricular wall. A biopsied specimen obtained from the metastatic subcutaneous tumor in the right popliteal fossa showed pathologic findings consistent with hemangiopericytoma.

Adult↗

Effects of long-term treatment with angiotensin-converting enzyme inhibitor on angiotensin II and prostacyclin release from mesenteric arteries in spontaneously hypertensive rats.

To evaluate the long-term effects of an angiotensin-converting enzyme inhibitor (ACEI) on vascular angiotensin II (AII), eicosanoid production and vascular reactivities, we treated spontaneously hypertensive rats (SHR) with alacepril for 6 weeks and perfused the isolated mesenteric arterial bed which contains resistance vessels. Alacepril significantly lowered the arterial blood pressure. Changes in perfusion pressure in response to norepinephrine (NE) were attenuated, and isoproterenol-stimulated AII release from the perfused mesenteric arterial beds was inhibited in the alacepril-treated SHR. Vasodilation induced by acetylcholine (Ach) and prostacyclin (PGI2) release was significantly increased in the vasculature of the alacepril-treated SHR. Alacepril exerted no effect on cyclic GMP (cGMP) formation, but increased cAMP formation in the vasculature. These findings suggest that ACEI inhibits AII formation and facilitates PGI2 production in the resistance vessels, which leads to blunting of the pressor response to NE and improvement of endothelial function in SHR. These humoral and mechanical changes in the vasculature may contribute to the depressor and organ protective effects of ACEI.

Acetylcholine↗

Enhancement effect of carteolol on the clonidine-induced vasodilation of rat mesenteric arteries.

It has demonstrated that carteolol can increase the endothelium-dependent vasodilation induced by alpha-2 adrenergic agonist. In order to evaluate the effect of carteolol, and to clarify the mechanism, we examined the effects of 10 microM carteolol on the vasodilation induced by increasing doses (10(-7)-10(-4) M) of clonidine in perfused rat mesenteric arteries preconstricted with 100 microM phenylephrine. Clonidine elicited a dose-dependent vasodilation of the mesenteric arteries preconstricted with phenylephrine. Carteolol enhanced the vasodilation induced by higher doses (10(-5) and 10(-4) M) of clonidine, although carteolol itself exerted no direct vasodilating effect. On the other hand, 10 microM propranolol or 10 microM metoprolol did not augment the clonidine-induced vasodilation. In the presence of 100 microM NG-monomethyl L-arginine (LNMMA), an analogue of L-arginine, the enhancement of the clonidine-induced vasodilation by carteolol was abolished. This inhibition by LNMMA was restored with 300 microM L-arginine, but not with 300 microM D-arginine. These results suggest that carteolol enhances the clonidine-induced vasodilation by an endothelial-related mechanism mediated by the release of endothelium-derived nitric oxide in resistance vessels.

Animals↗

Characteristics and expression of transforming growth factor-beta receptor subtypes on vascular smooth muscle cells from spontaneously hypertensive rats.

OBJECTIVE: To investigate the characteristics and expression of transforming growth factor (TGF)-beta receptor subtypes on vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. METHODS: The effects of TGF-beta 1 on DNA synthesis were evaluated by [3H]-thymidine incorporation into quiescent VSMC plated at high (5 x 10(4) cells/cm2) or low (5 x 10(3) cells/cm2) cell density. Specific binding of TGF-beta to VSMC was assessed by incubation of the cells with [125I]-TGF-beta 1. Affinity labelling of receptor subtypes was achieved by exposure of the cells to [125I]-TGF-beta 1 and cross-linking with disuccimidyl suberate. RESULTS: VSMC from SHR displayed a biphasic DNA synthesis response to TGF-beta 1 at high cell density, with DNA synthesis stimulated by low concentrations of TGF-beta 1 but not by high concentrations, whereas at low cell density there was a small increase in DNA synthesis in response to TGF-beta 1. TGF-beta 1 inhibited DNA synthesis in VSMC from WKY rats at both high and low cell densities. Binding assays revealed that VSMC from SHR had a larger number of TGF-beta receptors and a higher affinity for TGF-beta at high and at low cell densities. The affinity labelling with [125I]-TGF-beta 1 revealed the presence of receptor subtypes with relative molecular masses of 280-300, 85, 70, 60 and 50 x 10(3) on vascular smooth muscle cells from both rat strains at high cell density. The abundance of the 85 x 10(3) molecular mass receptor subtype was greater in VSMC from SHR. The 85 x 10(3) molecular mass receptor subtype was not detected on VSMC from either strain at low cell density. CONCLUSION: The present results suggest a different expression of TGF-beta receptor subtypes on VSMC from SHR and WKY rats. These differences may account for the exaggerated proliferative response of VSMC from SHR to TGF-beta.

Animals↗

Distinct expression of transforming growth factor-beta receptor subtypes on vascular smooth muscle cells from spontaneously hypertensive rats and Wistar-Kyoto rats.

1. We investigated the characteristics and expression of transforming growth factor-beta (TGFbeta) receptor subtypes on vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. 2. TGFbeta binding assays revealed that VSMC from SHR showed higher number and affinity of TGFbeta receptors than cells from WKY rats. 3. The affinity labelling with [125I]-TGFbeta1 revealed the presence of TGFbeta receptor subtypes with molecular sizes of 280, 85, 70 and 60kDa on VSMC from both strains at high cell density. The abundance of the 85kDa receptor subtype was greater in VSMC from SHR than cells from WKY rats. The 85kDa receptor subtype was not detected on VSMC from both strains at low cell density. 4. These results suggest distinct expression of TGFbeta receptor subtypes on VSMC from SHR and WKY rats, which may account for the exaggerated proliferative response of VSMC from SHR to TGFbeta.

Affinity Labels↗

Hemodynamic effects and pharmacokinetics of oral milrinone for short-term support in acute heart failure.

The present study evaluated the acute hemodynamic response, effects on subjective symptoms and physical findings, and the pharmacokinetics of a single oral dose (2.5, 5, or 10 mg) of milrinone in 31 patients with acute or decompensated heart failure. We found a significant increase in cardiac index (29, 31, and 29%, respectively, p < 0.01) and a significant decrease in pulmonary capillary wedge pressure (39, 43, and 47%, respectively, p < 0.01) accompanied with improvement in subjective symptoms and physical findings. These hemodynamic effects persisted for 4-8 h after each dosage of milrinone. Dose-dependent hemodynamic response was observed between the drug concentration and percent maximum changes in pulmonary capillary wedge pressure (peak milrinone concentration, 2.5 mg: 99.99 +/- 57.49, 5 mg: 187.11 +/- 71.37, and 10 mg: 300.94 +/- 158.5 ng/ml). The finding, together with results of the Prospective Randomized Milrinone Survival Evaluation (PROMISE) study, suggests lower dose of milrinone will be useful for the short-term inodilator support in patients with acute or decompensated heart failure.

Acute Disease↗

Thrombolytic therapy for acute myocardial infarction-effects, problems and strategies.

The effects and problems of coronary thrombolysis (CT) were investigated in 652 patients with initial acute myocardial infraction (AMI). Nosocomial mortality obtained by matching factors which determined prognosis was significantly lower in patients treated by CT (8.3%) than in those who did not undergo CT (18.1%). Regardless of whether the treatment was intracoronary arterial (ICT) or intravenous (IVCT), the primary cause of the decreased mortality was reperfusion of the coronary artery responsible for infarction (mortality 6.1% in the reperfused group vs 21.5% in the ineffective group). CT therapy improved left ventricular ejection fraction (LVEF), the nosocomial mortality rate, and regional wall motion at the site of infarction in cases that were reperfused less than 3 h, 3-6 h, and even 6 or more hours after the therapy. The long-term prognosis was significantly better in the reperfused group than in the ineffective group for 5 years and 7 months after therapy. However, CT was accompanied by both (1) poor prognosis in the ineffective group; and (2) unfavorable effects on the prognosis and on the daily life of patients with severe stenosis even after treatment. Accordingly, supplemental ICT and rescue PTCA (strategy (A)) were performed to treat the first problem, and deferred PTCA (strategy (B)) was conducted to treat the second problem in 80 patients with initial AMI. As a result, strategy (A) increased the coronary reperfusion rate to 94.3%, and strategies (A) and (B) together decreased the nosocomial mortality rate of 8.5% to 3.8%, and reduced the risk of death by 55.3%.

Humans↗

Effects of recombinant human erythropoietin (rHuEPO) on nutritional status of hemodialysis patients: investigation of direct anabolic effects of rHuEPO.

To investigate whether the nutritional improvement achieved by recombinant human erythropoietin (rHuEPO) treatment is the result of anemia correction with rHuEPO or the direct anabolic effects of rHuEPO per se, nutritional assessment was performed in 2 studies (study I and II) on hemodialysis (HD) patients. Nutritional assessment included blood biochemistry determinations, anthropometric measurements, daily protein intake (DPI) and dialysis efficiency. In study I, 5 HD patients who had not been given rHuEPO and had a hematocrit (Hct) of < or = 25%, were administered rHuEPO at the initial dose of 96.2 U/kgBW. Nutritional assessment of these patients was performed before rHuEPO treatment and every 4 weeks until the 24th week after rHuEPO treatment. In study II, the same nutritional assessment as in study I except for DPI, was performed in 2 groups with the same Hct level and dialysis regimen; an EPO group (n = 8) previously given rHuEPO (88.2 +/- 13.7 U/kgBW, 25.8 +/- 2.5 mos) and a non-EPO group (n = 8) not given rHuEPO. In study I, the mean Hct level was significantly increased 4 weeks after rHuEPO treatment (23.3 +/- 0.6 to 26.9 +/- 0.9%). However, the nutritional parameters and dialysis efficiency were nearly constant over 24 weeks, suggesting either the absence of a short-term direct anabolic effect of rHuEPO or masking of such an effect due to general condition improvement by anemia correction with rHuEPO. In study II, no significant differences in nutritional assessment were confirmed between the groups, suggesting that a long-term direct anabolic effect of rHuEPO may not exist and nutritional improvement may result from correction of anemia with rHuEPO.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Compensatory adrenal growth and steroidogenesis after unilateral adrenalectomy.

To examine the effect of unilateral adrenalectomy on compensatory growth and steroidogenesis in the remaining adrenal gland, we determined the tissue concentrations of protein, DNA and corticosterone in the remaining adrenal gland and the circulating corticosterone and ACTH concentrations at 1, 3, 5, 7 and 14 days after unilateral adrenalectomy in male rats. The remaining adrenal weight and total protein content increased steadily over the 14 days after the operation, while the plasma ACTH increased transiently on the 1st day. The adrenal total DNA level was not significantly changed after unilateral adrenalectomy, whereas the protein/DNA ratio was significantly increased by the 14th day. These findings suggest that compensatory growth is not induced by an increase in ACTH and that hypertrophy may occur rather than hyperplasia in the remaining gland. The serum corticosterone levels and corticosterone concentration in the remaining gland were significantly increased by the 3rd day, when the plasma ACTH levels returned to normal. The aldosterone/corticosterone ratio in the remaining gland did not change during the experiment. These results indicate that steroidogenesis stimulating factors other than ACTH may be present and stimulate rather the early stages than the late stages of steroidogenesis under conditions of unilateral adrenalectomy.

Adrenal Glands↗