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F Dexter

Publications and source records attributed to F Dexter.

142 records · Page 8Linked to original sources
PubMed1989

Muscarinic autoreceptors do not modulate kinetics of acetylcholine release in hearts.

We determined the time course of the cellular mechanism that mediates the attenuation of the chronotropic response in anesthetized dogs to decreases in the time interval (interpulse interval) between pulses of vagal stimuli. We injected propranolol, cut the cervical vagi, and repetitively stimulated the cardiac segment of the right vagus nerve with one brief burst of electrical pulses during each cardiac cycle. We recorded the initial and steady-state changes in cardiac cycle length that were induced by the phasic vagal stimulation. The decrease in the interpulse interval decreased the initial and steady-state responses. The time delay between the release of acetylcholine (ACh) from the vagal nerve endings in the heart and inhibition of the release of additional ACh was less than 4 ms. Published delays between the time of ACh release and the time of the resulting change in membrane potential, in other biological systems, are 30-12,000 ms. We conclude that the time delay was too brief for muscarinic autoreceptors to have mediated the attenuation of ACh release from postganglionic vagal nerve endings in the heart in response to decreases in interpulse interval.

Acetylcholine↗
PubMed1989

Mathematical model of the changes in heart rate elicited by vagal stimulation.

We developed a mathematical model of the underlying cellular mechanisms responsible for the changes in sinus cycle length (SCL) elicited by vagal stimulation in intact animals. The model incorporated a stimulation-mediated depletion of the releasable pool of acetylcholine (ACh) in the nerve endings, the in vitro reaction kinetics of acetylcholinesterase, and the electrical activity of a pacemaker cell with six membrane ionic currents. SCL increased linearly with the frequency of simulated vagal stimulation, as it does in animal experiments, because the concentration of ACh in the neuroeffector junction [( ACh]) saturated as the frequency of stimulation was increased and because SCL increased geometrically in response to increases in [ACh]. The dependence of SCL on the timing of vagal stimulation in the cardiac cycle resulted, in part, from the dependence of [ACh] on SCL. Simulated vagal stimulation entrained the sinus node because the rate of activation and inactivation of ACh-activated K+ channels depended only weakly on membrane potential during diastolic depolarization. SCL increased geometrically with [ACh], because 1) during diastolic depolarization, the amplitude of the ACh-activated K+ current was approximately equal to the amplitude of the sum of the other ionic currents, 2) [ACh] was low enough to saturate neither acetylcholinesterase nor the cellular system that activates the ACh-activated K+ channels, 3) the pacemaker cell membrane behaved electrotonically like a capacitor, and 4) the sum of all the ionic currents increased linearly with the amplitude of the ACh-activated K+ current.

Acetylcholine↗
PubMed1978

[A tissue bank: aspects concerning its promotion and organization (author's transl)].

In spite of continued improvement in the production of artificial tissues, there are still many instances where replacement of the damaged part by a natural tissue grafts would be preferable. It is to satisfy this requirement that tissue banding has been developed. In this paper a brief description of the preparation of tissue grafts currently being carried out in the Yorkshire Regional Tissue Bank is given and the philosophy of tissue banking from a financial and scientifical point of view is explained.

Animals↗
PubMed1975

Light and electron microscopy studies on homograft and heterograft heart valves.

Light and electron microscopical changes were studied in 23 valvular homografts and six pig aortic heterografts, which had been inserted into patients for lengths of time varying from three days to 54 months. Prior to insertion, eleven of the homografts had been sterilised by beta-propriolactone and freeze-dried, the other twelve had been sterilised by gamma-radiation. The morphological changes in the freeze-dried group were characterised by moderate to severe structural changes including gross vacuolation, fibrinoid degeneration and calcification in the absence of any significant cellular events. It is concluded that the structural changes were due to physico-chemical degradation of the collagen due to improper preservation of the graft, prior to insertion. The morphological changes in the homografts treated with gamma-radiation were fewer and less severe in that there was less vacuolation of the matrix, less fibrinoid degeneration and no examples of calcification. Clear-cut examples of graft regeneration were never observed in either group, but the significance of minor cellular infiltrates in two of the gamma-irradiated grafts is discussed in terms of abortive regeneration. The heterografts showed moderate to intense cellularity, predominantly of macrophages. It is postulated that graft rejection phenomena are responsible for the graft failure in this group.

Animals↗
PubMed1971

Pseudomonas aeruginosa in a regional burns centre.

The construction of a Regional Burns Centre in Pinderfields General Hospital, Wakefield, presented an opportunity to study Pseudomonas aeruginosa infection in patients with extensive burns. During the first year (Barclay & Dexter, 1968) a system of disinfection and bacteriological control created conditions permitting more detailed studies to be undertaken which resulted in a significant reduction of infection and cross-infection.

Air Microbiology↗
PubMedDate not supplied

Ethanol increases uterine blood flow and fetal arterial blood oxygen tension in the near-term pregnant ewe.

Fetal hypoxia is a hypothesized mechanism of ethanol teratogenesis. The objective of this study was to test this hypothesis by determining the effects of maternal ethanol infusion on uterine blood flow (UBF) and fetal oxygen status. UBF was measured with an electromagnetic flow probe placed around the left maternal uterine artery of the surgically recovered instrumented near-term pregnant sheep at 124 +/- 3 days of gestation (term = 147 days). Experimental treatment involved maternal infusion of 2 g (n = 3) or 4 g (n = 5) ethanol/kg maternal body weight, or 0.9% saline (n = 4) over a 5-h period. Arterial blood samples were collected at regular intervals to monitor maternal ethanol concentration and fetal PO2. Maternal ethanol infusion produced a dose-dependent increase (p = 0.0009) in UBF. Ethanol infusion also increased (p = 0.03) fetal arterial PO2. Overall, these findings indicate that fetal hypoxia is not a mechanism of ethanol teratogenesis.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Bolus maternal cocaine administration does not produce a large increase in fetal sheep cerebral cortical glutamate concentration.

Human cocaine use during pregnancy may result in postnatal neurologic dysfunction and abnormal behavior. L-Glutamate, the major excitatory neurotransmitter in the brain, plays an important role in cerebral cortical development. An optimal level of glutamate is required for normal neuronal development. We tested whether acute cocaine exposure produces large increases in glutamate release in the intact cerebral cortex of the near-term fetal sheep. Cocaine 3.0 mg kg(-1) IV bolus produced the expected increase in maternal and fetal mean arterial pressure, increase in fetal heart rate, decrease in uterine blood flow, and decrease in fetal arterial blood pO2 (N = 5). The percentage increases in extracellular glutamate concentration in the fetal cerebral cortex measured by in utero microdialysis were 7%, 15%, 17%, 17%, and 43% in each fetus (upper 95% confidence bound for the median = 43%). We conclude that if cocaine increases glutamate concentration in the developing cerebral cortex, the increase in magnitude is small relative to the changes produced by other interventions such as ethanol or umbilical cord occlusion. Mechanisms other than increases in cerebral cortical glutamate concentration probably contribute to the neurologic injury associated with prenatal cocaine exposure.

Animals↗
PubMedDate not supplied

Regional anesthesia does not significantly change surgical time versus general anesthesia--a meta-analysis of randomized studies.

BACKGROUND AND OBJECTIVES: The major determinant of variable operating room costs is surgical time. A number of factors contribute to surgical time. This study was designed to determine whether regional anesthesia decreases surgical time when compared with general anesthesia over several surgical procedures. METHODS: A search was conducted for clinical trials that reported surgical times and which compared outcomes from regional versus general anesthesia. A meta-analysis of these trials was completed to determine whether, on average, among many surgeons and surgical procedures, the use of regional anesthesia affects surgical time. Confidence intervals were calculated and random effects meta-analysis was used to pool results. RESULTS: Twenty-six studies (with 1,874 patients) were used in the meta-analysis. Regional anesthesia does not significantly decrease surgical time versus general anesthesia (mean general minus regional difference was 1.7 minutes, 95% confidence interval -0.5 to 3.9 minutes). CONCLUSIONS: Overall, the use of regional anesthesia does not significantly decrease surgical time.

Anesthesia, Conduction↗