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Biomedical subjects

K Ueshima

Publications and source records attributed to K Ueshima.

At least 55 records · Page 3Linked to original sources
PubMed1994

A case of orthostatic and postexertional hypotension with ischemic electrocardiographic changes.

A case of orthostatic and postexertional hypotension with ischemic electrocardiographic changes is reported. The etiology was considered to be the partial dysfunction of efferent sympathetic nerve endings. Peripheral adrenergic receptors (alpha and beta) were up-regulated, which might have caused pseudoischemic electrocardiographic changes and abnormal vasodilation after exercise.

Autonomic Nervous System Diseases↗
PubMed1993

Prediction of cardiovascular death in men undergoing noninvasive evaluation for coronary artery disease.

OBJECTIVE: To develop prediction rules from clinical and exercise test data identifying patients at high and low risk for cardiovascular events among a group of male veterans. DESIGN: Prognostic study with prospective gathering of data and routine follow-up of consecutive patients referred for exercise testing. Patients only underwent noninvasive evaluation for coronary artery disease. No validation cohort is yet available. SETTING: A 1200-bed Veterans Affairs Medical Center. PATIENTS: Of 3609 men referred for exercise testing between 1984 and 1990, 2546 patients remained evaluable after exclusion of those who underwent subsequent cardiac catheterization, those with significant valvular heart disease, and those who had previous coronary artery bypass surgery. MEASUREMENTS: Evaluation included recording of clinical data on a standardized form and a standard treadmill test followed by assessment of cardiovascular events. RESULTS: During a mean follow-up period (+/- SD) of 2.75 (+/- 18) years, 119 cardiovascular deaths and 44 nonfatal myocardial infarctions occurred in 2546 patients. The Cox proportional hazards model showed the following characteristics to be statistically independent predictors of time until cardiovascular death: history of congestive heart failure or digoxin use, exercise-induced ST depression, change in systolic blood pressure during exercise, and exercise capacity. Using a simple score based on one item of clinical information (history of congestive heart failure or digoxin use) and three exercise test responses (ST depression, exercise capacity, and change in systolic blood pressure), 77% of patients were categorized as low risk (annual cardiac mortality rate, less than 2%), 18% as moderate risk (annual cardiac mortality rate, 7%), and 6% as high risk (annual cardiac mortality rate, 15%; hazard ratio, 10; 95% confidence interval, 6 to 17). This model has not yet been validated. CONCLUSIONS: Variables available from the usual non-invasive work-up of patients with known or suspected coronary artery disease can be used to predict future risk for cardiovascular death.

Aged↗
PubMed1993

Prediction of cardiovascular death by means of clinical and exercise test variables in patients selected for cardiac catheterization.

The objective of this report is the development of a population-specific prediction rule based on clinical and exercise test data that would estimate the risk of cardiovascular death in patients selected for cardiac catheterization. Prospective data and follow-up information were obtained from patients who underwent cardiac catheterization soon after clinical assessment and exercise testing. Males (n = 588) referred for evaluation of coronary heart disease from 1984 to 1990 were selected after exclusion of patients with significant valvular heart disease and patients with prior cardiac surgery. Half had a prior myocardial infarction and half complained of typical angina pectoris. All patients performed a treadmill test and were selected for clinical reasons to undergo coronary angiography within 3 months. Over a mean follow-up period of 2.5 years (+/- 1.4 years), there were 39 cardiovascular deaths and 45 nonfatal myocardial infarctions. The Cox proportional hazards model demonstrated the following characteristics to be statistically significant independent predictors of time until cardiovascular death: history of congestive heart failure (hazards ratio of 4), ST depression on the resting ECG (hazards ratio of 3), and a drop in systolic blood pressure below the resting value during exercise (hazards ratio of 5). Exercise-induced ST depression was not associated with either death or nonfatal myocardial infarction. A simple score based on one item of clinical information (history of congestive heart failure), a resting ECG finding (ST depression), and an exercise test response (exertional hypotension) stratified our patients for 4 years after testing from 75% with a low risk (annual cardiac mortality rate of 1%), 17% with a moderate risk (annual mortality rate of 7%), and 1% with a high risk (annual cardiac mortality rate of 12%, with a hazards ratio of 20 and 95% confidence interval from 6 to 70X). It was concluded that the variables available from the usual noninvasive workup of patients with known or suspected coronary artery disease enable prediction of risk of cardiovascular death. Three quarters of those usually undergoing cardiac catheterization can be identified by simple noninvasive variables as being at such low risk that invasive intervention is unlikely to improve prognosis.

Aged↗
PubMed1993

Hemodynamic determinants of exercise capacity in chronic atrial fibrillation.

To evaluate the response of patients with chronic atrial fibrillation (AF) to exercise, 79 male patients (mean age 64 +/- 1 years) with AF underwent resting two-dimensional and M-mode echocardiography and symptom-limited treadmill testing with ventilatory gas exchange analysis. Patients were classified by underlying disease into five subgroups: no underlying disease (LONE: n = 17), hypertension (HT: n = 11), ischemic heart disease (n = 13), cardiomyopathy or history of congestive heart failure (CHF: n = 26), and valvular disease (n = 12). A higher maximal heart rate than expected for age was observed (175 vs 157 beats/min), which was most notable in the LONE and HT subgroups. Maximal oxygen uptake (VO2 max) was lower than expected for age in all groups. Patients with CHF had a lower resting ejection fraction than all other patients (p < 0.001), a lower VO2 max, and a lower maximal heart rate than LONE and HT patients (p < 0.001). Stepwise regression analysis demonstrated that echocardiographic measurements at rest were poor predictors of VO2 max and VO2 at the ventilatory threshold. Among clinical, morphologic, and exercise variables, maximal systolic blood pressure accounted for the greatest variance in exercise capacity, but it explained only 35%. In patients with AF the higher than predicted maximal heart rates may be a compensatory mechanism for maintaining exercise capacity after the loss of normal atrial function. However, even in the absence of underlying disease, it does not appear to compensate fully for a compromised exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Nomogram based on metabolic equivalents and age for assessing aerobic exercise capacity in men.

OBJECTIVES: The goal of this study was to create a nomogram, based on maximal exercise capacity (in metabolic equivalents [METs]) and age, for assessing a patient's ability to perform dynamic exercise to quantify the level of physical disability or relative capacity for physical activity. BACKGROUND: Providing an estimation of exercise capacity relative to age is clinically useful. Such an estimate can be derived from measured or estimated maximal oxygen uptake (in METs) from treadmill exercise testing and age. It is an effective means of communicating to patients their cardiopulmonary status, encouraging improvement in exercise capacity and quantifying disability. METHODS: Exercise test results of 1,388 male patients (mean age 57 years, range 21 to 89) free of apparent heart disease who were referred for exercise testing for clinical reasons were retrospectively reviewed. This referral group as well as subgroups of active (n = 346) and sedentary (n = 253) patients were analyzed to determine norms for age and for age by decades for exercise test responses, including METs, maximal heart rate and maximal systolic blood pressure. Regression equations were calculated from this information, and a nomogram for calculating degree of exercise capacity from age and MET level achieved by a patient was created. A similar analysis was performed in a separate group of 244 apparently healthy, normal male volunteers (mean age 45 +/- 14 years, range 18 to 72) who underwent exercise testing with direct measurement of expired gases. RESULTS: Equations for predicted METs for age were derived for the entire clinical referral group (METs = 18.0-0.15[Age]) and for the subgroups of active (METs = 18.7-0.15[Age]) and sedentary (METs = 16.6-0.16[Age]) patients. All results achieved statistical significance, with p values < 0.001. In the volunteer group of normal men who performed exercise testing with ventilatory gas exchange, the decline in maximal heart rate and METs with age was not as steep as in the referral group. Although the normal group confirmed nomograms published previously among similar subjects, the equations derived from the patients differed from those previously reported; in contrast to previous studies using healthy volunteers, the equations and nomograms for the referral group are more appropriate for patients typically referred for testing in a hospital or office-based internal medicine practice. CONCLUSIONS: Norms for METs based on age are presented as well as population-specific nomograms that enable physicians to assess patients' exercise capacity relative to their age group.

Adult↗
PubMed1993

Predictors of disease severity and survival in patients with coronary artery disease.

BACKGROUND: The objective of this study was to determine whether coronary angiographic findings and survival could be predicted using standard clinical and exercise-test data. METHODS: Five hundred and ninety-five men who had undergone both exercise treadmill testing and cardiac catheterization were followed for up to 5 years. Left main (LM) disease (> or = 50% stenosis) was present in 42 patients, whereas 30 patients had LM equivalent disease (> or = 70% stenosis of both the proximal left anterior descending and circumflex coronary artery disease (n = 152), one-vessel disease (n = 186), two-vessel disease (n = 118), three-vessel disease (n = 67), LM or LM equivalent disease without significant (> or = 70%) right coronary artery involvement (n = 26), and LM or LM equivalent disease with right coronary artery involvement (n = 46). RESULTS: ST-segment depression was more marked, whereas ejection fraction, maximal heart rate, maximal systolic blood pressure, and exercise capacity were lower in each group as disease severity worsened. Using Kaplan-Meier analysis, the subgroup with the poorest survival was found to be those with LM or LM equivalent disease with right coronary artery disease, and the next worse was the three-vessel disease group, in which survival was poorer than in all other subgroups (P < 0.01). Stepwise regression analysis revealed that the most powerful predictor for coronary artery disease severity was exercise-induced ST depression (P < 0.001), but it predicted survival poorly. History of congestive heart failure, low ejection fraction (50% or lower), and poor exercise capacity (5 metabolic equivalents or less) emerged as strong predictors of survival using stepwise Cox regression analysis (P < 0.001). CONCLUSION: Exercise-induced ST depression predicted the severity of angiographic disease but not survival, whereas the strongest predictors of survival were history of congestive heart failure, low ejection fraction, and poor exercise capacity.

Adult↗
PubMed1993

Endogenous sulfhydryls in healing gastric mucosal injury induced by HCl in the rat.

The role of endogenous sulfhydryls (SH) in the healing of HCl-induced gastric injury was investigated in the rat. The animals fasted for 18 h were given 1 ml of 0.6 N HCl by gavage, and they were fed normally from 1 h later and killed various days after HCl treatment. Gastric lesions induced by HCl healed to quiescent states within 7 days both macroscopically and histologically. Mucosal SH levels were markedly reduced after induction of damage by HCl, but recovered gradually to or above normal values within 5 days. Gastric acidity was also significantly reduced after administration of 0.6 N HCl (induction of lesions), followed by a return to normal values within 5 days, although the volume of gastric contents remained unchanged before and after HCl treatment. The healing of HCl-induced gastric lesions was significantly impaired by diethylmaleate (DEM 0.3 ml/kg x 2) when this drug was given subcutaneously for 5 days. Glutathione (GSH: 100 mg/kg x 2) alone did not affect the healing of gastric lesions, but the combined administration of GSH with DEM significantly antagonized the delayed healing caused by DEM. Administration of DEM caused a marked and persistent reduction in the mucosal SH contents, while GSH by itself significantly increased the mucosal SH levels and partially reversed the reduced SH contents caused by DEM. Gastric acid secretion was not significantly altered by either DEM or GHS. These results suggest that endogenous SH may play some roles in the healing process of gastric mucosal lesions. DEM caused a deleterious effect on the healing of gastric lesions, probably by reducing the mucosal SH.

Animals↗
PubMed1992

Role of capsaicin-sensitive afferent neurons in mucosal blood flow response of rat stomach induced by mild irritants.

The role of capsaicin-sensitive sensory nerves in gastric mucosal blood flow (GMBF) responses to mild irritants was investigated in the rat stomach mounted on a lucite chamber using hypertonic NaCl and 0.2 N HCl. Exposure of the mucosa to hypertonic NaCl (0.5, 0.75, 1 M) for 10 min caused a reduction in the transmucosal potential difference (PD) in a concentration-related manner, followed by an increase of luminal pH and GMBF. In contrast, mucosal application of 0.2 N HCl caused no or little change in PD and pH, but increased GMBF significantly. Functional ablation of capsaicin-sensitive sensory nerves significantly inhibited the increase of GMBF after exposure to these irritants, although the PD and pH responses induced by 1 M NaCl remained unaltered by this treatment. Pretreatment with indomethacin (5 mg/kg, subcutaneously) significantly attenuated the GMBF responses to 1 M NaCl and 0.2 N HCl and inhibited the increase of pH caused by 1 M NaCl. Mucosal application of capsaicin (0.1 mg/ml for 10 min) produced an increase of GMBF without being accompanied by change in PD and pH, and this effect was significantly blocked by either indomethacin or chemical deafferentation. These results suggest that capsaicin-sensitive sensory nerves as well as endogenous prostaglandins may be involved in the mechanism of GMBF responses induced by mild irritants, and the latter might sensitize these nerves to mucosal irritation. PD reduction may be obligatory for pH but not GMBF responses.

Animals↗
PubMed1992

Role of capsaicin-sensitive sensory nerves in acid-induced bicarbonate secretion in rat stomach.

The effect of capsaicin-sensitive afferent nerves on the alkaline secretory response induced by mucosal acidification was investigated in the ex vivo stomachs of anesthetized rats. The stomach was mounted on a Lucite chamber and perfused with saline (pH 4.5) in the absence of acid secretion (omeprazole pretreatment: 60 mg/kg, intraperitoneal), and luminal pH and transmucosal potential difference (PD) were monitored simultaneously. Under these conditions the gastric mucosa responded to intravenous injection of prostaglandin E2 (PGE2: 300 micrograms/kg) and mucosal acidification (0.2 N HCl for 10 min) by a significant increase of pH with a slight decrease of PD; the HCO3- output was 9.2 +/- 0.7 mumol and 8.4 +/- 0.8 mumol, respectively. The increased pH and HCO3- responses were significantly inhibited by prior administration of indomethacin (5 mg/kg, subcutaneously) or chemical deafferentation following capsaicin injections (total dose: 100 mg/kg, subcutaneously), whereas those induced by PGE2 remained unchanged after either treatment. On the other hand, the mucosal application of capsaicin (0.3-6 mg/ml) increased the luminal pH and HCO3- output in a concentration-related manner, and this action was also significantly attenuated by either indomethacin or chemical deafferentation of capsaicin-sensitive sensory neurons. These results suggest that capsaicin-sensitive sensory nerves may be involved in the mechanism of acid-induced HCO3- secretion in the stomach, in addition to endogenous PGs, and these two pathways may interact somewhere in the stimulatory process.

Animals↗
PubMed1992

Induction of duodenal ulcers in sensory deafferented rats following histamine infusion.

We used capsaicin as a selective probe for sensory neuronal mechanisms and examined in rats whether defunctionalization of the sensory nerves caused duodenal ulcers in the presence of acid hypersecretion. Chemical deafferentation was performed by subcutaneous injection of capsaicin for 3 days (total dose: 100 mg/kg) 2 weeks before the experiment. This treatment did not cause by itself any damage in the duodenum. However, intravenous infusion of histamine (4, 8 and 16 mg/kg/h) in these animals caused hemorrhagic lesions in the proximal duodenum within 6 h in a dose-dependent manner with an incidence of 100%. Histamine alone in the control animals did not induce macroscopically visible lesions at lower doses and caused only slight damage at the highest dose (16 mg/kg/h), although acid secretion was stimulated to the maximal degree at 8 mg/kg/h. Ablation of capsaicin-sensitive sensory neurons did not have any effect on acid secretion induced by histamine (8 mg/kg/h), but significantly inhibited the increase in duodenal HCO3- secretion in response to mucosal acidification. We conclude that functional ablation of capsaicin-sensitive sensory nerves impairs duodenal HCO3- secretory response to acid and results in duodenal ulcers if acid hypersecretion is present. These sensory nerves may be important in the defense mechanism of the duodenum against luminal acid.

Animals↗
PubMed1992

Effects of sulfhydryl-related compounds on indomethacin-induced gastric lesions in rats: role of endogenous sulfhydryls in the pathogenesis.

The role of mucosal sulfhydryl (SH) in the pathogenesis of indomethacin-induced gastric lesions was investigated in rats. Indomethacin (25 mg/kg, s.c.) caused high-amplitude gastric contractions, resulting in linear hemorrhagic lesions in the corpus mucosa within 4 hr, but did not induce any changes in the mucosal SH levels. These lesions were prevented significantly by prior s.c. administration of cysteamine, glutathione (GSH) or diethylmaleate (DEM), irrespective of whether the mucosal SH was increased by the former two agents or reduced by the latter. N-Ethylmaleimide (NEM) tended to worsen such lesions without any effect on the mucosal SH contents. Gastric hypermotility caused by indomethacin was inhibited significantly by DEM, cysteamine and GSH, while acid secretion was reduced by DEM and NEM. Both cysteamine and GSH prevented the indomethacin-induced linear lesions even in the stomach perfused with 150 mM HCl, whereas in the animals treated with DEM, nonlinear damage was induced exclusively in the antrum by indomethacin in the presence of acid. We conclude that the mucosal SH has no relation to the ulcerogenicity of indomethacin in the gastric corpus mucosa.

Animals↗
PubMed1992

Stimulation by capsaicin of gastric alkaline secretion in anesthetized rats.

Effects of mucosal application of capsaicin on alkaline secretion were examined in the stomachs of anesthetized rats and compared with those in the duodenum. The stomach (acid secretion was inhibited by omeprazole given i.p.) or the duodenum was perfused with saline (pH 4.5); both the pH of the perfusate and transmucosal potential difference (PD) were continuously monitored; and the HCO3- output was determined by the pH change. Under these conditions, the mucosal application of capsaicin (0.3-6 mg/ml for 30 min) caused significantly increased pH and HCO3- output in a concentration-related manner in both tissues, while PD increased in the duodenum and decreased in the stomach. The HCO3- stimulatory action of capsaicin was markedly attenuated by sensory deafferentation, significantly mitigated by prior administration of indomethacin, and exhibited a marked tachyphylaxis after the repeated exposure at a high concentration (6 mg/ml). None of these treatments had any effect on the pH, PD and HCO3- responses induced by prostaglandin E2 (300 micrograms/kg, i.v.) in these tissues. These results indicate that mucosal application of capsaicin increased the gastroduodenal HCO3- output by stimulation of capsaicin-sensitive sensory neurons. This action may be in part mediated by endogenous prostaglandins.

Afferent Pathways↗
PubMed1992

Induction of gastric lesions by 2-deoxy-D-glucose in rats following chemical ablation of capsaicin-sensitive sensory neurons.

Effects of chemical ablation of capsaicin-sensitive sensory nerves on functional and mucosal ulcerogenic responses to 2-deoxy-D-glucose (2DG) were investigated in the rat stomach, in comparison with those of indomethacin, a prostaglandin (PG) biosynthesis inhibitor. Intravenous injection of 2DG (200 mg/kg) followed by infusion of this agent (100 mg/kg/hr, i.v.) significantly increased gastric acid secretion and motility, but rarely induced macroscopic damage in the gastric mucosa of normal conscious rats. Chemical ablation of capsaicin-sensitive sensory nerves or pretreatment with indomethacin (5 mg/kg, s.c.) did not significantly affect the acid secretory and motility responses to 2DG, but induced severe hemorrhagic lesions in the stomach within 4 hr. Gastric mucosal blood flow (GMBF) determined by laser Doppler flowmetry under anesthetized conditions did not consistently change during 2DG treatment in any of these three groups, but the rise in GMBF in response to mucosal acidification (0.2 N HCl) was significantly inhibited in the animals pretreated with indomethacin or following chemical deafferentation. We conclude that functional ablation of capsaicin-sensitive sensory neurons, similar to the PG deficiency, increases the gastric mucosal vulnerability during 2DG infusion (acid hypersecretion and hypermotility due to vagal excitation), resulting in hemorrhagic lesions, and that the mechanism may be accounted for at least partly by the impairment of gastric mucosal blood flow response to mucosal acidification.

Animals↗
PubMed1992

Angiographic patterns and severe coronary artery disease. Exercise test correlates.

In a Veterans Affairs Medical Center, we studied 607 male patients to determine whether patterns and severity of coronary artery disease could be predicted by means of standard clinical and exercise test data. We found significant differences in clinical, hemodynamic, and electrocardiographic measurements among patients with progressively increasing disease severity determined by angiography. Left main disease produced responses significantly different from those of three-vessel disease only when accompanied by a 70% or greater narrowing of the right coronary artery. Discriminant function analysis revealed that the maximum amount of horizontal or downsloping ST depression in exercise and/or recovery was the most powerful predictor of disease severity, with 2-mm ST depression yielding a sensitivity of 55% and a specificity of 80% for prediction of severe coronary artery disease (three-vessel disease plus left main disease). Patients with increasingly severe disease also demonstrated a greater frequency of abnormal hemodynamic responses to exercise.

Chi-Square Distribution↗
PubMed1991

Vagally mediated acid hypersecretion and lesion formation in anesthetized rat under hypothermic conditions.

The pathophysiological changes associated with hypothermia were investigated in the rat stomach under anesthetized conditions. The animal was placed in a styrene foam box and the core body temperature was kept between 24 and 36 degrees C using a heat lamp and refrigerant pack. Lowering of body temperature (less than 30 degrees C) produced acid hypersecretion and induced hemorrhagic lesions in the gastric mucosa; these responses reached the maximum at 28 degrees C, and a significant relationship was found between acid output and lesion score. Hypothermia (28 degrees C) also caused a marked increase of gastric contractile activity and mucosal blood flow (MBF), but the ratio of acid output to MBF became greater when compared to that obtained under normothermic conditions. These changes induced by hypothermia (28 degrees C) were completely blocked by vagotomy and were significantly inhibited by atropine, hexamethonium, clonidine, or TRH antiserum. However, lowering body temperature did not significantly affect acid secretory, motility, and ulcerogenic responses induced by carbachol in the vagotomized rat, excluding local mechanisms (suppression of the inhibitory nerves) in the hypothermia-induced changes. We conclude that hypothermia alone stimulates vagally dependent acid secretion and motility, resulting in damage in the gastric mucosa. These changes may be centrally mediated by TRH, which is released in association with the thermogenic response to hypothermia.

Animals↗