Biomedical subjects

K Ueshima

Publications and source records attributed to K Ueshima.

At least 73 records · Page 4Linked to original sources

PubMed1991

The prognostic value of exercise capacity: a review of the literature.

While there is still much debate in the literature regarding the specific MET levels at which there are differences in survival, the following points have become clear with the growing body of reports in the literature. Exercise capacity seems to be an independent predictor of mortality, and when it is combined with other clinical, exercise, or angiographic data, it becomes very powerful in this regard. This relates to both overall mortality and to that from cardiovascular disease. There is still a need for the establishment of mortality data related to MET levels adjusted for age and activity status. A low exercise capacity of less than 6 METs indicates a higher mortality group, probably regardless of the underlying extent of coronary disease or left ventricular function. Analysis of the CASS data has indicated that these patients benefit from coronary artery bypass surgery with respect to survival. An exercise capacity of greater than 10 METs designates an excellent survival group, again despite the extent of coronary artery disease or left ventricular function. If 10 METs truly exerts a "protective effect" that obviates any survival benefit from coronary artery bypass surgery, this has enormous implications for cost containment and medical care. It is nonetheless important to remember that this level of exercise capacity does not imply the absence of either coronary disease or triple-vessel coronary disease. Exercise capacity is related to more than just cardiovascular fitness and integrity. It is dependent upon a combination of other physiologic components as well, including pulmonary function, health status of other organ systems, nitrogen balance, nutritional status, medications, orthopedic limitations, and others.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular Diseases↗

PubMed1991

Role of capsaicin-sensitive afferent neurons in alkaline secretory response to luminal acid in the rat duodenum.

The role of capsaicin-sensitive afferent neurons in acid-induced HCO3- secretion was investigated in the duodenum of anesthetized rats. The proximal duodenum was perfused with saline (pH 4.5), the pH of perfusate and the transmucosal potential differences were continuously monitored, and HCO3- output was determined by pH change. Under these conditions, duodenal pH, potential difference, and HCO3- output were significantly increased in response to IV injection of prostaglandin E2 (300 micrograms/kg) and luminal acidification (10 mmol/L HCl, 10 minutes). These responses induced by luminal acid were significantly attenuated by SC pretreatment with indomethacin (5 mg/kg), preexposure of the mucosa to lidocaine (4%, 15 minutes), functional ablation of capsaicin-sensitive afferent neurons, or even prior application of capsaicin (6 mg/mL, 30 minutes) to the duodenum. Although capsaicin application by itself (0.3-6 mg/mL) produced a concentration-dependent increase of HCO3- output, this effect was significantly reduced by lidocaine, indomethacin, or chemical deafferentation and exhibited a tachyphylaxis after repeated application at a high concentration (6 mg/mL). Neither of these treatments significantly affected the HCO3- response induced by prostaglandin E2. It was concluded that stimulation of capsaicin-sensitive afferent neurons increased duodenal HCO3- secretion and that these neurons may be involved in the mechanism of HCO3- response induced by luminal acid in the duodenum.

Animals↗

PubMed1991

Oxygen free radicals and lipid peroxidation in the pathogenesis of gastric mucosal lesions induced by indomethacin in rats. Relation to gastric hypermotility.

The relationship of gastric hypermotility to mucosal hemodynamics, lipid peroxidation and vascular permeability changes was investigated in the pathogenesis of indomethacin-induced gastric lesions in rats. Subcutaneous administration of indomethacin (25 mg/kg) produced an increase in both the amplitude and frequency of stomach contraction from 30 min after treatment, resulting in hemorrhagic damage 2 h later. Gastric mucosal blood flow measured by a Laser flowmetry showed oscillatory fluctuations under hypercontractile states: a decrease during contraction followed by an increase during relaxation. Mucosal lipid peroxidation and vascular permeability were significantly increased with time after indomethacin treatment, and these changes preceded the appearance of hemorrhagic damage. All these events were prevented when gastric hypermotility was inhibited by atropine or 16,16-dimethyl prostaglandin E2. Pretreatment of the animals with allopurinol and hydroxyurea or continuous infusion of superoxide dismutase and dimethyl sulfoxide during a test period also attenuated these functional changes and mucosal lesions induced by indomethacin, without affecting the motility response. We conclude that oxygen free radicals may play a role in the development of mucosal lesions associated with gastric hypermotility in indomethacin-treated rats.

16,16-Dimethylprostaglandin E2↗

PubMed1991

Gastric motility changes in capsaicin-induced cytoprotection in the rat stomach.

We have examined the effect of orally administered capsaicin on gastric motility in the rat to investigate a possible relationship between motility change and cytoprotection induced by this agent. Capsaicin, given orally (1-30 mg/kg), dose-dependently inhibited hemorrhagic band-like lesions induced by ethanol (60% in 150 mM HCl). This protection was significantly mitigated by desensitization of afferent neurons following capsaicin pretreatment 2 weeks before the experiment, and it was also significantly attenuated by prior administration of indomethacin, but not by spantide. Intragastric administration of capsaicin (30 mg/kg) significantly inhibited gastric motility and increased the mucosal blood flow, but had no effect on the transmucosal potential difference of the stomach. These functional changes induced by capsaicin were also less marked in the afferent neuronal desensitized rat, and they were significantly attenuated by indomethacin but not by spantide. These results suggest that the mucosal protection by intragastric capsaicin may be associated with the inhibition of gastric motility and the increase of mucosal blood flow. These responses may be induced by activation of primary afferent neurons which are probably sensitized by endogenous prostaglandins.

Animals↗

PubMed1991

Capsaicin-sensitive afferent neurons in adaptive responses of the rat stomach induced by a mild irritant.

Exposure of rat stomach to 1 M NaCl reduced the transmucosal potential difference (PD) followed by an increase of luminal pH and gastric mucosal blood flow (GMBF). Desensitization of capsaicin-sensitive afferent neurons significantly mitigated the increase in GMBF without affecting PD and pH responses. Mucosal application of capsaicin increased GMBF with no effect on PD and pH. The findings suggest that capsaicin-sensitive afferent neurons may be involved in the regulatory mechanism of GMBF responses induced by a mild irritant.

Adaptation, Physiological↗

PubMed1991

Duodenal ulcers induced by diethyldithiocarbamate, a superoxide dismutase inhibitor, in the rat: role of antioxidative system in the pathogenesis.

Pathogenesis of duodenal ulcers induced by diethyldithiocarbamate (DDC), a superoxide dismutase (SOD) inhibitor, was investigated in the rat. Repeated s.c. administration of DDC (750 mg/kg) every 12 hr induced duodenal ulcers in the fed rats, and the severity of the ulcers reached the maximum after three injections. DDC not only reduced basal acid output but also impaired duodenal alkaline secretion. These ulcers were significantly prevented by antioxidative agents such as SOD (50000 units/kg, s.c.), allopurinol (50 mg/kg, s.c.) or glutathione (200 mg/kg, s.c.) as well as the antisecretory agent cimetidine (100 mg/kg, s.c.). The impaired HCO3- response caused by DDC was partially but significantly reversed by either SOD (15000 units/kg/hr, i.v.), allopurinol or glutathione; and SOD by itself significantly elevated the rate of basal alkaline secretion. 16,16-Dimethyl prostaglandin E2 (10 micrograms/kg, s.c.) increased duodenal HCO3- output in the presence of DDC and significantly prevented the development of duodenal ulcers in response to DDC. These results suggest that the mucosal antioxidative system including SOD may play a role in the regulatory process of alkaline secretion and contribute to the mucosal defensive ability in the duodenum. The insufficiency of this system may be involved in the pathogenesis of DDC-induced duodenal ulcers.

Allopurinol↗

PubMed1991

[Non-supervised home exercise programs in a convalescent phase of acute myocardial infarction: their effectiveness and the usefulness of the heart rate at the anaerobic threshold].

The effectiveness of 2 different exercise programs in the convalescent phase of acute myocardial infarction (AMI) was assessed. One hundred and five patients with AMI were enrolled for one of these 2 non-supervised home exercise programs immediately after discharge from the hospital. Before discharge and one month later, they underwent submaximal graded treadmill exercise tests with the application of expiratory gas analysis. All patients were assigned to perform 2 km of walk-jog exercise daily for one month. The heart rate during exercise, duration of exercise and the total steps during 24 hrs were measured. Eighty patients (group A) underwent the exercise program in which their heart rates were maintained at 100-110 beats/min during exercise; while 25 patients (group B) underwent the other program in which their heart rates were maintained at 90-100% of those obtained at their anaerobic threshold (AT). The ventilatory AT was calculated by the standard technique using the Horizon System. In group A, AT increased from 13.4 ml/min/kg to 15.1 ml/min/kg (p < 0.01) after the exercise program and in group B, from 12.8 ml/min/kg to 14.9 ml/min/kg (p < 0.01). In group B, AT increased in all patients, while it remained unchanged in 30% of the patients in group A (p < 0.01). In conclusion, a non-supervised home exercise program can be effective and easily instituted for rehabilitation in a convalescent phase of AMI. The program using 90-100% of the heart rates at the anaerobic threshold seemed to be more suitable for obtaining better effects on exercise tolerance than that using 100-110/min heart rate.

Aged↗

PubMed1991

Stimulation of gastric bicarbonate secretion by an analog of thyrotropin-releasing hormone, YM-14673, in the rat.

The effects of YM-14673, a thyrotropin-releasing hormone analog, on gastric alkaline secretion were investigated in the anesthetized rat pretreated with omeprazole (60 mg/kg, intraperitoneally) by measuring the luminal pH, transmucosal PD and HCO3- output. The whole stomach was perfused at a flow rate of 0.7 ml/min with saline (pH 4.5) in the absence of acid secretion, the pH of the perfusate and PD were continuously monitored and the HCO3- output was measured as acid-neutralizing capacity by back-titration of the perfusate to pH 4.5. YM-14673, given intravenously at the doses (0.1-1 mg/kg) that stimulated acid secretion, increased the pH and HCO3- output in a dose-dependent fashion, but did not significantly affect the PD. Prostaglandin E2 (1 mg/kg) elevated the pH and HCO3- output with concomitant decrease in the PD, whereas carbachol (4 micrograms/kg), similar to YM-14673, produced an increase of the pH and HCO3- output with no change in the PD. The net HCO3- output (4.3 +/- 0.3 muEq) induced by 0.3 mg/kg of YM-14673 was about 60 and 150% of that induced by prostaglandin E2 and carbachol, respectively. The increased pH and HCO3- responses caused by YM-14673 were almost completely abolished by vagotomy, significantly inhibited by atropine (0.3 mg/kg, intravenously) and indomethacin (5 mg/kg, subcutaneously) but not affected by pirenzepine (1 mg/kg, intravenously). These results suggest that YM-14673, a thyrotropin-releasing hormone analog, produced vagally mediated HCO3- secretion in the rat stomach, and the mechanism may involve the cholinergic system, which is mediated with muscarinic M2 receptors and interacts with endogenous prostaglandins.

Animals↗

PubMed1991

[Clinical significance of ST segment shifts during chest pain in predicting the pathogenesis of impending myocardial infarction].

To know whether the pathogenesis of impending myocardial infarction(IMI) could be predicted by the direction of ST segment shifts during an ischemic chest pain, we studied 62 patients with IMI and undergoing emergent coronary angiography(CAG). They were selected from a consecutive number of 474 patients with unstable angina. IMI was defined when patients had more than 2 episodes of chest pain at rest under intensive pharmacological interventions after their CCU admission, and at least one of those was not relieved by nitroglycerin given intravenously. They were divided into 2 groups according to ST segment shifts during chest pain; 35 patients with ST elevation (G-1) and 27 patients with ST depression (G-2). The time of CAG was individually determined in each patient according to the severity of illness. Those with acute MI within 3 months before the study and 24 hours following the chest pain just before CAG were excluded from the study. New onset angina accounted for 49% in G-1 and 4% in G-2(p less than 0.01). Average history length of IMI, frequency of symptoms after CCU admission, and interval from the last symptom to CAG were similar in each groups. Single vessel disease was more predominant in G-1 than in G-2 (54% vs 11% p less than 0.01). Intracoronary thrombus(IT) in an ischemia related artery(IRA) was found in 97% of G-1 and 22% of G-2(p less than 0.001), while complex lesions(CL) proposed by Ambrose as another genesis of IMI were in 26% of G-1 and 74% of G-2(p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina, Unstable↗

PubMed1990

Determination of gastroduodenal alkaline responses in the rat.

We set up a new system for measuring the gastroduodenal HCO3- responses using pH change and potential difference (PD) in the anesthetized rat. The stomach or the proximal duodenum was perfused at the flow rate of 0.7 mL/min with saline (pH 4.5), the pH of the perfusate and PD were continuously monitored, and HCO3- output was determined by back-titrating the perfusate and by measuring the area of pH change. In the case of the stomach, acid secretion was inhibited by omeprazole (60 mg/kg, i.p.). Output of both pH and HCO3- in these tissues was significantly increased by intravenous administration of prostaglandin (PGE2), 16, 16-dimethyl PGE2, carbachol, and YM-14673 (a thyrotropin-releasing hormone (TRH) analog), whereas the PD responded to these agents by a significant rise in the duodenum and decrease in the stomach. These parameters also responded to physiological stimulation such as mucosal acidification. When the area of pH change caused by various agents was plotted against the net amount of HCO3- output determined from back-titration, a significant relationship was found between these two factors (r = 0.98). These results indicate that this system using pH change may be useful for quantitative determination of HCO3- response in the gastroduodenal mucosa.

Animals↗

PubMed1990

Management and evaluation of non-supervised home exercise program in a convalescent phase of acute myocardial infarction.

Out of 636 patients with acute myocardial infarction (AMI) admitted to our institution, 183 patients enrolled in our non-supervised home exercise program immediately after their discharge from the hospital. The first 40 patients were randomized to control and training group, while the remaining 143 patients were included in the training group. Before and after the trial, all patients underwent cardiopulmonary exercise testing; submaximal graded treadmill exercise test with the application of expiratory gas analysis. In the training group, patients performed 2 km walk-jog exercise everyday for 1 month, keeping their heart rate (HR) at 90-100% of that in the anaerobic threshold. HR during exercise was monitored by patients themselves, using HR-meter. The anaerobic threshold significantly increased in the training group; while control group had no significant changes. VO2 and HR significantly increased at the same Borg's indices. Psychological improvement was also obtained in the training group compared to control group. It is concluded that non-supervised home exercise program is effective and easily applicable in the convalescent phase of AMI.

Aged↗

PubMed1989

Clinical and prognostic significance of silent myocardial ischemia in survivors after acute myocardial infarction.

To clarify the clinical and prognostic significance of silent myocardial ischemia (SMI) after acute myocardial infarction (MI), the clinical characteristics and long-term prognosis after discharge in 525 medically treated survivors after acute MI were investigated. According to the presence of post-infarction angina and results of all exercise tests during hospitalization, 309 patients without ischemic episodes were classified into control group, 59 patients with SMI into SMI group and 157 patients with post-infarction angina into AP group. Previous MI (29%, 24%, 11%, respectively), non-Q wave MI (34%, 34%, 15%) and multivessel disease (69%, 61%, 33%) were more frequent in the SMI and AP groups than in the control group. These indicated clinical characteristics in patients with SMI were similar to those in patients with angina pectoris. The incidence of angina prior to MI onset in patients with SMI was lower than in patients with post-infarction angina. This may suggest that there is some common mechanism keeping them silent in the pre- and post-MI period. During the mean follow-up period of 5.5 years, 93 patients died and 78 had a recurrent MI. Cumulative total and cardiac mortality, and incidence of recurrent MI by actuarial method were higher in the SMI as well as AP group than in the control group. There was no statistically significant difference in prognosis between SMI and AP group. We conclude total ischemic burden, not only symptomatic but SMI, should be treated using currently available therapeutic modalities for further improvement of long-term prognosis in survivors after acute MI.

Actuarial Analysis↗

PubMed1989

Neurotransmitter release and vascular responsiveness in mesenteric vasculatures from two-kidney, one-clip Goldblatt hypertensive rats.

In order to investigate the peripheral neuroeffector functions of renal hypertension, norepinephrine release from the sympathetic nerve endings and vascular responsiveness were evaluated in the mesenteric vasculatures from two-kidney, one-clip Goldblatt hypertensive rats (2K, 1C-HT). Norepinephrine release and pressor responses during periarterial nerve stimulation (40 V, 5 msec rectangular pulses for 1 min, 5, 10 and 15 Hz) were unchanged during the acute phase (3 weeks after surgery), and were rather reduced during the chronic phase (7-8 weeks after surgery) in 2K, 1C-HT compared to sham-operated normotensive control rats. By contrast, the vasoconstrictor responses to exogenously applied norepinephrine were significantly greater in 2K, 1C-HT than in the normotensive controls. From these observations, it seems unlikely that peripheral adrenergic function in the blood vessels plays an important role in the pathogenesis of 2K, 1C-HT. However, the increased sensitivity of vascular smooth muscle cells to norepinephrine may contribute to the maintenance of high blood pressure in the face of reduced vascular sympathetic tone in this form of hypertension.

Animals↗

PubMed1989

[Efficacy of home exercise program in a convalescent phase of acute myocardial infarction evaluated by Borg's indices, expiratory gas analysis and blood lactate].

The Borg's indices, the rate of perceived exertion have been widely accepted to evaluate subjective symptoms semi-quantitatively in exercise tests. We applied the indices to evaluate the efficacy of our home exercise program in patients with acute myocardial infarction. Eighty-five patients were entered in our home exercise program after their discharge from the hospital. This program consisted of everyday 2 km walk-jog exercise for 1 month keeping their heart rate at 100-110/min during the exercise. Before and 1 month after their discharge, they underwent treadmill exercise tests with expiratory gas analysis and a measurement of blood lactate. In the treadmill tests performed before and after the training, VO2 and heart rate increased linearly with Borg's indices, however VE and blood lactate had disproportionate increases after Borg's 13 which is considered to be the anaerobic threshold (AT). In fact, AT measured individually by expiratory gas analysis and blood lactate, appeared at Borg's 13 in 53% of the patients. After 1 month physical training, VO2 and heart rate significantly increased at the same Borg's indices, but there was no significant changes in blood lactate at the same Borg's score before and after the training. These results suggest that, in patients with acute myocardial infarction, exercise performance significantly increased at any score of subjective symptoms and that Borg's indices may reflect the blood lactate levels. It is concluded that Borg's indices, closely related to the dynamics of blood lactate, are not only useful in quantifying subjective symptoms but also to estimate the efficacy of physical training.

Adult↗

PubMed1988