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Biomedical subjects

J R Foster

Publications and source records attributed to J R Foster.

At least 109 records · Page 6Linked to original sources

The electrophysiological substrate of atrial fibrillation.

The electrophysiological substrate that predisposes the human atrium to sustain atrial fibrillation is incompletely understood. However, abnormalities of atrial size, refractory period and conduction are important precursors to this arrhythmia. The propensity of various disease states, cardioactive drugs and the autonomic nervous system to potentiate atrial fibrillation may be explained by changes in these electrophysiological properties.

Animals↗

Atrial excitability and conduction in patients with interatrial conduction defects.

Prolongation of P-wave duration is an accepted indicator of an interatrial conduction disturbance and may predispose patients to atrial arrhythmias. This study was performed to monitor electrophysiologic characteristics of the atria in patients with a prolonged P-wave duration. Atrial excitability and conduction times were compared in 7 patients with a P-wave duration of less than 115 ms (Group I), and 13 patients with a duration of greater than of equal to 115 ms (Group II). In contrast of the Group I patients, most of the 13 patients in Group II had atrial arrhythmias, including sinus nodal dysfunction (3 patients) and a history of atrial fibrillation or ectopic atrial tachycardia (6 patients). Electrophysiologic differences between the 2 groups included a higher late diastolic threshold in Group II (0.8 +/- 0.2 mA versus 1.3 +/- 0.2 mA; p less than 0.005), and a greater increase in intraatrial conduction time (5 +/- 10 ms versus 30 +/- 20 ms; p less than 0.005) and interatrial conduction time (5 +/- 15 ms versus 30 +/- 15 ms; p less than 0.05) of early premature responses. There were no differences between the 2 groups in refractory periods, shape of the strength interval curve, or conduction times of premature responses occurring late in diastole. These abnormalities in conduction time and excitability found in patients with a prolonged P-wave duration may predispose to the initiation of certain atrial tachyarrhythmias.

Adult↗

Peroxisome proliferation in cultured rat hepatocytes produced by clofibrate and phthalate ester metabolites.

Adult rat hepatocytes cultured for 48 h in the presence of 0.2 mM clofibrate, mono-(2-ethylhexyl)-phthalate (MEHP) or 2-ethylhexanol (2-EHA) contained increased numbers of peroxisomes. In keeping with the effects of these compounds in vivo, the peroxisome proliferation was associated with marked increases (up to 15-fold) in the activity of carnitine acetyltransferase. No such effects were produced by n-hexanol or two microsomal enzyme inducers, phenobarbital and 1,2-benzanthracene. These results suggest that cultured hepatocytes may provide a useful model system for studying chemically induced peroxisome proliferation.

Animals↗

Studies on the effects of orally administered dicyclohexyl phthalate in the rat.

The oral administration of 500-2500 mg/kg/day dicyclohexyl phthalate (DCHP) to young male Sprague-Dawley rats for 7 days resulted in liver enlargement and induction of some parameters of hepatic xenobiotic metabolism. Additional studies indicated that the hepatic enzyme induction resembled that of sodium phenobarbitone rather than that of polycyclic hydrocarbons. Morphological examination of the livers of DCHP treated rats revealed centrilobular cell hypertrophy and ultrastructural examination demonstrated marked proliferation of the smooth endoplasmic reticulum. Mitochondrial structure and numbers of peroxisomes (microbodies) were not affected. DCHP treatment did not affect kidney and testes weights but some histological evidence of testicular damage was obtained with 2500 mg/kg/day of DCHP. The metabolites of DCHP, namely monocyclohexyl phthalate (MCHP) and cyclohexanol, also induced certain parameters of hepatic xenobiotic metabolism. MCHP, but not cyclohexanol also produced marked testicular atrophy. It is concluded that DCHP is a weak drug-type inducer of hepatic xenobiotic metabolism in the rat and the hepatic effects of this phthalate diester are different from those of di-(2-ethylhexyl) phthalate.

Animals↗

Arrhythmogenic effects of carbon monoxide in experimental acute myocardial ischemia: lack of slowed conduction and ventricular tachycardia.

To investigate the possibility that carbon monoxide (CO) at high clinically encountered levels may have arrhythmogenic effect in initial minutes of acute myocardial ischemia, 14 dogs underwent thoracotomy and recording of bipolar epicardial electrograms during brief (6-minute) left anterior descending coronary artery (LAD) occlusions. Eight of the 14 dogs were studied both before and after CO pretreatment in which carboxyhemoglobin levels of 6.8% to 14.6% (mean 10.4 +/- 2.8%) were achieved. Epicardial electrograms showed no change in degree of ischemic myocardial conduction slowing after CO, and there was no significant difference between CO and no-CO LAD occlusions in incidence of spontaneous ventricular tachycardia. Since the degree of myocardial conduction slowing is thought to be importantly related to susceptibility to ventricular arrhythmias in acute ischemia, this study suggests that CO may not be arrhythmogenic during early minutes of acute myocardial ischemia.

Animals↗

Evidence of transient effect by lignocaine on alveolar macrophage morphology.

Alveolar macrophages were extracted from rat lung by pulmonary lavage. The lavage fluid consisted of Joklik's minimum essential medium alone, containing lignocaine, or lignocaine with the addition of 10% foetal calf serum. Although the presence of lignocaine increased the macrophage yield 3-fold, in the absence of foetal calf serum the resulting macrophage population exhibited gross cytoplasmic vacuolation. The presence of foetal calf serum prevented this vacuolar formation. There was no difference in either the osmolarity or pH of the media and although the vacuolation failed to produce changes in a cell viability assay, the presence of the morphological change is obviously undesirable when functional studies are to be carried out.

Animals↗

A study of the initiation of biliary hyperplasia in rats infected with Fasciola hepatica.

Following infection of rats with Fasciola hepatica, an increase in the number of epithelial cells in the common bile duct, labelled with [3H]thymidine, was detected autoradiographically as early as 5 days post-infection (p.i.). This initial mitogenic effect of the infection was limited to that region of the bile duct lying adjacent to the liver, while the region lying next to the duodenum failed to show any increase in labelling until 41 days p.i. Mechanical contact between the parasite and the biliary epithelium did not occur until 41 days p.i. and the initial hyperplasia was evidently not a result of mechanical irritation. The study serves to emphasize the chemical aetiology of the precocious biliary hyperplasia and to more accurately identify its onset.

Animals↗

Prescription of gain-setting and prognosis for use and benefit of post-aural hearing aids.

Degree of hearing aid use, aid gain setting and the improvement given by the aid in a speech identification task were determined for a sample of post-aural hearing aid users. Measures of the spectral effects of gain settings received by individuals suggested that the poor frequency responses of the aids examined severely restricted the overall gain and hence the frequency range of useful gain. The outcome variables of use, gain and improvement in identification were each examined in relation to a selection of audiological predictor variables that would be easily obtained clinically. Multiple-regression analysis furnished equations accounting for a considerable proportion of the variance in gain setting and in use and for a moderate proportion of the variance in the identification improvement score. These results suggest that it is valid to predict use on an individual basis when determining the emphasis of rehabilitative programmes and it is helpful to predict gain for individuals when advising them on the gain setting to be attempted. The patterns of correlations obtained justify determining the speech detection threshold and the uncomfortable loudness level in order to predict a most comfortable level and when assessing the benefit and use of an aid.

Audiometry, Speech↗

Use and benefit of postaural aid in sensory hearing loss.

A sample of postaural hearing aid users was followed through adaptation to use of an aid over an 18-month period subsequent to issue. Minor assistance and advice was given but no intensive hearing therapy or other instruction. A miniature timing device was installed in an aid substituted for a few days to provide a check on self-reported extent of use. On both objective and self-report measures, postaural aids receive substantially greater use than the body-worn aids in comparable previous investigations, about half the aids being used over 4 hours per day. Word-identification of free-field listening in aided and unaided conditions showed advantages of 10% or more in only 45% of those tested, yet questionnaire responses suggested reliable subjective benefits in specific listening situations. The results justify taking not only measures of speech identification improvement but also questionnaire measures and measures of time of use in field trials when evaluating overall effectiveness of aid provision.

Aged↗

The effect of lidocaine on reentry within the His-Purkinje system in man.

The effects of intravenous lidocaine were assessed in 11 patients with normal intraventricular conduction in whom reentry within the His-Purkinje system (RE-HPS) occurred consistently over a narrow range of ventricular (S1S2) coupling intervals. RE-HPS was characterized by a spontaneous beat (V3) inducible by critically timed premature stimuli (S2) during constant ventricular drive (S1S1), and was dependent upon critical retrograde conduction delay within the HPS (S2H2 interval). Lidocaine abolished RE-HPS in six of 11 patients (group 1) and shortened the zone of RE-HPS in five of 11 patients (group 2). In group 1 after lidocaine, critical S2H2 intervals for RE-HPS were not attained at any S1S2 in four patients and critical S2H2 intervals were equaled but not exceeded in two patients without resulting in RE-HPS. In group 2 after lidocaine. RE-HPS was present in all patients at S2H2 intervals comparable to control values; however, significantly closer S1S2 intervals were necessary to achieve these requisite S2H2 delays (p < 0.005). The longest S2H2 intervals at comparable S1S2 intervals were significantly shortened by lidocaine in 11 of 11 patients (p < 0.001). Thus, lidocaine causes a significant decrease in retrograde refractoriness within the HPS in patients with normal intraventricular conduction.

Blood Pressure↗