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Biomedical subjects

A Henderson

Publications and source records attributed to A Henderson.

At least 199 records · Page 11Linked to original sources
PubMed1978

Action of caffeine on calcium transport by isolated fractions of myofibrils, mitochondria, and sarcoplasmic reticulum from rabbit heart.

We studied the effects of caffeine on calcium transport by subcellular organelles isolated from rabbit myocardium. Caffeine increased myofibrillar basic and calcium-activated ATPase activity at 20 mM but not at lower concentrations. Mitochondrial and sarcoplasmic reticulum (SR) calcium accumulation was measured both by dual wavelength spectrophotometry with the calcium-sensitive dye, murexide, and by Millipore filtration with 45Ca. In mitochondria, caffeine impaired phosphate-assisted calcium transport but did not alter the closely related parameters of oxygen uptake, P/O ratio (nmol adenosine diphosphate consumed/n ats oxygen consumed, state 3 respiration) or limited calcium loading. In SR, caffeine impaired calcium accumulation. New methods were used to characterize calcium accumulation in the absence of oxalate according to first order reaction kinetics. Caffeine increased the rate constant while decreasing the calcium accumulated. It also increased the associated calcium-activated ATPase activity at low (30 mM) but not high (240 micrometer) external calcium concentration. In the presence of oxalate, caffeine decreased the rate of calcium accumulation, more with low than high calcium concentration. Net efflux of 45Ca from preloaded SR also was increased by caffeine. The findings indicate that caffeine impairs active calcium accumulation by making SR vesicle membranes more permeable to calcium.

Animals↗
PubMed1976

Serial 3 orthogonal lead electrocardiographic abnormalities after pulmonary embolism. Computer assisted study.

The 3 orthogonal lead electrocardiogram has been evaluated with computer assisted interpretation in 20 patients with acute pulmonary embolism confirmed by pulmonary angiography. Initial 3-lead electrocardiographic abnormalities were found to be at least as helpful as the 12-lead electrocardiogram in supporting the clinical diagnosis. In addition, however, sequential changes in both the maximum QRS and T vector orientations in frontal and transverse planes were more often apparent than any sequential changes in the 12-lead electrocardiogram. While no specific 3 lead electrocardiographic criterion for pulmonary embolism could be determined, this technique was more helpful than conventional methods in following serial electrocardiographic changes in patients with this condition.

Adult↗
PubMed1976

The effects of iron deficiency on the respiratory function and cytochrome content of rat heart mitochondria.

We have examined the effects of total body iron deficiency on the function of mitochondria isolated from rat hearts. Male Wistar rats were weaned at 21 days and divided into an experimental iron-deficient group and a control group. Both groups received identical diet but an iron supplement (180 mg of ferrous sulfate per kg of diet) was added for the control group. Rats were studied at 7 and 14 weeks. Iron-deficient rats weighed less than controls but showed significantly increased ventricle to body weight ratio at both 7 and 14 weeks, indicating relative cardiac hypertrophy. Isolated mitochondrial fractions from iron-deficient and control rats contained similar proportions of whole homogenate protein and succinic cytochrome c reductase activity, indicating that the fractions isolated from the experimental and control rats were comparable. In iron-deficient rats NADH cytochrome c reductase, succinic cytochrome c reductase, succinic dehydrogenase, and NADH ferricyanide oxidoreductase activities were all significantly reduced at 7 and 14 weeks. Cytochrome c oxidase activity was significantly reduced only at 14 weeks as were the concentrations of cytochromes a3, c1, and b. The rate of oxygen uptake by mitochondria was significantly lower at both 7 and 14 weeks but the P/O ratio was unaltered. We conclude that iron deficiency is associated with impairment of myocardial mitochondrial electron transport.

Anemia, Hypochromic↗
PubMed1976

A NEW Escherichia coli O-group, O159, associated with outbreaks of enteritis in infants.

An outbreak of enteritis occurred amongst babies in a nursery unit. 25 babies were affected and 5 required intravenous therapy; there were not fatalities. From 24 of the 25 babies affected, an Escherichia coli with a previously undescribed O-antigen was isolated. An outbreak of diarrhoea had taken place in the same hospital a year before and re-examiniation of cultures of E. coli isolated at that time showed that 5 of the 15 babies affected had been excreting E. coli with the same O-antigen. Isolates from 10 of the babies were tested for enterotoxin production in the infant mouse model and 4 gave a positive response. The new O-antigen has been accepted into the international serotyping scheme and has been designated E. coli O159.

Antigens, Bacterial↗
PubMed1975

Melioidosis in a child in papua new guinea successful treatment with kanamycin and trimethoprim-sulphamethoxazole.

An instance of melioidosis is described in a five-year-old Papua New Guinean. The disease did not involve the lungs, but the patient presented with an abscess on the abdomen and with numerous abscesses on the feet. The disease was successfully treated with kanamycin and trimethoprim-sulphamethoxazole. This is the fourth case known to have occurred in Papua New Guinea, and the patient is the first to have survived.

Child, Preschool↗
PubMed1975

Catecholamine effects on cyclic AMP levels and ion secretion in rabbit ileal mucosa.

Effects of catecholamines on cyclic AMP (cAMP) levels and ion fluxes were examined in isolated rabbit ileal mucosa. The base-line cAMP level was unaffected by epinephrine (Epi), norepinephrine (Norepi), and isoproterenol. The theophylline-augmented cAMP level was decreased slightly be Epi in one series of experiments but not in another. Propranolol did not enhance this effect. The increase in cAMP level produced by cholera toxin was almost completely reversed by addition of Epi or Norepi. This reversal was prevented by phenoxybenzamine. Epi also partially reversed the increase in cAMP level produced by prostaglandin E1. Effects of Epi on ion fluxes were determined following addition of secretagogues. Epi significantly decreased theophylline-induced but not cAMP or cholera toxin-induced Cl secretion. A decrease in short-circuit current was nonetheless observed in the latter two instances. The observed discrepancies between alpha-adrenergic effects on cAMP levels and ion fluxes suggest the following possibilities: 1) ion transport-related cAMP is only a small fraction of total mucosal cAMP; 2) cAMP-induced active ion secretion is only slowly reversible, or 3) effects of alpha-adrenergic stimuli on ion transport are not due to inhibition of cAMP accumulation.

Adrenergic alpha-Agonists↗
PubMed1974

Effects of prostaglandins and cholera enterotoxin on intestinal mucosal cyclic AMP accumulation. Evidence against an essential role for prostaglandins in the action of toxin.

Both cholera enterotoxin and certain prostaglandins have been shown to stimulate intestinal fluid secretion in vivo, to cause ion flux changes in vitro similar to those caused by addition of cyclic 3',5'-adenosine monophosphate (cyclic AMP), and to activate intestinal mucosal adenyl cyclase. It has been suggested that the effects of the enterotoxin on intestinal cyclic AMP metabolism may be indirect, and that locally synthesized prostaglandins may serve as required intermediates for the effects of the enterotoxin in activating intestinal mucosal adenyl cyclase. In order to clarify certain aspects of the mechanisms by which these two agents alter intestinal mucosal cyclic AMP metabolism and ion transport, their effects on cyclic AMP accumulation in rabbit ileal mucosa were examined in vitro. Addition of 5 mug per ml (75 mug per 150 mg mucosa) of purified cholera enterotoxin produced a peak increase in cyclic AMP level in 3 h but there was a time delay of at least 30 min before any effect was observed. Inhibition of cyclic nucleotide phosphodiesterase with theophylline failed to reduce this time delay. In contrast, addition of prostaglandin E(1) (PGE(1)) increased the cyclic AMP level rapidly, a peak effect being observed in 2 min. The time of the peak prostaglandin-induced changes in cyclic AMP level and short-circuit current correlated closely. A maximal increment in cyclic AMP level was achieved with 5 x 10(-5) M PGE(1). When 10(-4) M PGE(1) was added to mucosa already maximally stimulated with cholera toxin, the resulting cyclic AMP level was equal to the sum of the levels reached when each agent was added alone. Furthermore, the effects of the enterotoxin on mucosal cyclic AMP levels were not influenced by indomethacin under conditions where mucosal prostaglandins synthesis was inhibited. The results suggest that endogenous prostaglandins do not provide an essential link in the activation of intestinal mucosal adenyl cyclase by cholera enterotoxin. The present study also indicates that the effect of cholera enterotoxin on intestinal mucosal cyclic AMP metabolism involves a definite time delay which is not due to cyclic nucleotide phosphodiesterase activity.

Adenylyl Cyclases↗
PubMed1973

Preoperative sterilization of the perineum: a comparison of six antiseptics.

Nine preparations of six antiseptic substances were applied to the perineum of pregnant women at term in order to assess their efficacy in sterilizing the skin. The efficacy, in descending order of effectiveness, after three minutes' exposure, was p-chlor-m-xylenol in alcohol (surgical Dettol); chlorhexidine gluconate in detergent (Hibiscrub), followed by the aqueous preparations p-chlor-m-xylenol (Dettol), chlorhexidine gluconate (Hibitane), cetrimide (Cetavlon), povidoneiodine (Disadine), benzalkonium chloride (Resiguard), and merthiolate. Surgical Dettol was the only alcohol-based preparation used.

Alcohols↗
PubMed1973

Effects of cycloheximide on the response of intestinal mucosa to cholera enterotoxin.

Prior studies have indicated that effects of cholera enterotoxin (CT) on the small intestine are delayed in onset and involve an interaction with adenyl cyclase in the mucosa. It has also been shown that the administration of cycloheximide to rabbits in doses which inhibit crypt cell mitoses (20 mg/kg), diminishes CT-induced fluid production in jejunal loops. These latter studies have been interpreted as indications that CT-related intestinal secretion is a crypt cell function and that it is mediated by a CT-induced protein. The present study was undertaken to delineate more precisely the nature of the interaction in the intestine between cycloheximide and cholera toxin. Pretreatment of rabbits with cycloheximide reduced by 60% the secretory response to CT in isolated ileal loops with intact blood supply. Sodium and chloride flux measurements on mucosa isolated from these and control loops indicated that this antisecretory effect of cycloheximide persists in vitro. Measurements of radioactive leucine incorporation into mucosal protein indicated that the dose of cycloheximide employed inhibited protein synthesis by 90%. This inhibitory effect was shown to be independent of any effect of cycloheximide on amino acid uptake across the brush border. Measurements of adenyl cyclase activity and cyclic AMP levels in ileal mucosa of cycloheximide pretreated and control animals indicated that cycloheximide did not diminish the CT-induced increases in these parameters. These observations demonstrate that cycloheximide reduces CT-induced intestinal fluid production without interfering with the CT-induced augmentation of adenyl cyclase activity or the consequent rise in cyclic. AMP concentration. Since the antisecretory effect of cycloheximide persists in vitro, it probably involves a direct interaction of the antibiotic with mucosal cell ion transport mechanisms rather than an indirect effect mediated by other humoral or neurogenic factors. The present observations also suggest that the secretory response of the intestine to CT involves neither the synthesis of new adenyl cyclase nor that of a protein modifying its activity.

Adenylyl Cyclases↗
PubMed1972

Acute villous inflammation in the placenta following intrauterine transfusion.

Infection is well recognized as a complication of intrauterine transfusion. The majority of cases are fortunately mild and consist merely of chorio-amnionitis. The present case, of severe type, resulted from contamination of the donor blood with Acinetobacter calcoaceticus. Spread of infection from foetus to mother has been carefully studied and an entirely new type of lesion in the placenta described. This takes the form of acute villous inflammation with resultant micro-abscess formation beneath the trophoblast layer and eventual rupture into the intervillous space. Attempts at localization are poor.

Abscess↗