Effects of peripheral chemo- and baro-receptor denervation on responses of preoptic thermosensitive neurons to inspired CO2

Tamaki, Yoko; Nakayama, Teruo; Kanosue, Kazuyuki

doi:10.1007/bf00580983

Cited by 4 publications

(3 citation statements)

References 11 publications

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“…Electrophysiological observations show that cold nerve activity in cat skin is inhibited by CO 2 (Dodt 1956) and that warm neurons in the preoptic area of the rat hypothalamus are facilitated by CO 2 (Tamaki et al 1989). Cold exposure generally induces a metabolic increase that results in an increased HR (Fisher et al 1985), and also suggests that inhibition of the cold 17 sensation would reduce HR.…”

Section: Discussionmentioning

confidence: 99%

Spinal cord transection inhibits HR reduction in anesthetized rats immersed in an artificial CO2-hot spring bath

Yamamoto

Hashimoto

2006

Int J Biometeorol

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Like humans, the heart rate (HR) of anesthetized rats immersed in CO 2 -water is lower than that when immersed in tap water at the same temperature. To investigate the afferent signal pathway in the mechanism of HR reduction, Wistar rats were anesthetized with urethane and then the spinal cord was transected between T 4 and T 5 . The animals were immersed up to the axilla in a bathtub of tap-water (CO 2 contents:10-20 mg·L -1 ) or of CO 2 -water (965-1400 mg·L -1 ) at 35°C while recording HR, arterial blood pressure, and arterial blood gas parameters (PaCO 2 , PaO 2 , pH). Arterial blood gas parameters did not change during immersion irrespective of CO 2 concentration of the bath water, whereas the HR was reduced in the CO 2 -water bath. The inhalation of CO 2 -mixed gas (5 % CO 2 , 20% O 2 , 75 % N 2 ) resulted in increased levels of blood gases and an increased HR during immersion in all types of water tested. The HR reduction observed in sham transected control animals immersed in CO 2 -water disappeared after subsequent spinal cord transection. These results show that the dominant afferent signal pathway to the brain, which is involved in inducing the reduced HR during immersion in CO 2 -water, is located in the neuronal route and not in the bloodstream.

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Section: Discussionmentioning

confidence: 99%

Spinal cord transection inhibits HR reduction in anesthetized rats immersed in an artificial CO2-hot spring bath

Yamamoto

Hashimoto

2006

Int J Biometeorol

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“…The presence of respiratory alkalosis, metabolic acidosis or both will be dependent on the contributing factors and duration of heat exposure. Elevated CO 2 with accompanying tissue acidosis and reduced pH may impair thermoregulation via excitation of hypothalamic warm-sensitive neurons that receive afferent input from peripheral chemo-and baroreceptors (367)(368)(369). Stimulation of warm-sensitive neurons within the POAH would cause a reduction in heat-loss responses and facilitate the development of severe hyperthermia during heat exposure.…”

Section: Acid Base Disturbancesmentioning

confidence: 99%

Heat Stroke

Leon

Bouchama

2015

Comprehensive Physiology

360

356

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Heat stroke is a life-threatening condition clinically diagnosed as a severe elevation in body temperature with central nervous system dysfunction that often includes combativeness, delirium, seizures, and coma. Classic heat stroke primarily occurs in immunocompromised individuals during annual heat waves. Exertional heat stroke is observed in young fit individuals performing strenuous physical activity in hot or temperature environments. Long-term consequences of heat stroke are thought to be due to a systemic inflammatory response syndrome. This article provides a comprehensive review of recent advances in the identification of risk factors that predispose to heat stroke, the role of endotoxin and cytokines in mediation of multi-organ damage, the incidence of hypothermia and fever during heat stroke recovery, clinical biomarkers of organ damage severity, and protective cooling strategies. Risk factors include environmental factors, medications, drug use, compromised health status, and genetic conditions. The role of endotoxin and cytokines is discussed in the framework of research conducted over 30 years ago that requires reassessment to more clearly identify the role of these factors in the systemic inflammatory response syndrome. We challenge the notion that hypothalamic damage is responsible for thermoregulatory disturbances during heat stroke recovery and highlight recent advances in our understanding of the regulated nature of these responses. The need for more sensitive clinical biomarkers of organ damage is examined. Conventional and emerging cooling methods are discussed with reference to protection against peripheral organ damage and selective brain cooling.

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“…While hypercapnia and acidosis often inhibit spontaneous neuronal activity in different parts of the central nervous system (6,15,22,26,29), previous electrophysiological recordings in anesthetized rats found that warm-sensitive POAH neurons were generally excited by brief periods of CO 2 inhalation (38,40). This excitation, however, appears to be due to afferent input from peripheral chemoreceptors and baroreceptors (39) since extracellular recordings in rat hypothalamic tissue slices found the opposite response; i.e., in vitro POAH neurons tended to decrease their firing rates during perfusions with hypercapnic solutions (28). Because of this disparity in neuronal responses to hypercapnia, further investigation is warranted.…”

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confidence: 99%

Carbon dioxide and pH effects on temperature-sensitive and -insensitive hypothalamic neurons

Wright

Boulant²

2007

Journal of Applied Physiology

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The preoptic-anterior hypothalamus (POAH) controls body temperature, and thermoregulatory responses are impaired during hypercapnia. If increased CO(2) or its accompanying acidosis inhibits warm-sensitive POAH neurons, this could provide an explanation for thermoregulatory impairment during hypercapnia. To test this possibility, extracellular electrophysiological recordings determined the effects of CO(2) and pH on the firing rates of both temperature-sensitive and -insensitive neurons in hypothalamic tissue slices from 89 male Sprague-Dawley rats. Firing rate activity was recorded in 121 hypothalamic neurons before, during, and after changing the CO(2) concentration aerating the tissue slice chamber or changing the pH of the solution bathing the tissue slices. Increasing the aeration CO(2) concentration from 5% (control) to 10% (hypercapnic) had no effect on most (i.e., 69%) POAH temperature-insensitive neurons; however, this hypercapnia inhibited the majority (i.e., 59%) of warm-sensitive neurons. CO(2) affected similar proportions of (non-POAH) neurons in other hypothalamic regions. These CO(2) effects appear to be due to changes in pH since the CO(2)-affected neurons responded similarly to isocapnic acidosis (i.e., normal CO(2) and decreased pH) but were not responsive to isohydric hypercapnia (i.e., increased CO(2) and normal pH). These findings may offer a neural explanation for some heat-related illnesses (e.g., exertional heat stroke) where impaired heat loss is associated with acidosis.

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Effects of peripheral chemo- and baro-receptor denervation on responses of preoptic thermosensitive neurons to inspired CO2

Cited by 4 publications

References 11 publications

Spinal cord transection inhibits HR reduction in anesthetized rats immersed in an artificial CO2-hot spring bath

Spinal cord transection inhibits HR reduction in anesthetized rats immersed in an artificial CO2-hot spring bath

Heat Stroke

Carbon dioxide and pH effects on temperature-sensitive and -insensitive hypothalamic neurons

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