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Biomedical subjects

M A MacKenzie

Publications and source records attributed to M A MacKenzie.

33 records · Page 2Linked to original sources

Thermoregulation and afterdrop during hypothermia in patients with poikilothermia.

The pathophysiology of afterdrop of core temperature during rewarming in patients with induced or accidental hypothermia remains controversial. We studied the effect of cooling and rewarming in four female patients with acquired poikilothermia and in four normal females. Exposure to cold air (16.5 degrees C) induced shivering and adequate vasoconstriction in normal individuals, without a fall in rectal temperature (Tr; 36.3 +/- 0.2 degrees C [mean +/- SD]); subsequent heating (40 degrees C) induced a rise in Tr to 37.0 +/- 0.3 degrees C and generalized sweating. The four patients all had spontaneous hypothermia (Tr 34.1 +/- 0.9 degrees C) before cooling. Tr decreased by 0.3-0.9 degrees C during cold exposure, and a marked afterdrop of Tr (0.3-0.5 degrees C) occurred during rewarming: this did not occur in normal individuals. Cooling failed to induce shivering and vasoconstriction in three patients. No patient showed visible sweating during heating despite a Tr of up to 38.0-38.5 degrees C and skin temperature of up to 37.7-38.5 degrees C. The basal metabolic rate was decreased by 71-82% in all patients during steady-state hypothermia and remained lowered during normothermia in two patients. We conclude that during hypothermia three of the four patients showed severe disorders of peripheral vasomotor function and shivering response. These data provide evidence for thermal conduction as the major mechanism of afterdrop during hypothermia.

Adult↗

Electrocardiographic changes during steady mild hypothermia and normothermia in patients with poikilothermia.

1. ECG changes observed in short-term induced and accidental hypothermia are well known. To assess the influence of steady-state spontaneous hypothermia on the ECG, we subjected four patients with acquired poikilothermia (severe thermolability) to 24 h ECG recording, exercise testing and thermal stress. 2. Twenty-four hour Holter monitoring showed a significant reduction in heart rate and a prolongation of the QT interval during steady-state mild hypothermia (rectal temperature 33.9 +/- 0.7 degrees C, mean +/- SD) compared with during normothermia; no significant changes occurred in the PR interval, QRS complex and QTc interval (QT interval corrected for heart rate). 3. Unlike during normothermia, during steady hypothermia atrioventricular Wenckebach blocks were observed in two patients, whereas another patient showed markedly more atrioventricular Wenckebach blocks during hypothermia. 4. During steady hypothermia the heart rate variability was significantly enhanced in comparison with normothermia. 5. Exercise tolerance was similar during mild hypothermia and normothermia. 6. Heat exposure (ambient temperature 40 degrees C) induced significantly greater changes in rectal temperature, heart rate and PR interval, QRS complex and QT interval in the patients than in the control subjects (n = 8). 7. The present study reveals that even mild steady spontaneous hypothermia can elicit ECG changes, presumably mediated by relatively enhanced cardiac vagal tone. Hence, spontaneous abnormalities in core temperature should be taken into account in interpreting the ECG in clinical practice.

Adult↗

Poikilothermia in man: pathophysiology and clinical implications.

Poikilothermia, the inability to maintain a constant core temperature independent of ambient temperature, markedly influences both the mental and physical function of affected patients; furthermore, prolonged hypothermia can induce numerous complications. To establish the pathophysiology of thermoregulation underlying poikilothermia in man, we compared 4 women with acquired poikilothermia, with 9 female control subjects. The activity of the main thermoregulatory effector mechanisms was assessed in a thermoneutral environment, and during subsequent cold stress and heat exposure. At thermoneutrality the patients had a significantly lower rectal temperature and resting metabolic rate compared with the controls; no patient showed peripheral vasoconstriction or shivering. Cooling revealed markedly reduced peripheral vasoconstriction in 3 patients and failure of the metabolic response in 2 patients; unlike controls, no patient exhibited shivering. Heat challenge revealed severely reduced capacity for heat dissipation in all patients. We conclude that in patients with poikilothermia, the mechanisms for both heat conservation and heat dissipation are seriously attenuated. Careful monitoring of the core temperature and adequate measures to maintain normothermia are of great importance in patients with poikilothermia in order to provide adequate treatment, improve the quality of life, and prevent serious complications.

Adipose Tissue↗

Effects of steady hypothermia and normothermia on the electrocardiogram in human poikilothermia.

The electrocardiographic changes observed in (short-term) induced and accidental hypothermia are well known. We studied the electrocardiographic effects of steady mild hypothermia in 4 female patients with poikilothermia. 24h Holter recording revealed during mild hypothermia significantly decreased heart rate and prolongation of the QT interval in comparison with normothermia. During hypothermia the short-term heart rate variability and the circadian rhythm of heart rate variability were significantly higher than during normothermia. We conclude that in our patients even mild steady hypothermia induces electrocardiographic alterations. In patients with disorders of thermoregulation one should be on the alert for cardiovascular complications, especially in cold climates.

Adult↗

The influence of glycyrrhetinic acid on plasma cortisol and cortisone in healthy young volunteers.

Based on studies in laboratory animals and on measurements of the urinary metabolites (allo)tetrahydrocortisol and tetrahydrocortisone in human volunteers it has been claimed that liquorice-induced mineralocorticoid excess is caused by a unique defect in the conversion of cortisol to cortisone. To further evaluate this hypothesis we have investigated the influence of glycyrrhetinic acid (GA), the mineralocorticoid-active constituent of liquorice, on plasma cortisol and cortisone in 10 healthy young normotensive volunteers. Pure GA (500 mg/day), administered orally from days 3-10 of the study, exerted pronounced mineralocorticoid activity. Ingestion of GA resulted in an elevated urinary excretion of free cortisol and virtually unchanged plasma cortisol levels in the presence of markedly decreased levels of both plasma cortisone and urinary free cortisone. These results provide direct clinical support for the hypothesis that GA induces an inhibition of the activity of 11 beta-dehydrogenase, resulting in a blockade in the conversion of cortisol to cortisone.

11-beta-Hydroxysteroid Dehydrogenases↗

An X;9 translocation, primary amenorrhea, and hypothalamic dysfunction.

A white girl presented at age 16 yr with delayed puberty and primary amenorrhea. She had 46 chromosomes with a de novo reciprocal X;9 translocation. The normal X chromosome was found to be heterochromatic, thus preserving the function of the translocation portion of the 9. Her total estrogen and serum estradiol levels were low and her serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were at the lower end of the normal adult range. She had a reasonably good FSH and LH response to GnRH, but an inadequate response to 100 mg of clomiphene daily for 1 wk. This would suggest that the abnormality of function is probably hypothalamic, a hitherto unreported association. De novo translocations between X chromosomes and autosomes are rare and none identical to this case has been described. The breakpoint of the X chromosome was at p22, well outside the "critical region" for female reproductive function. It seems probable that her chromosome abnormality is responsible for her clinical state.

Adolescent↗

Tenosynovitis in chickens.

An adenovirus was isolated from the tendon fluid of broilers and meat breeders with clinical tenosynovitis. The viral infection was in many cases accompanied by a staphylococcal infection. The significance of the adenovirus is not yet known, although initial transmission studies indicate that it may play a role in the tendon thickening process.

Animals↗

Dissemination of Salmonella serotypes from raw feed ingredients to chicken carcases.

During a Salmonella survey in a large integrated poultry organization it was observed that a significant correlation existed between Salmonella serotypes isolated from the raw feed ingredients and those from finished carcases. A number of serotypes hitherto unrecognized in the organization were detected in the raw feed ingredients, and were later recognized in live birds and carcases from the processing plant. It appears that a significant reduction in carcase contamination rate could be achieved by minimizing Salmonella in the meal and grain constituents of poultry feed.

Animal Feed↗

Selenium-responsive myopathy in broiler breeder hens in Queensland.

A syndrome characterised by bilateral paralysis and associated with degenerative changes in skeletal musculature, has been noted in adult breeder hens, and their progeny broilers, in a commercial poultry organisation in Queensland. Paralysis occurred between the ages of 24 to 63 weeks in broiler breeder hens and at approximately 6 weeks in the broiler chickens. Onset is slow, taking up to 2-3 days from the time leg weakness if first noticed until paralysis was complete. Other than the paralysis the birds appeared normal. Histopathological and experimental observations indicate that the muscular dystrophy is caused by a selenium deficiency. Supplementation of the diet with selenium at a level of 0.1 ppm completely alleviated the symptoms such that the birds may be returned to the mating pens.

Animals↗