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Biomedical subjects

Y Kudoh

Publications and source records attributed to Y Kudoh.

At least 91 records · Page 5Linked to original sources
PubMed1988

The dual effects of hemodialysis on cardiac function assessed by pulsed Doppler echocardiography.

To assess the effect of hemodialysis on cardiac function, a change of preload due to water removal was considered. In order to keep the preload constant during hemodialysis, extracorporeal ultrafiltration was induced before hemodialysis (step 1), and then hemodialysis without water removal was achieved (step 2). Cardiac performance in 8 patients was evaluated before and at the end of each step using pulsed doppler echocardiography. Step 1: Ultrafiltration was 1350 +/- 410 ml and hematocrit increased significantly. Left ventricular end-diastolic dimension (LVDd) decreased from 40.3 +/- 4.2 (mean +/- standard deviation) mm to 36.1 +/- 4.6 mm (p less than 0.005) and aortic peak flow velocity (PFV) also decreased from 59.9 +/- 16.0 cm/s to 49.0 +/- 11.0 cm/s (p less than 0.005). Step 2: In contrast, after hemodialysis without water removal, the mean velocity of circumferential fiber shortening (mVcf) increased from 1.36 +/- 0.26 circ/s to 1.86 +/- 0.36 circ/s (p less than 0.005). PFV and average acceleration (Aa) increased from 49.0 +/- 11.0 cm/s to 63.8 +/- 11.4 cm/s (p +/- 0.001) and from 750 +/- 220 cm/s/s to 1270 +/- 280 cm/s/s (p less than 0.001), respectively. During this step, serum potassium and osmolality decreased significantly. In conclusion, hemodialysis improves cardiac function under constant preload condition and this is due to the direct effects of hemodialysis by the correction of electrolytes and osmolar components such as uremic toxin.

Adult↗
PubMed1988

Benign ventricular tachycardia in systemic sarcoidosis--a case of false tendon.

A 22-year-old female patient was diagnosed as having systemic sarcoidosis with pulmonary, skin and ocular lesions, and ventricular tachycardia in resting ECG. Although cardiac sarcoidosis was strongly suspected at diagnosis, no clinical symptom such as palpitation or syncope developed during the three year observation period. Cardiac silhouette was unchanged in chest X-ray and 201thallium myocardial scintigraphy revealed no abnormality. Ventricular complex was suppressed by exercise or tachycardia. Two-dimensional echocardiogram showed abnormal fascicular bands attached from the mid-septum to the apex (false tendon). Therefore, it was concluded that this benign form of ventricular tachycardia might be due to the false tendon, rather than to the cardiac involvement of sarcoidosis. The cause of arrhythmia is important when evaluating the prognosis of a patient with a systemic disease.

Adult↗
PubMed1988

[Effects of guanfacine on the levels of cyclic nucleotides in anesthetized rat brain regions].

Effects of an antihypertensive drug, guanfacine, on brain regional cyclic AMP and cyclic GMP levels were studied in anesthetized rats. Cyclic nucleotides were analyzed in seven brain regions. Guanfacine decreased blood pressure and heart rate 20 min after administration. Yohimbine inhibited these hemodynamic effects of guanfacine. Guanfacine reduced cyclic AMP levels in the hypothalamus. The reducing effect of guanfacine on cyclic AMP was antagonized by yohimbine in the hypothalamus. Guanfacine lowered cyclic GMP in the cerebellum, medulla oblongata and hypothalamus. Yohimbine inhibited the effect of guanfacine on cyclic GMP in the cerebellum, medulla oblongata and hypothalamus. Prazosin showed no effect on guanfacine induced change of cyclic nucleotides in any brain region. From these results, it is concluded that guanfacine decreased cyclic AMP and cyclic GMP in the hypothalamus. In addition, it is suggested that alpha-2 adrenoceptors mainly modulate these changes of cyclic nucleotides.

Animals↗
PubMed1988

Effect of methotrexate on local cerebral blood flow in conscious rats.

The effect of methotrexate (MTX) on local cerebral blood flow (I-CBF) was studied with autoradiographic [14C]-iodoantipyrine methods in normal conscious rats. I-CBF was reduced by 30-57% in the rats given MTX (100 mg or 200 mg/body) as compared to that in the saline injected control group, but no dose-dependent effect was observed. The mechanism of I-CBF reduction by MTX was discussed.

Animals↗
PubMed1987

Sympathetically induced myocardial ischaemia causes the heart to release plasma kinin.

A recently developed highly sensitive radioimmunoassay method for detecting plasma kinin was used to re-evaluate the results of previous studies, in which plasma kinin had been measured with a bioassay method. To clarify the mechanism of plasma kinin release in global myocardial ischaemia the left main coronary artery was cannulated using a Griggs type autoperfusing cannula after pentobarbital anaesthesia in open chest dogs. The animals were divided into a non-coronary constricted group (n = 4) and a moderately coronary constricted group (n = 7). Cardiac sympathetic nerve stimulation (10 V, 4 Hz, 2 ms duration) was given to both groups. Haemodynamic recordings and blood samples were taken before and after coronary constriction as well as after sympathetic nerve stimulation. The arterial and coronary sinus plasma kinin concentrations were determined with the new radioimmunoassay method. After sympathetic nerve stimulation apparent myocardial ischaemia occurred and the plasma kinin concentration in coronary sinus blood increased significantly in the constricted group. In the non-constricted group, however, myocardial ischaemia did not appear and no significant change in coronary sinus plasma kinin concentrations was seen. These findings show that there was a pronounced release of plasma kinin from the heart when apparent myocardial ischaemia occurred.

Animals↗
PubMed1987

Study on the atherosclerosis mechanism in chronic hemodialysis.

In order to clarify whether hemodialysis treatment accelerates atherosclerosis, forty-two patients undergoing chronic hemodialysis were investigated. Because it is non-invasive and repeatable, aortic calcification on chest-XP was used as an index of atherosclerosis. No patients had evidence of calcified atherosclerosis at the start of hemodialysis therapy. The patients were divided into three groups according to vascular changes. Group 1 (20 patients) showed no calcification during the observation period. Group 2 (11 patients) had mild or moderate aortic calcification (thin linear aortic calcification). In group 3 (11 patients), massive and severe calcification was accelerated by hemodialysis. 18 parameters which might be considered to promote atherosclerosis were evaluated in each group. The age in group 3 was 53.8 +/- 10.4 (mean +/- standard deviation) years, which was older than the 42.1 +/- 12.6 year age in group 1 (p less than 0.025). Duration of dialysis in group 3 was 121.9 +/- 30.5 months, which was significantly longer than the 82.0 +/- 31.0 months in group 2 (p less than 0.01) and the 77.3 +/- 55.3 months in group 1 (p less than 0.025). Serum HDL-cholesterol levels in groups 2 (23.0 +/- 4.5 mg/dl) and 3 (20.9 +/- 6.6 mg/dl) were significantly lower than the 28.6 +/- 8.3 mg/dl in group 1, (p less than 0.025 and p less than 0.05, respectively). Serum parathormone-C level in group 3 was 14.7 +/- 8.6 ng/ml, which was significantly higher than the 6.1 +/- 6.0 ng/ml level in group 1 (p less than 0.01) and the 5.0 +/- 7.8 ng/ml level in group 2 (p less than 0.025). In discriminant analysis, age, duration of dialysis, hematocrit, serum HDL-cholesterol, parathormone-C, and alkaline phosphatase level were the independent factors used to distinguish the three groups. These findings suggest that 1) aging is a basal factor in the promotion of atherosclerosis, 2) hypo-HDL cholesterolemia is a major factor in the early phase of atherosclerosis, 3) hyperparathyroidism could have an important role in the late phase of atherosclerosis, 4) dialysis itself might promote atherosclerosis directly, and 5) blood pressure level is not major factor for atherosclerosis over a long observation period, at least in our study.

Adult↗
PubMed1987

Spatial and temporal characteristics of the transmural distribution of collateral flow and energy metabolism during regional myocardial ischemia in the dog.

To characterize the temporal and spatial characteristics of transmural gradients of flow, ATP and CP, dogs (n = 17) were subjected to coronary artery ligation for either 30 minutes or 24 hours. Different radioactive microspheres were given at the onset and end of the ischemic period. Simultaneous multiple transmural biopsies (up to 20 per heart) were obtained (in situ freezing) from central ischemic and surrounding normal tissue after either 30 minutes or 24 hours of elapsed ischemia. After lyophilization each biopsy was divided into up to 6 transmural sub-fragments, each of which was analysed for flow, ATP and CP. At the onset of ischemia flow declined to less than 15% throughout the ischemic zone and there was a slight transmural gradient of flow from epi- to endocardium (12.4 +/- 1.6, 13.5 +/- 2.0, 11.0 +/- 1.8, 10.3 +/- 1.7, 8.5 +/- 1.9 and 8.3 +/- 3.1% of non-ischemic tissue). After 30 minutes of ischemia, collateral flow to the epicardial tissue had increased substantially but endocardial flow remained unchanged, the epi- to endo- gradient was 20.8 +/- 2.5, 18.9 +/- 2.4, 13.7 +/- 2.1, 10.8 +/- 1.5, 8.5 +/- 1.2, 7.6 +/- 1.7. After 24 hours there were further increases in the epi- and mid- myocardial regions but the endocardial flow remained severely depressed, the epi- to endo- gradient was 23.9 +/- 3.2, 24.5 +/- 3.0, 23.6 +/- 4.8, 16.4 +/- 3.3, 9.8 +/- 2.9, 5.8 +/- 2.9%. ATP and CP were severely depressed after 30 minutes of ischemia and reflected flow closely with sharp linear epi- to endo- gradients (17.5 to 10.9 muMol/g dry wt for ATP and 7.4 to 3.1 muMol/g dry wt for CP). After 24 hours, the decline in ATP had been slowed and there was a striking recovery of CP in the epi- and mid- myocardial regions which had experienced increasing collateral flow. CP in the endocardium remained severely depressed. Progressive supplementation of collateral flow early and throughout a 24 hour period of regional myocardial ischemia and the selective delivery of this flow to subepi- and mid- myocardial tissue accounts in part for the natural salvage of this tissue and the deterioration of the endocardium to necrosis. Gradients of flow and metabolism further influence these events and account for the "wave front" of cell death.

Adenosine Triphosphate↗
PubMed1986

Calcium antagonists and evolving myocardial infarction: studies of the effects of nifedipine on tissue ATP, collateral flow and infarct size in the closed chest dog.

In previous studies nifedipine has been shown to limit infarct size during 24 h of regional ischemia in the dog. Using a closed chest embolization procedure, autoradiographic (141-cerium at onset of ischemia) microsphere risk zone analysis and tetrazolium staining, the ability of nifedipine to influence collateral flow, energy metabolism and infarct size over 48 h was assessed in the dog. A second microsphere (46-scandium), which did not interfere with the autoradiography, was given after 48 h of ischemia to allow temporal changes in flow to be assessed. Transmural biopsies, taken after 48 h from non-ischemic tissue, ischemic tissue which had become necrotic and ischemic tissue which had survived (tetrazolium-positive tissue within the risk zone) were assayed for flow, adenosine triphosphate (ATP) and creatine phosphate (CP). The results indicate: nifedipine may still afford some small degree of protection up to 48 h of elapsed ischemia, (infarct size as a percent of risk zone size was 86.1 +/- 3.0 in control vs 70.4 +/- 4.5 in drug group (p less than 0.025 n = 9 in each group), 'salvage' in both the control and the nifedipine-treated groups was predominantly subepicardial and in the transmural plane. The extent and location of salvage and necrosis was determined by the epicardial to endocardial distribution of collateral flow. In tissue which was destined to necrosis (mainly in the subendocardium) collateral flow at the onset of ischemia (7.2 +/- 1.2% relative to surrounding non-ischemic tissue) did not increase over 48 h (8.0 +/- 1.4) whereas in tissue which was 'salvaged' (mainly in the subepicardium) flow was greater (27.4 +/- 3.2%) at onset of ischemia) and increased substantially (to 64.6 +/- 5.9%) over 48 h; nifedipine does not increase the amount of flow per g of tissue in salvaged tissue but rather it may increase the amount of tissue receiving sufficient flow to promote salvage; it follows that in nifedipine-treated animals more flow is delivered to the ischemic zone; tissue ATP and CP parallel flow and the results support the concept of a critical threshold of flow (approx. 25% at onset of ischemia) below which tissue eventually deteriorates to necrosis and above which tissue is likely to amenable to salvage. However, for sustained survival this flow level must eventually increase to above 40-50%. In conclusion, while nifedipine can achieve a substantial delay in the onset of tissue necrosis, for sustained salvage there must be early and substantial reflow to the tissue.

Adenosine Triphosphate↗
PubMed1985

Studies on experimental coronary insufficiency. Effect of L-carnitine on myocardial ischemia produced by sympathetic-nerve stimulation with high plasma fatty acids.

Our previous studies revealed that sympathetic-nerve stimulation (SNSt) plays an important role in the precipitation and the augmentation of myocardial ischemia in dogs with coronary constriction. To clarify the underlying mechanism of the detrimental effect of free fatty acids (FFA) at a high plasma concentration and the beneficial effect of L-carnitine on myocardial ischemia, ischemic changes following SNSt were compared among three groups of dogs with mild or moderate coronary constriction: a saline control group, an intralipid [(IL) 0.1 ml/kg per min + heparin 5 mg/kg] group, and an IL + L-carnitine (200 mg/kg) group. High plasma concentration of FFA aggravated the ischemic changes induced by SNSt in dogs with coronary constriction, in which no signs of increase in myocardial oxygen consumption were seen. L-Carnitine clearly alleviated the mechanical dysfunction, acceleration of anaerobic metabolism, depletion of myocardial contents of high-energy phosphates, myocardial accumulation of lactate, and ECG ischemic changes that were augmented by high plasma FFA in the coronary-constricted dogs with SNSt. From these findings, it was suggested that an increased plasma FFA might aggravate myocardial ischemia, at least, produced by SNSt in dogs with mild or moderate coronary constriction and that L-carnitine might improve the ischemia augmented by FFA, presumably by reducing myocardial accumulation of FFA intermediates.

Animals↗
PubMed1983

The role of L-carnitine in the pathogenesis of cardiomegaly in patients with chronic hemodialysis.

Many reports have suggested that cardiac dysfunction with cardiomegaly is more often observed in patients with chronic hemodialysis. Moreover, cardiac dysfunction has been thought as one of the most important factors affecting the prognosis of these patients. In this study, in order to clarify the role of l-carnitine in the pathogenesis of cardiomegaly, 33 patients with chronic hemodialysis were studied using the multivariate analysis method. Among the factors which may affect cardiac function, the following 10 variables were examined. 1) age, 2) duration of dialysis, 3) plasma carnitine, 4) serum total cholesterol, 5) serum HDL-cholesterol, 6) triglyceride, 7) systolic blood pressure, 8) diastolic blood pressure, 9) left ventricular voltage on a electrocardiogram at rest and 10) hematocrit. The plasma carnitine levels in these patients were markedly reduced and inversely correlated with the cardiothoracic ratio (CTR) on the chest X-ray films (r = 0.38, p less than 0.05). In principal component analysis, the CTR was closely related to hematocrit and plasma carnitine levels. By multiregression analysis, both hypo-carnitinemia and anemia were independently shown to be important causes of cardiomegaly. Thus, it is suggested that the cardiomegaly in patients with chronic hemodialysis may be improved by supplemental therapy with l-carnitine, even in cases with severe anemia.

Adolescent↗