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Biomedical subjects

T A Gray

Publications and source records attributed to T A Gray.

47 records · Page 3Linked to original sources
PubMed1987

Hyperlactataemia and metabolic acidosis following paracetamol overdose.

Plasma lactate concentrations and acid-base status were determined in 53 patients poisoned with paracetamol. Eleven patients (Group 1) had plasma paracetamol concentrations below the standard treatment decision line; 19 cases (Group 2) presenting within 15 h of overdose had plasma paracetamol concentrations above the treatment line and received N-acetylcysteine. The remaining 23 patients (Group 3) arrived at hospital too late (more than 15 h after overdose) for treatment with N-acetylcysteine to be completely effective. Compensated metabolic acidosis was present on admission in 55 per cent of Group 1 and 42 per cent of Group 2 patients, and a further 21 per cent of cases in Group 2 had an uncompensated metabolic acidosis. Half the patients in Group 3 were acidotic: 22 per cent had a compensated and 26 per cent an uncompensated metabolic acidosis. On admission, the mean plasma lactate concentration was elevated in both Group 2 and Group 3 patients though not in Group 1 cases. Plasma lactate concentration then fell to normal in patients in Group 2 but became mildly elevated again in some cases at a time which coincided closely with the peak in serum aspartate aminotransferase activity. In patients presenting within 15 h of overdose there was a significant correlation between the elevation in plasma concentrations of lactate and paracetamol at admission. In patients presenting late (Group 3), plasma lactate remained elevated for longer than in Group 2 and acidosis and hyperlactataemia were prominent features in the four patients who died. This study demonstrates first that hyperlactataemia, with or without significant acid-base disturbance, is common following paracetamol overdose particularly in those who are severely poisoned. As uncompensated metabolic acidosis is found in 20 per cent of patients who present early and require protective therapy, it should be sought and corrected if it does not remit spontaneously. Second, half the patients presenting too late for effective treatment are acidotic and those with an uncompensated metabolic acidosis resistant to correction have a poor prognosis. Paracetamol poisoning should be considered in the differential diagnosis of metabolic acidosis of unknown aetiology.

Acetaminophen↗
PubMed1986

Plasma ionized calcium monitoring during liver transplantation.

Plasma ionized calcium and citrate concentrations were measured in 11 patients undergoing liver transplantation. During the anhepatic phase of the procedure, ionized calcium concentrations fell to as low as 40% of normal, in spite of calcium supplementation. Simultaneously, citrate concentrations rose to between 20 and 100 times preoperative levels. In two patients low plasma ionized calcium concentrations were associated with hypotension that responded to calcium infusion. Intraoperative monitoring of plasma ionized calcium during liver transplantation is helpful in the rational control of the patient's calcium status.

Calcium↗
PubMed1986

Effects of chronic ethanol treatment on neocortex.

Neocortical inhibition and neuronal morphology were studied in rats following chronic ethanol treatment (CET). In terminal acute experiments, spontaneous neuronal discharges in pair-fed and naive rats were inhibited by epicortical stimulation, a procedure known to produce postsynaptic inhibition. Few units in CET rats were inhibited by such stimulation. Cortical recurrent inhibition, indicated by a surface-negative potential in response to antidromic stimulation of the cerebral peduncle, was little affected by a challenge dose of ethanol, compared with the response in pair-fed animals. Recurrent inhibition involves inhibitory interneurons. CET apparently made inhibitory interneurons and inhibitory postsynaptic receptors less responsive to ethanol. Apical dendritic spines on some portions of pyramidal neurons increased in number with CET. This could reflect a compensatory growth in neurons not damaged by CET. The overall observations are consistent with ethanol affecting one or more specific systems of cortical motor control as opposed to its presumed general disinhibitory effect.

Animals↗
PubMed1984

Inflammatory myelopathy presenting as a cystic intramedullary spinal cord lesion.

A case of subacute progressive spinal tetraparesis had myelographic evidence of cervical spinal cord swelling and a delayed metrizamide computed tomographic myelogram (MCTM) suggested cavitation within the swollen spinal cord. Surgical exploration of the cervical cord revealed inflammatory changes only. No syrinx or intramedullary tumour was found. The accumulation of metrizamide within the spinal cord, as demonstrated by MCTM, did not represent a syrinx or a cystic tumour, but more likely an area of inflammation. Because inflammatory myelopathy may simulate an intramedullary tumor or syrinx, careful analysis of all clinical and radiological information is necessary to help make a correct diagnosis.

Adult↗
PubMed1984

Filamentous axonopathy in disulfiram neuropathy.

A 52-year-old female developed a sensorimotor polyneuropathy while on treatment with disulfiram. Electron microscopic examination of a sural nerve biopsy disclosed occasional axons distended by intermediate filaments. Identical changes can be induced in animals by carbon disulfide (CS2), a metabolite of disulfiram. Our findings suggest that disulfiram neurotoxicity is mediated by CS2 and is exerted on the distal axon.

Alcoholism↗
PubMed1977

The relationship between stimulation-induced potassium release and amylase secretion in the mouse parotid.

1. The output of amylase from superfused mouse parotid segments in response to stimulation with acetylcholine (ACh), phenylephrine and isoprenaline during exposure to solutions with varying potassium concentrations was monitored by an on line automated fluorometric method. 2. During stimulation with ACh or phenylephrine a 10-fold increase in superfusion fluid potassium concentration caused an immediate very marked reduction in amylase output which was fully reversible. A 10-fold reduction in potassium concentration resulted in a prominent rise in amylase output. During stimulation with isoprenaline there was no effect on the amylase output of varying the extracellular potassium concentration. Acetylcholine and phenylephrine caused potassium release from the mouse parotid whereas isoprenaline had no such effect. 3. It appears that under conditions where stimulation-induced potassium release is enhanced there is also an enhanced amylase secretion and vice cersa. There may therefore be a link between passive potassium transport and amylase secretion.

Acetylcholine↗
PubMed1975

Electron-paramagnetic-resonance spectroscopy studies of iron-sulphur centres of submitochondrial particles from iron- and sulphur-deficient. Candida utilis.

1. Measurements were made at 12 degrees K of the electron-paramagnetic-resonance (e.p.r.) spectra of submitochondrial particles from Candida utilis cells grown under conditions that alter the amount of the mitochondrial NADH dehydrogenase (EC 1.6.99.3). 2. Iron-limited growth decreases the extent of iron-sulphur e.p.r. signals to undetectable values that are less than 1 percent of those normally found with glycerol-limited growth. 3. Small but significant signals attributable to the NADH dehydrogenase were detected in submitochondrial particles from sulphate-limited cells. 4. Measurements made on submitochondrial particles prepared from these and other phenotypically modified cells lead us to conclude that the presence of low-temperature e.p.r.-detectable iron-sulphur centres attributable to the NADH dehydrogenase are necessary but not sufficient for the coupling of ATP synthesis to the NADH dehydrogenase reaction in the mitochondrial membrane of C. utilis. 6. The amplitude of the g=2.01 signal observed in non-reduced submitochondrial particles is approximately tenfold diminished by iron limitation but not significantly altered by sulphate limitation.

Adenosine Triphosphate↗
PubMedDate not supplied

Personal and family history of affective illness in patients with multiple sclerosis.

There is a high prevalence of affective illness, both depression and bipolar disorder, in patients with multiple sclerosis. In this study, the family history method was used to assess the prevalence of affective illness in first-degree relatives of patients with multiple sclerosis. There was not an excess of affective illness in the relatives suggesting that affective disorder associated with multiple sclerosis does not have a familial pattern similar to primary affective disorder. Clinical and theoretical implications of these findings are discussed.

Adult↗