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Biomedical subjects

E C Meyer

Publications and source records attributed to E C Meyer.

At least 55 records · Page 3Linked to original sources
PubMed1989

Effect of exercise on met-enkephalin in unfit and superfit individuals.

Twenty-four unfit volunteers and twenty-three superfit athletes were subjected to a progressive intensity treadmill exercise to total exhaustion in order to study the plasma met-enkephalin response to exercise. Blood samples were collected before and 5 min post-exercise. The basal met-enkephalin levels were significantly higher in the superfit individuals (180 fmol.ml-1) than in the unfit individuals (126 fmol.ml-1). Post-exercise the increase from basal levels of plasma met-enkephalin was significantly higher in the superfit athletes (180-278 fmol.ml-1) than in the unfit individuals (126-157 fmol.ml-1). The magnitude of the met-enkephalin responses to exercise therefore appears to be dependent on the amount of work performed and the degree of previous physical training. Peripherally circulating opioid peptides may, therefore, possibly play a role in the body's adaptation to exercise training.

Adult↗
PubMed1988

Aldosterone response to metoclopramide is mediated through the autonomic nervous system in man.

This study primarily examines the role of the autonomic nervous system in the aldosterone response to metoclopramide since there is conflicting evidence as to the involvement of a dopaminergic mechanism in this response. Six normal male volunteers in metabolic balance at 100 mmol sodium/day and 60 mmol potassium/day constant intake received metoclopramide, 10 mg i.v., on five different occasions. The dosing was either metoclopramide alone or combined with ganglionic, muscarinic, beta-adrenergic or calcium-channel blockade. Metoclopramide increased serum aldosterone significantly to 163.3% of basal level at 10 min. Atropine blunted this response and the 10 min level was significantly reduced to 116.03% of the basal value. The highest aldosterone levels were attained when metoclopramide was administered during a trimethaphan infusion and a peak of 292.8% of basal level occurred at 90 min. In the presence of atenolol, with or without nifedipine, the metoclopramide-induced aldosterone response was significantly greater at 15 min than with metoclopramide alone. The results of this investigation suggest that the aldosterone response to metoclopramide is mediated by acetylcholine released from post-ganglionic cholinergic nerve terminals, and that an adrenergic mechanism exerts a tonic inhibitory influence on aldosterone secretion in man.

Adult↗
PubMed1988

Possible mechanisms of anti-cholinergic drug-induced bradycardia.

Atropine-induced bradycardia is traditionally ascribed to central vagal stimulation, although bradycardia has also been observed after administration of quarternary amines. Pirezepine, a selective M1-antagonist, causes bradycardia in therapeutic doses for which a peripheral mechanism is postulated. This hypothesis has been investigated in healthy volunteers. Atropine 0.5 mg caused significant bradycardia from 210 min and pirenzepine 10 mg after 60 min. After prior beta-blockade, the bradycardic action of the anti-cholinergic drugs was more marked. Pirenzepine-induced bradycardia was reversed by higher doses of atropine. It is suggested that atropine- and pirenzepine-induced bradycardia results from M1-blockade of sympathetic ganglia. In addition, low concentrations of atropine and therapeutic doses of pirenzepine may cause an increase in acetylcholine, perhaps due to a presynaptic effect on nerve endings.

Adult↗
PubMed1987

A comparative study of pipemidic acid and nitrofurantoin in the treatment of uncomplicated urinary tract infections.

In an open uncontrolled trial 60 women with confirmed uncomplicated urinary tract infections were randomly allocated to receive either pipemidic acid (Septidron; Ethimed) or nitrofurantoin for 10 days. Urine cultures were done on day 1 and day 10. No statistical difference was found in the subjective and objective assessments of the response to the two medications and it is concluded that pipemidic acid is a satisfactory and effective alternative to nitrofurantoin in the treatment of uncomplicated urinary tract infections in women.

Adult↗
PubMed1979

Central nervous system maturation in the stressed premature.

The developmental sequence of sleep cycles has been found to be a useful index of central nervous system maturation in premature infants. To determine the effects of severe reversible stress on the maturation of sleep cycles, 6- to 8-hour sleep studies were done on 10 premature infants with severe hyaline membrane disease (HMD) and 10 healthy premature babies. The studies were done in the neonatal intensive care unit and included patients from 30 weeks' gestation to term and in all stages of the disease. Prior studies were confirmed showing that percentage of quiet sleep increases, transitional sleep changes little, and active sleep decreases from 30 weeks' gestation to term. In infants with severe HMD, the percentage of quiet sleep was less and active sleep higher than in unstressed infants of similar age who acted as controls. Once the infants recovered from HMD, sleep patterns became similar to those found in the control group. These data suggest that when respiratory distress occurs in the premature infant, there is a transient delay in central nervous system maturation as measured by sleep cycle analysis.

Brain↗
PubMed1979

Fibrinogen clearance from the pulmonary interstitium.

Previous experiments demonstrated that 125I-human fibrinogen (125-RIF) instilled into the distal airway of the right lower lobe in intact dogs passed through the microairway into the interstitium. This report analyzed the subsequent interstitial clearance of this fibrinogen by analyzing plasma and lymph samples for 125I activity. This activity was separated into clottable, and trichloroacetic acid (TCA) insoluble and soluble components. Clottable and TCA-insoluble 125-RIF in the same ratio appeared in lymph from the right lymphatic duct (RD) and thoracic duct (TD). From standard mixing equations we calculate that 1.4 times as much lymph from the right lower lobe flows into the TD as into the RD. With one exception, clottable 125-RIF appeared in plasma only in the absence of an RD; this suggested the presence of accessory lymphatico-venous communications rather than back flux of 125-RIF at the capillary wall. By injecting 131I-human fibrinogen intravenously, we observed a small reduction in clottability (maximum of 10%) in lymph both from the RD and TD. Equilibration in RD lymph was only 1/5 as fast as albumin, and from the measured equilibration rate constant, and the assumption that interstitial fibrinogen clearance is entirely convective, we estimate that the pulmonary interstitial distribution volume for fibrinogen is 70% that for albumin. Non dialyzable 125-RIF products generated in the distal airway adhered to intracapillary, circulating erythrocytes. These products retained fibrinogen antigenicity, and appeared to be further degraded in the vascular compartment.

Animals↗
PubMed1978

Fibrinogen clearance from alveoli.

In experiments lasting 311 +/- 8 (SE) min, we studied the clearance of 125I-fibrinogen ([125I])RIF) from distal lung units of anesthetized, ventilated dogs. We instilled varying concentrations of isosmolar, citrated [125I]RIF ranging from 0.75 to 4 mg/ml into alveoli of individual dogs, and we monitored clearance by the use of external detectors and blood and lymph sampling. Approximately 9% [125I]RIF passed into proximal airways according to detector signal analysis. Excluding airway flow, whole lung clearance of [125I]RIF occurred by degradation to small molecules that rapidly became evenly distributed in body extracellular water. The degradation appeared to take place within the distal airway and not within the lung interstitium because 131I-fibrinogen, injected intravenously, was degraded less in passing from plasma to right duct lymph. The intra-alveolar kinetics of [125I]RIF had 1.5 reaction order with a specific rate of 1.27 X 10(-5) ml(3/2)-mg(-1/2)-min(-1). The data indicate that fibrinogen clearance from alveoli occurs by both transbronchial bulk flow and intraalveolar degradation.

Animals↗
PubMed1977

Albumin clearance from alveoli: tissue permeation vs. airway displacement.

In anesthetized, ventilated dogs, clearance of 2 +/- 0.2 ml alveolar-instilled 1% isosmolar [125I]albumin ([125I]RISA) was separated into bulk airway displacement and transalveolar tissue permeation by the use of collimated external detectors and by sampling of blood and lymph. The detectors were positioned perpendicular to the plane of bronchial drainage, and collimator resolution was characterized by a 50% decrease in count rate for a 5-mm lateral (transbronchial) instillate shift. Detector signals demonstrated no airway shift in 10 dogs studied, the signal decay equaling [125I]RISA absorption determined by lung homogenates. The mean rate constants of [125I]RISA lung clearance and epithelial permeation were 4.08 X 10(-4)-min-1 and 5.48 X 10(-4)-min-1, respectively. The diffusional permeability coefficient of alveolar epithelium for albumin was 4.06 X 10(-9) CM-S-1. Absorbed [125I]RISA was separated into blood and lymph components by collecting lymph from the right lymphatic duct (RLD) and thoracic duct. Mean blood/lymph removal ratio was 6.3/1, and correlated with plasma/RLD lymph steady-state albumin concentration ratios in individual animals. Over a mean observation period of 5.4 h, an average of 12.3% [125I]RISA was cleared from the instilled region. The data suggest that this amount was cleared by permeation; there was little evidence of airway clearance.

Animals↗