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M.a. Mackenzie - One of the best experts on this subject based on the ideXlab platform.
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Skin blood flow and autonomic reactivity in human Poikilothermia
Clinical Autonomic Research, 1996Co-Authors: M.a. Mackenzie, A. R. M. M. Hermus, Hub Wollersheim, J. W. M. Lenders, T ThienAbstract:Autonomic reactivity is pivotal in maintaining a constant body core temperature. Skin vasomotor reflexes and cardiovascular reactivity were investigated in four women (aged 28–37 years) with acquired Poikilothermia, during steady-state spontaneous hypothermia (rectal temperature (T_r)=33.7 ± 1.0°C [mean ±SD]) and steady-state normothermia (T_r=36.7 ± 0.3°C), as well as in 12 normothermic control subjects. Baseline finger temperature (T_f) during hypothermia was significantly lower than during normothermia (T_f=32.4 ± 1.2 compared with 36.2 ±0.3°C, respectively), and than in the controls (T_f=34.8 ±0.8°C). No significant differences in baseline skin blood flow and forearm blood flow were found between subjects during hypothermia or normothermia and controls, suggesting a failure of sympathetic drive to counter-regulate hypothermia in the subjects. Skin vasoconstrictor responses to the contralateral cooling test and neck cooling test were markedly attenuated in three subjects, and to the finger cooling test in two subjects, during normothermia compared with hypothermia. Blood presure responses to the Valsalva manoeuvre and head-up tilting were normal in all subjects, whereas the heart rate response to head-up tilting was blunted in three subjects during hypothermia. The responses of blood pressure and forearm blood flow to the cold pressor test in the subjects during both thermal conditions were comparable with the controls. We conclude that in our subjects, without generalized autonomic failure, Poikilothermia has to be attributed predominantly to disorders of the central thermoregulatory pathways. Our findings during hypothermia and normothermia indicate that variations in core and skin temperature significantly affect skin vasomotor reactivity.
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Sudomotor function in human Poikilothermia
Neurology, 1995Co-Authors: M.a. Mackenzie, E. Schonbaum, A. R. M. M. Hermus, Hub Wollersheim, Th. Thien, A. G. H. Smals, Peter W. C. KloppenborgAbstract:Hypohidrosis predisposes to hyperthermia and may indicate generalized thermoregulatory failure.To assess the sweating capacity in human Poikilothermia, we performed a quantitative analysis of the central and peripheral sudomotor pathways in four women with acquired Poikilothermia (aged 29 to 38 years) and nine controls. Heat challenge in a climatic chamber (ambient temperature 40 degrees C, 50% relative humidity) for 180 minutes revealed that both sweat secretion and evaporative weight loss were significantly lower in the patients than in the controls (p less than 0.01). Temperature thresholds for thermal sweating were markedly elevated in at least two patients, whereas a third patient showed no sweating response. Stimulation of the eccrine sweat glands by intradermally injected acetylcholine during reduced core temperature (34.9 plus minus 0.7 degrees C) revealed a significantly reduced sweating response in all patients (p less than 0.01); the sudomotor response to pilocarpine iontophoresis was reduced or absent in three patients. We conclude that the generalized thermoregulatory sudomotor failure in these patients was attributable primarily to disorders of the central sudomotor drive; the impaired postganglionic sudomotor response is temperature related and possibly secondary to (long-standing) Poikilothermia. Quantification of heat-dissipating capacity is pivotal for diagnosing severe thermolability and may help to prevent serious heat illness. NEUROLOGY 1995;45: 1602-1607
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Effect of Steady Hypothermia and Normothermia on Multimodality Evoked Potentials in Human Poikilothermia
Archives of neurology, 1995Co-Authors: M.a. Mackenzie, Dick M. Vingerhoets, Ernst J Colon, Alfred J. L. G. Pinckers, Servaas L. H. NotermansAbstract:Objective: To assess the effects of steady-state spontaneous hypothermia on multimodality evoked potentials and on peripheral nerve conduction in human Poikilothermia. Design and Setting: Case series at a university hospital. Patients: Four patients (four women, aged 28 to 37 years) with acquired Poikilothermia. Main Outcome Measures: Short-latency somatosensory, brain-stem auditory, and visual evoked potentials as well as motor and sensory peripheral nerve conduction velocity during steady-state spontaneous hypothermia and normothermia. Results: The marked latency prolongation of all evoked potentials and decreased peripheral nerve conduction velocity observed during steady-state spontaneous hypothermia (mean±SD core temperature, 33.5±0.3°C) compared with normothermia (36.9±0.4°C) agrees with previous findings during short-term induced hypothermia. Conclusions: The unequivocal effect of sustained mild spontaneous hypothermia on evoked potentials and peripheral nerve conduction velocity underlines the importance of meticulous attention to even small alterations in core temperature in interpreting neurophysiological investigations.
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Thermoregulation and afterdrop during hypothermia in patients with Poikilothermia
The Quarterly journal of medicine, 1993Co-Authors: M.a. Mackenzie, A. R. M. M. Hermus, Hub Wollersheim, R A BinkhorstAbstract: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.
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Electrocardiographic changes during steady mild hypothermia and normothermia in patients with Poikilothermia.
Clinical science (London England : 1979), 1992Co-Authors: M.a. Mackenzie, A. R. M. M. Hermus, A. G. H. Smals, Wim R.m. Aengevaeren, Tjeerd Van Der Werf, Gerlach F. F. M. Pieters, Peter W. C. KloppenborgAbstract: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.
M Zegil - One of the best experts on this subject based on the ideXlab platform.
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Synergistic induction of severe hypothermia (Poikilothermia) by limbic seizures, acepromazine and physical restraint: role of noradrenergic alpha-1 receptors.
Pharmacology biochemistry and behavior, 2001Co-Authors: M A Persinger, R P O'connor, Y R Bureau, G H Parker, O Peredery, M ZegilAbstract:The maintained production of extreme reductions in core temperature (20-22 degrees C) or Poikilothermia can be reliably produced by the synergistic interaction of limbic seizures (induced by lithium and pilocarpine), postseizure administration of a single injection of acepromazine, and physical restraint. Administration of the specific and nonspecific dopamine antagonists haloperidol, chlorpromazine, SCH23390, or clozapine did not simulate the effect at clinically effective dosages. Single injections of phentolamine and prazosin but not of propranolol instead of acepromazine following the seizures produced the Poikilothermia. This effect was also reproduced by reducing the amount of the rats' adipose weight before the induction of the seizures and physical restraint. Rats that had been restrained or not restrained and displayed either euthermia or hypothermia exhibited significantly different patterns in brain damage within limbic and thalamic structures.
A. R. M. M. Hermus - One of the best experts on this subject based on the ideXlab platform.
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Skin blood flow and autonomic reactivity in human Poikilothermia
Clinical Autonomic Research, 1996Co-Authors: M.a. Mackenzie, A. R. M. M. Hermus, Hub Wollersheim, J. W. M. Lenders, T ThienAbstract:Autonomic reactivity is pivotal in maintaining a constant body core temperature. Skin vasomotor reflexes and cardiovascular reactivity were investigated in four women (aged 28–37 years) with acquired Poikilothermia, during steady-state spontaneous hypothermia (rectal temperature (T_r)=33.7 ± 1.0°C [mean ±SD]) and steady-state normothermia (T_r=36.7 ± 0.3°C), as well as in 12 normothermic control subjects. Baseline finger temperature (T_f) during hypothermia was significantly lower than during normothermia (T_f=32.4 ± 1.2 compared with 36.2 ±0.3°C, respectively), and than in the controls (T_f=34.8 ±0.8°C). No significant differences in baseline skin blood flow and forearm blood flow were found between subjects during hypothermia or normothermia and controls, suggesting a failure of sympathetic drive to counter-regulate hypothermia in the subjects. Skin vasoconstrictor responses to the contralateral cooling test and neck cooling test were markedly attenuated in three subjects, and to the finger cooling test in two subjects, during normothermia compared with hypothermia. Blood presure responses to the Valsalva manoeuvre and head-up tilting were normal in all subjects, whereas the heart rate response to head-up tilting was blunted in three subjects during hypothermia. The responses of blood pressure and forearm blood flow to the cold pressor test in the subjects during both thermal conditions were comparable with the controls. We conclude that in our subjects, without generalized autonomic failure, Poikilothermia has to be attributed predominantly to disorders of the central thermoregulatory pathways. Our findings during hypothermia and normothermia indicate that variations in core and skin temperature significantly affect skin vasomotor reactivity.
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Sudomotor function in human Poikilothermia
Neurology, 1995Co-Authors: M.a. Mackenzie, E. Schonbaum, A. R. M. M. Hermus, Hub Wollersheim, Th. Thien, A. G. H. Smals, Peter W. C. KloppenborgAbstract:Hypohidrosis predisposes to hyperthermia and may indicate generalized thermoregulatory failure.To assess the sweating capacity in human Poikilothermia, we performed a quantitative analysis of the central and peripheral sudomotor pathways in four women with acquired Poikilothermia (aged 29 to 38 years) and nine controls. Heat challenge in a climatic chamber (ambient temperature 40 degrees C, 50% relative humidity) for 180 minutes revealed that both sweat secretion and evaporative weight loss were significantly lower in the patients than in the controls (p less than 0.01). Temperature thresholds for thermal sweating were markedly elevated in at least two patients, whereas a third patient showed no sweating response. Stimulation of the eccrine sweat glands by intradermally injected acetylcholine during reduced core temperature (34.9 plus minus 0.7 degrees C) revealed a significantly reduced sweating response in all patients (p less than 0.01); the sudomotor response to pilocarpine iontophoresis was reduced or absent in three patients. We conclude that the generalized thermoregulatory sudomotor failure in these patients was attributable primarily to disorders of the central sudomotor drive; the impaired postganglionic sudomotor response is temperature related and possibly secondary to (long-standing) Poikilothermia. Quantification of heat-dissipating capacity is pivotal for diagnosing severe thermolability and may help to prevent serious heat illness. NEUROLOGY 1995;45: 1602-1607
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Thermoregulation and afterdrop during hypothermia in patients with Poikilothermia
The Quarterly journal of medicine, 1993Co-Authors: M.a. Mackenzie, A. R. M. M. Hermus, Hub Wollersheim, R A BinkhorstAbstract: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.
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Electrocardiographic changes during steady mild hypothermia and normothermia in patients with Poikilothermia.
Clinical science (London England : 1979), 1992Co-Authors: M.a. Mackenzie, A. R. M. M. Hermus, A. G. H. Smals, Wim R.m. Aengevaeren, Tjeerd Van Der Werf, Gerlach F. F. M. Pieters, Peter W. C. KloppenborgAbstract: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.
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Poikilothermia in man : Pathophysiology and clinical implications
Medicine, 1991Co-Authors: M.a. Mackenzie, A. R. M. M. Hermus, Hub Wollersheim, R A Binkhorst, T Thien, Peter W. C. KloppenborgAbstract: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.
M A Persinger - One of the best experts on this subject based on the ideXlab platform.
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Synergistic induction of severe hypothermia (Poikilothermia) by limbic seizures, acepromazine and physical restraint: role of noradrenergic alpha-1 receptors.
Pharmacology biochemistry and behavior, 2001Co-Authors: M A Persinger, R P O'connor, Y R Bureau, G H Parker, O Peredery, M ZegilAbstract:The maintained production of extreme reductions in core temperature (20-22 degrees C) or Poikilothermia can be reliably produced by the synergistic interaction of limbic seizures (induced by lithium and pilocarpine), postseizure administration of a single injection of acepromazine, and physical restraint. Administration of the specific and nonspecific dopamine antagonists haloperidol, chlorpromazine, SCH23390, or clozapine did not simulate the effect at clinically effective dosages. Single injections of phentolamine and prazosin but not of propranolol instead of acepromazine following the seizures produced the Poikilothermia. This effect was also reproduced by reducing the amount of the rats' adipose weight before the induction of the seizures and physical restraint. Rats that had been restrained or not restrained and displayed either euthermia or hypothermia exhibited significantly different patterns in brain damage within limbic and thalamic structures.
Peter W. C. Kloppenborg - One of the best experts on this subject based on the ideXlab platform.
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Sudomotor function in human Poikilothermia
Neurology, 1995Co-Authors: M.a. Mackenzie, E. Schonbaum, A. R. M. M. Hermus, Hub Wollersheim, Th. Thien, A. G. H. Smals, Peter W. C. KloppenborgAbstract:Hypohidrosis predisposes to hyperthermia and may indicate generalized thermoregulatory failure.To assess the sweating capacity in human Poikilothermia, we performed a quantitative analysis of the central and peripheral sudomotor pathways in four women with acquired Poikilothermia (aged 29 to 38 years) and nine controls. Heat challenge in a climatic chamber (ambient temperature 40 degrees C, 50% relative humidity) for 180 minutes revealed that both sweat secretion and evaporative weight loss were significantly lower in the patients than in the controls (p less than 0.01). Temperature thresholds for thermal sweating were markedly elevated in at least two patients, whereas a third patient showed no sweating response. Stimulation of the eccrine sweat glands by intradermally injected acetylcholine during reduced core temperature (34.9 plus minus 0.7 degrees C) revealed a significantly reduced sweating response in all patients (p less than 0.01); the sudomotor response to pilocarpine iontophoresis was reduced or absent in three patients. We conclude that the generalized thermoregulatory sudomotor failure in these patients was attributable primarily to disorders of the central sudomotor drive; the impaired postganglionic sudomotor response is temperature related and possibly secondary to (long-standing) Poikilothermia. Quantification of heat-dissipating capacity is pivotal for diagnosing severe thermolability and may help to prevent serious heat illness. NEUROLOGY 1995;45: 1602-1607
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Electrocardiographic changes during steady mild hypothermia and normothermia in patients with Poikilothermia.
Clinical science (London England : 1979), 1992Co-Authors: M.a. Mackenzie, A. R. M. M. Hermus, A. G. H. Smals, Wim R.m. Aengevaeren, Tjeerd Van Der Werf, Gerlach F. F. M. Pieters, Peter W. C. KloppenborgAbstract: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.
-
Poikilothermia in man : Pathophysiology and clinical implications
Medicine, 1991Co-Authors: M.a. Mackenzie, A. R. M. M. Hermus, Hub Wollersheim, R A Binkhorst, T Thien, Peter W. C. KloppenborgAbstract: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.