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Biomedical subjects

S R Wall

Publications and source records attributed to S R Wall.

11 recordsLinked to original sources
PubMed1990

Glucose and palmitate oxidation in isolated working rat hearts reperfused after a period of transient global ischemia.

Alterations in energy substrate utilization during reperfusion of ischemic hearts can influence the functional recovery of the myocardium. Energy substrate preference by the reperfused myocardium, however, has received limited attention. Therefore, we measured oxidation rates of glucose and palmitate during reperfusion of ischemic hearts. Isolated working rat hearts were perfused with 1.2 mM palmitate and 11 mM [14C]glucose, 1.2 mM [14C]palmitate and 11 mM glucose, or 11 mM [14C]glucose alone, at an 11.5 mm Hg preload and 80 mm Hg afterload. Hearts were subjected to 60-minute aerobic perfusion or 25-minute global ischemia followed by 60-minute aerobic reperfusion. Steady-state oxidative rates of glucose or palmitate were determined by measuring 14CO2 production. In hearts perfused with glucose alone, oxidative rates during reperfusion were not significantly different than nonischemic hearts (1,008 +/- 335 vs. 1,372 +/- 117 nmol [14C]glucose oxidized/min/g dry wt, respectively). In the presence of palmitate, glucose oxidation was markedly reduced in reperfused and nonischemic hearts (81 +/- 11 and 101 +/- 15 nmol [14C]glucose oxidized/min/g dry wt, respectively). Palmitate oxidation rates were not significantly different in reperfused compared with nonischemic hearts (369 +/- 55 and 455 +/- 50 nmol [14C]palmitate oxidized/min/g dry wt, respectively). [14C]Palmitate was incorporated into myocardial triglycerides to a greater extent in reperfused ischemic hearts than in nonischemic hearts (26.0 and 13.8 mumol/g dry wt, respectively). Under the perfusion conditions used, palmitate provided over 90% of the ATP produced from exogenous substrates. Addition of the carnitine palmitoyltransferase I inhibitor, ethyl 2-[6-(4-chlorophenoxy)hexyl]oxirane-2-carboxylate (Etomoxir, 10(-6) M), during reperfusion stimulated glucose oxidation and improved mechanical recovery of ischemic hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Glucose oxidation rates in fatty acid-perfused isolated working hearts from diabetic rats.

The effect of fatty acids and the carnitine palmitoyltransferase I (CPT I) inhibitor, Etomoxir, on myocardial glucose oxidation in diabetes was studied. 14CO2 production from 11 mM [14C]glucose was measured in control or 6-week streptozotocin-diabetic isolated working rat hearts perfused with or without 1.2 mM palmitate (bound to 3% albumin). In control hearts, addition of palmitate to the buffer resulted in a marked reduction (13-fold) in glucose oxidation rates. Glucose oxidation in diabetic rat hearts perfused with palmitate was almost abolished. Even though glucose oxidation rates were low, exogenous palmitate oxidation rates, measured as 14CO2 production from [14C]palmitate, were not increased in diabetic versus control hearts. Addition of the CPT 1 inhibitor, Etomoxir (1.10(-6) M), resulted in a doubling of glucose oxidation rates in both control and diabetic rat hearts, in the presence or absence of palmitate. The effects of Etomoxir on glucose oxidation could not be explained by reduced exogenous palmitate oxidation or decreased levels of citrate. Cardiac function, as measured by the heart rate x peak systolic pressure product, was reduced in diabetic rat hearts. Etomoxir significantly increased heart function in palmitate-perfused hearts from both control and diabetic rats. These data suggest that fatty acids contribute to decreased glucose oxidation and cardiac function in diabetic rat hearts. These effects of fatty acids can be partially reversed with the CPT 1 inhibitor, Etomoxir.

Adenosine Triphosphate↗
PubMed1989

Thyroid hormone stimulates expression of 6-phosphofructo-2-kinase in rat liver.

The activity of liver 6-phosphofructo-2-kinase (PFK-2), the enzyme that catalyses the synthesis of fructose 2,6-bisphosphate, was markedly decreased in hypothyroid rats and partially restored after 3 days of treatment with triiodothyronine. The changes in PFK-2 activity were accompanied by parallel changes in enzyme content measured by immunotitration and in PFK-2 mRNA determined by dot blot and Northern blot hybridization with cDNA probes. It is concluded that thyroid hormone stimulates liver PFK-2 gene expression by a pre-translational mechanism.

Animals↗
PubMed1988

Etomoxir, a carnitine palmitoyltransferase I inhibitor, protects hearts from fatty acid-induced ischemic injury independent of changes in long chain acylcarnitine.

Fatty acids are known to increase the severity of injury during acute myocardial ischemia. In this study, we determined the effects of a carnitine palmitoyltransferase I inhibitor, ethyl 2-[6-(4-chlorophenoxy)hexyl]oxirane-2-carboxylate (Etomoxir) on reperfusion recovery of fatty acid perfused hearts. Following a 25-minute period of global ischemia, isolated working hearts reperfused with 1.2 mM palmitate, 11 mM glucose exhibited depressed function compared to hearts perfused with 11 mM glucose alone. A low dose of Etomoxir (10(-9) M) decreased long chain acylcarnitine and long chain acyl-coenzyme A (CoA) levels but did not prevent depressed function. In contrast, a high dose of Etomoxir (10(-6) M) prevented the palmitate-induced depression of function but did not decrease myocardial long chain acylcarnitine or long chain acyl-CoA levels. At this high dose of Etomoxir, oxygen consumption per unit work was decreased during reperfusion recovery, and ATP and creatine-phosphate levels were significantly higher after reperfusion. In aerobic hearts not subjected to ischemia, Etomoxir (10(-6) M) increased glucose oxidation both in the presence and absence of palmitate, while 10(-9) M Etomoxir had no effect. In these aerobic hearts, only the low dose of Etomoxir decreased long chain acylcarnitine and long chain acyl-CoA levels. These data demonstrate that Etomoxir (10(-6) M) increases functional recovery of fatty acid perfused ischemic hearts. This protection is unrelated to changes in levels of long chain acylcarnitines but may be due to increased glucose use by the reperfused heart, resulting in decreased oxygen consumption per unit work.

Acyl Coenzyme A↗
PubMed1987

Decrease in serum testosterone levels with maximal intensity swimming exercise in trained male and female swimmers.

Circulating testosterone levels have generally been reported to increase during short term, intense running or bicycle ergometer exercise. Swimming differs from such activity because of the strenuous arm activity and because it is conducted in a liquid medium in the horizontal position with the weight totally supported. To investigate whether such differences modify the serum testosterone response to exercise, we measured serum testosterone levels before and after a maximal intensity swimming test in ten elite male and ten elite female swimmers. Levels of circulating testosterone fell in 19 of 20 swimmers in contrast to previous reports of exercise in the vertical position. In women mean testosterone levels declined by 39.4% from baseline values and in males, mean testosterone levels declined by 19.0%. Since the incremental protocol was similar to in design to maximal intensity tests conducted on a treadmill or bicycle ergometer, these data suggest that the differing physical circumstances of swimming lead to a qualitatively different testosterone response to exercise.

Adolescent↗
PubMed1987

Reproductive hormone responses to resistance exercise.

To investigate if changes in circulating testosterone levels during isokinetic resistance exercise in women were similar to those during intense aerobic exercise and to examine concomitant changes in hemoconcentration, specific binding protein (sex hormone binding globulin-binding capacity), non-sex hormone binding globulin bound testosterone, luteinizing hormone, follicle-stimulating hormone, cortisol, and lactate, blood samples were obtained through an indwelling cannula at 30 and 15 min before exercise, after each of six exercises on upper and lower body muscle groups, and at 15 and 30 min after exercise in seven normal menstruating women. Investigations lasting approximately 60 min were performed in the early follicular phase beginning at 3.30 p.m. after two months of training with isokinetic ("Nautilus") equipment. Baseline testosterone and non-sex hormone binding globulin bound testosterone levels were significantly higher in subjects than in a control group. Increased total and non-sex hormone binding globulin bound testosterone was observed immediately prior to exercise with further increases late in exercise, then with proportional increases in cortisol and lactic acid. Sex hormone binding globulin-binding capacity increased before exercise. The testosterone increments exceeded hemoconcentration. Luteinizing hormone and follicle-stimulating hormone levels increased during exercise. The data suggest that origins of the exercise-associated testosterone increment are complex, resulting from hemoconcentration and specific gonadal and adrenal responses.

Adolescent↗
PubMed1986

Are anorexic tendencies prevalent in the habitual runner?

To investigate whether runners displayed any of the abnormalities characteristic of patients with anorexia nervosa, we conducted a cross sectional study of 31 high mileage, 18 low mileage runners and 18 non-running controls. Subjects completed a personal data questionnaire, the Jackson Personality Inventory (JPI) and the Eating Attitudes Questionnaire (EAT), underwent a body image test and a blood sample was obtained for measurement of reproductive, thyroid and adrenal hormones. High mileage runners scored significantly higher infrequency scores on the JPI than sedentary controls but there was no evidence of psychopathology. The high mileage runners also significantly overestimated waist width and there were small but statistically significant differences in EAT scores between controls and the runner groups. Ten of 49 runners had EAT scores beyond two standard deviations above the mean of non-running controls. Serum total, free and non-specifically bound testosterone and prolactin levels were significantly lower in high mileage runners than controls. LH, FSH, cortisol and thyroid hormones were not significantly different. There were no significant differences in any hormone between low mileage runners and controls. displayed no clear abnormalities characteristic of patients with anorexia The results suggested that running may have a chronic effect on serum testosterone and prolactin levels in high mileage but not low mileage runners. Although there was no significant evidence of anorexia nervosa on testing the runners with EAT, the overestimation of waist size provided some evidence of a distortion of body image in the high mileage runners. Runners displayed no clear abnormalities characteristic of patients with anorexia nervosa.

Adolescent↗
PubMed1985

The effect of acute exercise on pulsatile release of luteinizing hormone in women runners.

Endurance exercise has been associated with reproductive dysfunction. We have previously suggested that pulsatile release of luteinizing hormone is impaired at rest in normal menstruating runners compared with sedentary women. To determine whether acute exercise had any effect on pulsatile release of luteinizing hormone we investigated serum luteinizing hormone levels in six normal menstruating runners at rest and after 60 minutes of running exercise. Exercise induced an increment in circulating luteinizing hormone levels greater than the change in hematocrit. The luteinizing hormone pulse frequency, calculated as the number of luteinizing hormone pulses per 6 hours, was reduced after exercise compared with values obtained at rest. There was no significant difference in pulse amplitude or area under the 6-hour curve between resting and postexercise situations. These data suggest that acute exercise has an inhibitory effect on luteinizing hormone pulsatile release at the hypothalamic level in eumenorrheic runners that is in addition to the previously described effect of training.

Adult↗
PubMed1985

Defects in pulsatile LH release in normally menstruating runners.

Intense physical exercise has been associated with reproductive dysfunction and menstrual cycles may be abnormal in a majority of women with a heavy training load. To determine whether training influenced pulsatile LH release, we measured LH pulse frequency, LH pulse amplitude and area under the curve over six hours during the early follicular phase of the menstrual cycle in four sedentary women and six eumenorrheic women runners with a training volume of at least 32 km per week. All three LH variables were significantly lower in runners than in controls. These data suggest that there is a central inhibition of the hypothalamic-pituitary-gonadal axis in eumenorrheic runners.

Adult↗
PubMed1985

Non-sex hormone-binding globulin-bound testosterone as a marker for hyperandrogenism.

Recent evidence suggests that the biologically active testosterone includes both the free and albumin-bound fractions, while the sex hormone-binding globulin (SHBG)-bound steroid dissociates less readily. To examine the significance of the non-SHBG-bound testosterone (i.e. free plus albumin bound) in hyperandrogenism, we obtained single blood samples from 17 normal women, 20 regularly menstruating but hirsute women, and 20 oligoamenorrheic hirsute women. Each serum sample was analyzed for total testosterone by RIA, SHBG-binding capacity was determined by protein precipitation with 50% saturated (NH4)2SO4, and albumin was measured by colorimetry. Non-SHBG-bound and free testosterone and the testosterone to SHBG molar ratio were then calculated. Non-SHBG-bound testosterone was also assayed using differential protein precipitation. There were significant differences among the groups in the mean values of all variables (all P less than 0.05) except albumin. Measurement and calculation of serum non-SHBG-bound testosterone produced similar results, suggesting that the binding equation is valid. There was considerable overlap between normal (control mean +/- 2 SD) and abnormal subjects in all variables except non-SHBG-bound testosterone, for which only 3 regularly menstruating and 2 oligoamenorrheic hirsute subjects were in the normal range. As total testosterone levels increased, there was a significant increase in the ratio of non-SHBG-bound testosterone to free testosterone. These data suggest that albumin becomes increasingly more important in testosterone binding as the total serum testosterone level increases and that non-SHBG-bound testosterone may be the optimal marker to identify hyperandrogenism in hirsute women.

Amenorrhea↗