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Biomedical subjects

I A Silver

Publications and source records attributed to I A Silver.

At least 73 records · Page 4Linked to original sources
PubMed1984

Neurotransmitter amino acids in the CNS. I. Regional changes in amino acid levels in rat brain during ischemia and reperfusion.

The levels of amino acids in 6 regions of the brain (cortex, hippocampus, striatum, diencephalon, stem and cerebellum) were determined during an ischemic insult of 30 min and after recovery periods of up to 10 h. The results were analyzed in two groups: putative neurotransmitters (GABA, aspartate, glutamate, taurine, glycine and alanine) and non-neurotransmitters. In the neurotransmitter group, it was found that at the end of 30 min ischemia the levels of aspartate and glutamate slightly decreased whereas those of GABA and alanine rose substantially. The amounts of glycine and taurine remained unchanged. In 30 min after the ischemic insult, there were much larger decreases in aspartate and glutamate and increases in GABA and alanine with no change in glycine and taurine. At 2 h recovery the levels of the neurotransmitter amino acids had almost returned to control values and were fully recovered by 10 h after ischemia. It is postulated that glutamate and aspartate are released during ischemia into the extracellular space and subsequently 'washed-out' into the blood during the reperfusion. Release of GABA, if it occurs, is however, compensated by increase in its synthesis and decrease in its degradation under anaerobic conditions, both of which contribute to the rise in its steady-state level. In the non-transmitter category, increases were seen in amino acids present normally in very small concentrations; tyrosine, lysine, leucine and 3 hydrophobic amino acids: valine, methionine and phenylalanine, which were most pronounced at 2 h after ischemia. It is suggested that the rise in the levels of these molecules is the consequence of stimulation of protein breakdown caused by activation of intracellular proteases by calcium and H+ during the ischemic episode. Regional variations in the patterns of changes were small although in the ischemic models used the brainstem seemed to be least affected.

Alanine↗
PubMed1984

The distribution of types I and III collagen and fibronectin in the healing equine tendon.

During tissue response to injury the glycoproteins fibronectin and Type III collagen are synthesized in increased amounts. We have studied the distribution of these molecules in the healing tendon at various times after injury by comparison with that of the major constituent of normal tendon, Type I collagen. Immunofluorescent localization demonstrated the presence of fibronectin throughout the tendon within one week after injury. Staining was found in the matrix, both around capillaries and around fibroblast-like cells. Fibronectin was still apparent in the healing tendon at one month after injury, but after a further two months was no longer detectable. Type III collagen was present both in pericellular and matrix locations until three months after injury, and matrix staining was apparent during the entire fourteen-month period under study. Type III collagen was also found throughout the matrix of the contralateral superficial flexor tendon during this period.

Animals↗
PubMed1984

Studies on the pathogenesis of equine tendonitis following collagenase injury.

The histological and morphological characteristics of the scar tissue formed during healing after traumatic equine tendon injury have been compared with those of scar tissue produced in response to an enzyme-induced pony tendon injury. Several techniques are currently in use in the treatment of equine tendon sprain and this work formed part of a study of their respective efficacy. It was concluded that the enzyme-induced lesion is resolved by a reparative process very similar in its prognosis and extent to that following a naturally occurring tendon sprain. It may therefore justifiably be used as a model of naturally occurring tendon sprain in the comparative study of treatment methods.

Animals↗
PubMed1983

Cellular effects of endotoxin in vitro. II. Reversibility of endotoxic damage.

Administration of Escherichia coli endotoxin to NB41A3 neuroblastoma cells in culture produced decreases in 1) intracellular [ATP]/[ADP], 2) flux through pyruvate dehydrogenase (PDH), and 3) total intracellular calcium. These effects were reversible if endotoxin was washed off within 10-15 min, but not if it remained in contact with the cells for 30 min or more. Minor, reversible morphological and functional alterations occurred during the initial phase, but after 30-min exposure to the toxin, the damage was irreversible. A model is proposed in which early, reversible weak binding of endotoxin to the plasma membrane partially blocks inward calcium flux, lowering the intracellular [Ca2+] and consequently the PDH phosphatase activity which activates the PDH complex. If endotoxin is removed at this stage, these processes are reversed and the cell recovers. If not, the toxin becomes irreversibly incorporated into the cell with consequent damage to the plasma membrane and organelles, which leads to massive ion movements resulting in cellular hydration with ultimate disruption of mitochondria and cell death.

Adenosine Diphosphate↗
PubMed1983

A clinical and experimental study of tendon injury, healing and treatment in the horse.

This project was carried out over a five year period (1977 to 1981 inclusive) at the University of Bristol following discussion between the British Veterinary Association and the Royal College of Veterinary Surgeons about the efficacy of, and ethical justification for, the practice of 'firing' (cautery). These discussions had been promoted by parliamentary questions but led to no firm conclusions because previously reported clinical investigations on specific treatments lacked adequate comparisons and controls and thus did not provide scientifically acceptable, statistically valid data. The project was originally conceived as having two main sections, one clinical and the other experimental. The Veterinary Advisory Committee of the Horserace Betting Levy Board felt that primary attention should be given to the clinical investigation and this was done.

Animals↗
PubMed1982

Laboratory outbreak of Q fever acquired from sheep.

In April and May, 1981, an outbreak of Q fever occurred in a university department which used gravid sheep for fetal respiratory studies. During the subsequent investigation 91 people were studied and 28 were found to have complement-fixing antibodies to the phase II antigen of Coxiella burneti in their serum. Symptoms compatible with C. burneti infection occurred in 14 of the seropositive patients. The majority of symptomatic infections could be related to the delivery of twin fetuses in one laboratory, but some people remote from this incident who were exposed to sheep in other parts of the building also showed evidence of infection. Those people with serological evidence of recent infection were treated with tetracycline for 4 weeks. Defects were apparent in the facilities being used for the research and the risk of Q fever infection should be borne in mind by groups engaged in work with pregnant sheep.

Animals↗
PubMed1982

Anesthetic influence on arteriolar diameters and tissue oxygen tension in hemorrhaged rats.

Arteriolar diameters and tissue oxygen tensions were measured in the cremaster muscles of 68 hemorrhaged rats which were anesthetized with either intramuscular ketamine, 125 mg/kg, plus 30 mg/kg supplements as needed, or enflurane, 2.2% inspired. Animals breathed room air, or room air plus enflurane, throughout the experiments. Arterioles in the cremaster muscle were identified according to successive orders of branching, and the internal diameters of first-, third-, and fourth-order vessels were measured at 30-s intervals. Cremaster muscle oxygen tension was measured polarographically with platinum-iridium microelectrodes. Mean arterial pressure was controlled at 30-35 mmHg during 30 min of hemorrhage, and maximum shed blood volumes were similar (2.6 ml/100 g) in both groups. Principal responses to hemorrhage in rats receiving enflurane were 1) constriction in first-, third-, and fourth-order arterioles, and 2) tissue hypoxia. In hemorrhaged rats receiving ketamine, the constrictor response to hemorrhage either was diminished (first-, and third-order arterioles) or abolished (fourth-order arterioles), and tissue hypoxia did not occur. The authors conclude that ketamine, as compared with enflurane, diminishes or prevents arteriolar constriction and tissue hypoxia in the cremaster muscle of hemorrhaged rats.

Anesthetics↗
PubMed1982

Basic physiology of wound healing in the horse.

Wound healing is part of the normal general repair process of the body. Its efficient completion depends on many factors, some physical, eg, pH, oxygen tension and tissue tension, and some biological, eg, cell-cell interaction and feedback of extracellular matrix on to the cells which produce it. The factors which affect healing are discussed and failures and anomalies in the process described. New techniques which may improve the quality of healing in specialised tissues are explained. Recent research on wound healing has concentrated on the role of the different cell types in the process and also on the effects of micro-environment on the enhancement or inhibition of cellular activity. The wound is a situation in which cells are apparently operating at the limits of their powers of survival and very slight modification of the micro-environment can render the tissue either unduly hostile to the cell or can enhance cellular activity. While it is not possible to increase the rate of healing of a clean surgical wound to any useful degree, an understanding of the mechanics of wound healing is essential to a rational treatment of simple or indolent wounds. It is especially important that surgical or medical treatment should complement, rather than compete with, the natural process. Tight bandages, which compress circulation, or excessive washing, which may remove macrophages and dilute bacteriostatic or chemotaxic agents, should be avoided.

Animals↗
PubMed1982

Some aspects of tissue maturation in fetal and perinatal foals.

Collagen, elastin and structural glycoprotein content of the lungs of 38 fetal and neonatal foals, 8 of which were showing dysmaturity or convulsive syndrome, were measured by standard biochemical means. Glycoprotein content showed little or no change between 100 and 340 days of gestation; elastin remained constant from 100 to about 260 days when there was an exponential increase up to the time of birth, while collagen content rose linearly from 100 days to birth. In dysmature animals there was significantly less collagen in the lungs at birth but the difference in elastin content between the two groups was not statistically significant. There was no clear distinction between glycoprotein content of the dysmature and normal animals. Histological studies indicated that the lung of the fetal horse matures early and in the last third of pregnancy the adult pattern of blood vessels and trabeculae had already appeared. The reduced collagen content in the dysmature foals might be associated with anomalies of collagen synthesis and cross-linking. These could weaken the structure of the lungs and blood vessels and lead to haemorrhages, especially those in the central nervous system, which are a feature of the dysmature syndrome.

Animals↗
PubMed1981

The PO2 in venous valve pockets: its possible bearing on thrombogenesis.

The PO2 in the lumen and valve pockets of veins in 2 patients and 8 dogs was measured during streamline blood flow and in conditions of intermittent pulsatile flow. The blood within the valve pockets became rapidly hypoxic when undisturbed during streamline flow (i.e. when "static"), but the PO2 in the pockets rose to that of the lumenal blood when the column of venous blood was made to pulsate and so empty the valve pockets at short intervals. The observations suggest that the endothelium covering the valve cusps is entirely dependent on pocket or lumenal blood for its oxygen supply. The endothelium facing the pocket can therefore become hypoxic during non-pulsatile blood flow when that facing the lumen is adequately to oxygenated. Early thrombus formation was seen to develop on a valve cusp after only 2 h non-pulsatile flow. The demonstration that localized hypoxaemia occurs readily and can produce endothelial damage, in circumstances and situations where thrombi are commonly found to originate, is additional circumstantial evidence that hypoxia may trigger thrombogenesis.

Adult↗
PubMed1981

Effects of in vitro hypoxia and lowered pH on potassium fluxes and energy metabolism in rat brain synaptosomes.

Synaptosomes isolated on isosmotic Ficoll density gradients are an effective model for some aspects of neuronal function. They maintain metabolic energy levels ([ATP]/[ADP] [Pi]) and transplasma membrane electrical potentials very similar to those of neurons in the intact brain. The concentration of K+ in the external medium (K+-sensitive electrode), O2 uptake, and cytochrome c reduction (550 nm minus 540 nm) were simultaneously monitored in synaptosomal suspensions. Oxidative metabolism is the primary source of intrasynaptosomal ATP and at pH 7.4 anaerobiosis results in K+ leakage at 4.5 +/- 0.8 nmol/min/mg protein with glucose as substrate and 10.7 +/- 1.9 nmol/min/mg protein with lactate plus pyruvate (10:1) as substrate. Reintroduction of oxygen initiates complete (ouabain-sensitive) reuptake of K+ at initial rates of 35.4 +/- 3.2 nmol/min/mg protein and 18 +/- 1.7 nmol K+/min/mg protein, respectively. The rates of K+ leakage and reuptake fall when the pH is lowered from 7.4 to 6.0 but recover fully if the pH is raised to the original value. The rates of K+ release and uptake decrease when the Na+ concentration in the medium is decreased and increase when the Ca2+ concentration is decreased. The intrasynaptosomal [K+] under aerobic conditions was 77.3 +/- 3 mM and the calculated K+ diffusion potential was -72 mV. Anaerobic incubation of the synaptosomes from up to 20 min and at pH values from 7.4 to 6.0 did not produce irreversible impairment of any of the measured variables. These results suggest that permanent loss of brain function following prolonged hypoxia and ischemia is not due to irreversible damage to the synapses with respect to these parameters but rather to impairment of some other neuronal functions.

Adenosine Diphosphate↗