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Biomedical subjects

J B Halter

Publications and source records attributed to J B Halter.

At least 127 records · Page 7Linked to original sources
PubMed1984

Plasma catecholamines and hemodynamic responses to stress states in man.

The relationship between the plasma catecholamine and hemodynamic responses to stress in man was studied using radionuclide left ventricular angiography to assess changes in cardiac volumes. In 10 healthy men, the maximum plasma norepinephrine (NE) and epinephrine (EPI) responses to symptom-limited supine bicycle exercise were considerably greater than the responses to isometric handgrip exercise or to a cold pressor test. Similarly, increases in heart rate, systolic blood pressure, stroke volume, ejection fraction, and cardiac output were greatest with bicycle exercise. Both the plasma catecholamine and hemodynamic responses to handgrip exercise tended to be intermediate, and the smallest responses were observed during cold pressure testing. The plasma NE and EPI responses to symptom-limited upright treadmill exercise in another group of 10 men were greater than the responses to supine bicycle exercise. During bicycle exercise and during handgrip exercise there were significant correlations between plasma NE and EPI levels and changes of heart rate, blood pressure, and cardiac output. In addition, when data from all three stresses were combined and effects of heart rate and subject differences were controlled for, plasma NE and EPI levels were significantly correlated with ejection fraction. These findings suggest that release of EPI and NE during stress states may contribute to some of the hemodynamic responses that occur during stress.

Adult↗
PubMed1983

Aldose reductase inhibition improves nerve conduction velocity in diabetic patients.

To assess the potential role of polyol-pathway activity in diabetic neuropathy, we measured the effects of sorbinil--a potent inhibitor of the key polyol-pathway enzyme aldose reductase--on nerve conduction velocity in 39 stable diabetics in a randomized, double-blind, cross-over trial. During nine weeks of treatment with sorbinil (250 mg per day), nerve conduction velocity was greater than during a nine-week placebo period for all three nerves tested: the peroneal motor nerve (mean increase [+/- S.E.M.], 0.70 +/- 0.24 m per second, P less than 0.008), the median motor nerve (mean increase, 0.66 +/- 0.27, P less than 0.005), and the median sensory nerve (mean increase, 1.16 +/- 0.50, P less than 0.035). Conduction velocity for all three nerves declined significantly within three weeks after cessation of the drug. These effects of sorbinil were not related to glycemic control, which was constant during the study. Although the effect of sorbinil in improving nerve conduction velocity in diabetics was small, the findings suggest that polyol-pathway activity contributes to slowed nerve conduction in diabetics. The clinical applicability of these observations remains to be determined, but they encourage further exploration of this approach to the treatment or prevention of diabetic neuropathy.

Adult↗
PubMed1983

Differential changes of autonomic nervous system function with age in man.

To assess the relationship between aging and autonomic nervous system function, cardiovascular and pupillary autonomic nervous system reflexes were measured in subgroups of 103 normal male subjects ranging in age from 19 to 82 years (mean age = 39 years). Both the plasma norepinephrine level, a measure of cardiovascular sympathetic nervous system activity, and the mean arterial blood pressure increased with age (r = 0.68 and 0.67, respectively, both p less than 0.001). In contrast, the plasma epinephrine level, a measure of adrenomedullary sympathetic nervous system activity, was unrelated to age (r = 0.08, p = NS). Respiratory variation of heart rate during beta-adrenergic blockade, an index of cardiac parasympathetic nervous system activity, was reduced in older subjects (r = -0.54, p less than 0.001). Thus, there was evidence of an age-related increase of cardiovascular sympathetic nervous system activity and a reduction of cardiac parasympathetic nervous system activity. These findings are consistent with the hypothesis that there is sympathetic nervous system and parasympathetic nervous system compensation of cardiovascular function in response to an age-related decrease in baroreceptor sensitivity. However, dark-adapted pupil size during parasympathetic nervous system blockade, an index of iris sympathetic nervous system activity, declined with age (r = -0.81, p less than 0.001). The latency time for the pupillary response to a light stimulus, an index of iris parasympathetic nervous system activity, was prolonged in older subjects (r = 0.58, p less than 0.001). Thus, both sympathetic nervous system and parasympathetic nervous system inputs to the iris were diminished in older subjects, findings consistent with the generalized decrease of peripheral somatic nerve function that has been reported with aging in man. It is concluded that autonomic nervous system function also declines with aging, but that other age-related changes such as a decline of baroreceptor sensitivity may lead to compensatory autonomic nervous system response, which could mask underlying functional defects.

Adult↗
PubMed1983

Reduced thermic effect of feeding in obesity: role of norepinephrine.

Several studies have suggested that obese subjects have a reduced thermic effect of feeding when compared to normal weight controls. The present study was undertaken to further define this apparent abnormality, and evaluate the role of norepinephrine in the thermic response to food. A test formula meal of 800 calories (85% carbohydrate, 15% protein) was taken by 7 control and 6 moderately obese subjects whose obesity was adult in onset. The rise in resting oxygen consumption following the test meal was greater in the control than in the obese group (p less than 0.01), and there was a significant inverse correlation between the relative degree of obesity and this response to feeding (r = -0.59, p less than 0.05). Norepinephrine concentrations were greater in the obese than in the control group both before (p less than 0.05) and after (p less than 0.05) feeding. No correlations were found between the plasma norepinephrine concentrations and the rise in oxygen consumption after feeding. Four of the 6 obese subjects were restudied after weight reduction. The reduced-obese group showed a trend toward normalization of basal measurements and responses to feeding. It is concluded that the reduced thermic response to feeding seen in the obese subjects studied cannot be directly accounted for by diminished sympathetic nervous system activity as reflected by plasma levels of norepinephrine.

Adult↗
PubMed1983

Neurohumorally induced cardiac dysrhythmias during nitrous oxide-oxygen-thiopental anesthesia.

Barbiturate, nitrous oxide, and oxygen are commonly used by the oral and maxillofacial surgeon to anesthetize the ambulatory oral surgery patient. The authors report three cases of ventricular dysrhythmia occurring from surgical stimulation during nitrous oxide-oxygen-thiopental anesthesia. These dysrhythmias were most likely mediated via direct neural stimulation of cardiac sympathetic nerves. Concomitant with adrenergic stimulation, a rise in the arterial plasma norepinephrine level was documented, along with an increase in the rate-pressure product. Immediate recognition and treatment of ventricular dysrhythmia is mandatory to preclude further serious cardiovascular complications or death.

Anesthesia, Dental↗
PubMed1983

Comparative plasma catecholamine and hemodynamic responses to handgrip, cold pressor and supine bicycle exercise testing in normal subjects.

Serial hemodynamic and plasma catecholamine responses were compared among 10 healthy men (27 +/- 3 years) (+/- 1 standard deviation) during symptom-limited handgrip (33% maximal voluntary contraction for 4.4 +/- 1.8 minutes), cold pressor testing (6 minutes) and symptom-limited supine bicycle exercise (22 +/- 5 minutes). Plasma catecholamine concentrations were measured by radioenzymatic assays: ejection fraction and changes in cardiac volumes were assessed by equilibrium radionuclide angiography. During maximal supine exercise, plasma norepinephrine and epinephrine concentrations increased three to six times more than during either symptom-limited handgrip or cold pressor testing. Additionally, increases in heart rate, systolic blood pressure, rate-pressure product, stroke volume, ejection fraction and cardiac output were significantly greater during bicycle exercise than during the other two tests. A decrease in ejection fraction of 0.05 units or more was common in young normal subjects during the first 2 minutes of cold pressor testing (6 of 10 subjects) or at symptom-limited handgrip (3 of 10), but never occurred during maximal supine bicycle exercise. The magnitude of hemodynamic changes with maximal supine bicycle exercise was greater, more consistent and associated with much higher sympathetic nervous system activation, making this a potentially more useful diagnostic stress than either handgrip exercise or cold pressor testing.

Adult↗
PubMed1983

Tricyclic antidepressants and supine, standing, and exercise plasma norepinephrine levels.

Fourteen depressed patients were treated for 1 to 8 wk (4.1 +/- 0.6, mean +/- SEM) with imipramine, doxepin, or amitriptyline to study the effects of tricyclic antidepressants (TCAs) on sympathetic nervous system (SNS) function. Eight had chronic but medically stable cardiac disease and six were medically healthy. Supine plasma norepinephrine (NE) and epinephrine (EPI) levels, mean arterial blood pressure (MAP), and heart rate were measured at rest, after standing, and during graded, supine maximal bicycle exercise. Eight nondepressed patients with cardiac disease were studied without drug intervention as controls. There were no baseline differences in any of these measures among the medically healthy depressed subjects, the depressed cardiac patients, and the eight nondepressed patients matched for cardiac disease. After TCAs, NE was increased by 51 +/- 6% of basal values and heart rate rose, but EPI and MAP were unchanged. The supine to 10-min standing increment in NE increased from 309 +/- 51 pg/ml at baseline to 406 +/- 55 pg/ml during TCA treatment. These findings are compatible with an increase in SNS outflow after TCAs.

Adult↗
PubMed1983

Effect of intravenous aminophylline on plasma levels of catecholamines and related cardiovascular and metabolic responses in man.

Theophylline is thought to act by inhibiting the activity of phosphodiesterase, with a resultant increase in intracellular cyclic AMP. However, this concept is largely based on in vitro studies using concentrations of theophylline which greatly exceed therapeutic plasma concentrations. To investigate the relationship of the cardiovascular and metabolic effects of theophylline to activation of the sympathetic nervous system, i.v. aminophylline was administered to six healthy males under basal conditions. Each subject received four infusions. Mean theophylline concentrations (+/- SEM) of 4.5 +/- 0.2, 10.0 +/- 0.5, 14.0 +/- 0.5 and 20.0 +/- 1.2 micrograms/ml were achieved. Plasma epinephrine increased 262% (from 29 +/- 4 to 105 +/- 14 pg/ml, p less than 0.01) and plasma norepinephrine increased 64% (from 190 +/- 18 to 312 +/- 51 pg/ml, p less than 0.05) during the high-dose infusion. The increases in circulating catecholamines were dose-related (p less than 0.001 by analysis of variance). Dose-related increases in heart rate, systolic blood pressure, plasma glucose, free fatty acids and insulin were also observed (p less than 0.001 by analysis of variance). Although the duration of total electromechanical systole (QS2) and left ventricular ejection time adjusted for heart rate fell during the aminophylline infusions, this positive inotropic response was not influenced by dose, except possibly the high dose. Echocardiographic ejection fraction was not changed by the aminophylline infusions. We conclude that the acute cardiovascular and metabolic effects of theophylline may be mediated in part by stimulation of the sympathetic nervous system.

Adolescent↗
PubMed1983

Autonomic nervous system control of glucagon secretion during neuroglucopenia.

The role which the autonomic nervous system (ANS) plays in controlling glucagon (IRG) secretion is controversial. Strong activation of the ANS was achieved in baboons with 500 mg/kg 2-deoxyglucose, producing a 20-fold rise in epinephrine and a 15-fold rise in IRG. Under such circumstances, the IRG response was attenuated by both alpha- and beta-adrenergic blockade, strongly suggesting that this part of the IRG rise post 2-deoxyglucose was mediated via adrenergic mechanisms. The baboon is similar to man, with the sympatho-adrenal axis having little influence on IRG secretion during mild activation of the ANS. However, during stronger ANS activation with 2-deoxyglucose, a clear effect of the sympatho-adrenal axis on IRG secretion was demonstrated. Whether experiments in primates demonstrate an effect of the ANS on IRG secretion may depend primarily on the strength of the neural response elicted.

Animals↗
PubMed1983

Sodium-restricted diet increases nighttime plasma norepinephrine and impairs sleep patterns in man.

Plasma norepinephrine levels in 10 healthy young males were significantly elevated after 3 days of a low sodium (less than 500 mg/day) diet. The low sodium diet was also associated with disturbed sleep patterns: decreased rapid eye movement and slow wave sleep and increased wakefulness. These sleep changes are similar to those seen in normal aged adults, who also undergo elevations of daytime and nighttime plasma norepinephrine. These results suggest the possibility that increased sympathetic nervous system activity may affect sleep patterns, and that therapies altering sympathetic activity may affect sleep.

Adult↗
PubMed1983

Suppression of glucagon secretion during a tolbutamide infusion in normal and noninsulin-dependent diabetic subjects.

To determine the effect of tolbutamide on glucagon release in noninsulin-dependent diabetic and normal subjects and how plasma glucose levels may modulate this effect, the acute glucagon response (AGR) to a 5-g iv arginine pulse was determined before and during a tolbutamide infusion. There was a decrease in plasma glucose concentration in both normal and diabetic subjects (both P less than 0.001); there tended to be a suppression of the AGR (4 of 6 normals and 8 of 11 diabetics), but this suppression was not statistically significant. In separate studies, when the plasma glucose level was clamped at baseline values by a variable rate of glucose infusion, the AGR was suppressed during the tolbutamide infusion in all 7 normal [change in AGR (delta AGR) = -35 +/- 12 pg/ml; P less than 0.05] and all 6 noninsulin-dependent diabetic subjects (delta AGR = -14 +/- 5 pg/ml, p less than .05). In 6 insulin-dependent diabetic subjects, there was no evidence of glucagon suppression by tolbutamide (delta AGR = +2 +/- 2 pg/ml). These results are consistent with the hypothesis that sulfonylureas suppress glucagon secretion by augmenting insulin secretion, an effect that falling glucose levels can mask. Consideration of this observation is necessary when interpreting the effects of a sulfonylurea on islet cell responses.

Adult↗
PubMed1983

Modulation of arginine-induced glucagon release by epinephrine and glucose levels in man.

To assess how physiological epinephrine (EPI) elevations and EPI-induced hyperglycemia interact in the regulation of glucagon secretion, we measured acute glucagon responses (AGR) to arginine at controlled glucose levels during EPI infusions in man. With glucose levels matched at 166 +/- 5 mg/dl using glucose clamp techniques, the AGR (mean change at 2-5 min) to a 5-g iv arginine injection was greater in each subject during the infusion of 15 ng/kg . min EPI (low EPI) than during the control glucose infusion and was still greater during the infusion of 80 ng/kg . min EPI (high EPI; 69 +/- 15, 76 +/- 13, and 142 +/- 22 pg/ml, respectively; n = 8; P less than 0.003). With glucose levels matched at 256 +/- 5 mg/dl, a similar dose-related enhancement of AGR by EPI was seen (control, 53 +/- 12 pg/ml; low EPI, 63 +/- 5 pg/ml; high EPI, 130 +/- 20 pg/ml; P less than 0.008). During control infusions, raising the glucose level from 102 +/- 2 to 166 +/- 5 to 256 +/- 5 mg/dl suppressed AGR from 77 +/- 17 to 69 +/- 15 to 53 +/- 12 pg/ml (P less than 0.002). During low EPI, the same glycemic increments lowered GR from 108 +/- 19 to 76 +/- 13 to 63 +/- 5 pg/ml (P less than 0.02). This suppression of AGR by hyperglycemia was sufficient to obscure stimulation by EPI: at a glucose level of 102 +/- 2 mg/dl during control infusions, AGR was 77 +/- 17 pg/ml, compared to only 76 +/- 13 pg/ml during low EPI with the glucose level higher (166 +/- 5 mg/dl). Multiple linear regression analysis showed a highly significant dependence of AGR on both EPI and glucose levels, accounting for 80% of the within-subject variation in AGR (P less than 0.0001). These data show that 1) EPI is a dose-dependent amplifier of arginine-induced glucagon secretion in man, and 2) hyperglycemia suppresses arginine-induced glucagon secretion, potentially masking the stimulation caused by EPI. The findings suggest that the feedback effect of hyperglycemia on glucagon secretion may help regulate the level of hyperglycemia resulting from adrenergic stimulation.

Adult↗
PubMed1983

Hyperglycemia and beta-cell adaptation during prolonged somatostatin infusion with glucagon replacement in man.

To assess the relationship between beta-cell function and the level and duration of hyperglycemia during generalized beta-cell impairment, we studied the effects of acute and prolonged infusion of somatostatin in seven normal men. Twenty minutes after beginning an acute infusion of somatostatin (200 microgram/h) plus glucagon replacement (0.75 ng/kg/min), plasma glucose (PG) remained unchanged, but plasma insulin (IRI) and acute insulin response to isoproterenol had fallen markedly. Seventy minutes after beginning somatostatin-plus-glucagon, a rise in PG was associated with an increase in the acute insulin response to isoproterenol, though not to the control level. In a separate study, after 46 h of the somatostatin-plus-glucagon infusion, at a glucose level similar to the 70-min level, plasma insulin had returned nearly to the control level and the acute insulin response to isoproterenol had returned completely to the control level. Such increases inb basal and stimulated insulin secretion most likely represent a time-dependent adaptation by the beta-cells to the persistent hyperglycemia. First- and second-phase insulin responses to intravenous glucose were markedly inhibited after 46 h of somatostatin-plus-glucagon. In summary, a 46-h infusion of somatostatin with glucagon replacement in humans leads to hyperglycemia, a slightly diminished basal insulin level, markedly decreased insulin responses to glucose, and an insulin response to isoproterenol maintained at a normal level by acute and probably chronic adaptation to the hyperglycemia. We speculate that beta-cell adaptation to hyperglycemia may explain the similar abnormalities of islet function observed in patients with NIDDM.

Adaptation, Physiological↗
PubMed1983

The response of plasma triglyceride, cholesterol, and lipoprotein lipase to treatment in non-insulin-dependent diabetic subjects without familial hypertriglyceridemia.

The effects of treatment on plasma total triglyceride, total cholesterol, and plasma postheparin lipase activities have not been evaluated in non-insulin-dependent diabetic (NIDD) subjects without a coexisting familial lipid disorder. In 49 untreated NIDD subjects, there was a linear relationship between glycosylated hemoglobin (GHb) and triglyceride (r = 0.35, P less than 0.02). This correlation was improved after adjusting for the effects of obesity by a partial correlation analysis. After therapy, there was a significant relationship between the change in GHb and the change in triglyceride. To determine whether changes in lipid removal from plasma may contribute to the decrease in plasma lipid concentrations during treatment, the plasma postheparin lipoprotein lipase and hepatic lipase activities were evaluated in a subgroup (N = 8) of these NIDD subjects before and after 1 and 3 mo of therapy. Plasma postheparin hepatic lipase activity in the NIDD subjects was not different from that observed in six normal control subjects and did not change during therapy. In contrast, plasma postheparin lipoprotein lipase activity was lower in the untreated NIDD subjects than in the control subjects. Analysis of the two phases (early and late) of the postheparin lipoprotein lipase activity in plasma showed that the abnormal early phase in untreated NIDD corrected to normal values in less than a month, but the late phase was not corrected until the 3-mo measurement. These findings suggest that some NIDD subjects have a defect in heparin releasable lipoprotein lipase activity, which is reversed with improved glycemic control.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗