Respiratory and Vasomotor Effects of Variations in Carotid Body Temperature

Bernthal, Theodore; Weeks, William F.

doi:10.1152/ajplegacy.1939.127.1.94

Cited by 47 publications

(13 citation statements)

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“…These include various circulating hormones including catecholamines (537, 553), but see (534), angiotensin (30, 296, 413, 506, 521), adenosine (573, 759, 852), and extracellular ions, particularly K + (54, 412, 533) as well as changes in osmolarity (136, 300, 301, 590) and temperature (26, 61, 62, 69, 572). The carotid body responses to these stimuli are robust and reproducible and can in most cases also be observable at the level of cardiorespiratory reflexes (602, 672, 777, 942), which has led to the notion that the carotid body might act as a polymodal receptor within the stress axis of the body (478).…”

Section: Other Physiological Stimuli Of the Carotid Bodymentioning

confidence: 99%

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

461

572

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The discovery of the sensory nature of the carotid body dates back to the beginning of the 20th century. Following these seminal discoveries, research into carotid body mechanisms moved forward progressively through the 20th century, with many descriptions of the ultrastructure of the organ and stimulus-response measurements at the level of the whole organ. The later part of 20th century witnessed the first descriptions of the cellular responses and electrophysiology of isolated and cultured type I and type II cells, and there now exist a number of testable hypotheses of chemotransduction. The goal of this article is to provide a comprehensive review of current concepts on sensory transduction and transmission of the hypoxic stimulus at the carotid body with an emphasis on integrating cellular mechanisms with the whole organ responses and highlighting the gaps or discrepancies in our knowledge. It is increasingly evident that in addition to hypoxia, the carotid body responds to a wide variety of blood-borne stimuli, including reduced glucose and immune-related cytokines and we therefore also consider the evidence for a polymodal function of the carotid body and its implications. It is clear that the sensory function of the carotid body exhibits considerable plasticity in response to the chronic perturbations in environmental O2 that is associated with many physiological and pathological conditions. The mechanisms and consequences of carotid body plasticity in health and disease are discussed in the final sections of this article.

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Section: Other Physiological Stimuli Of the Carotid Bodymentioning

confidence: 99%

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

461

572

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“…The underpinning mechanisms for the hyperventilatory response to heat stress are elusive, but likely mediated by a combination of (i) integrated thermoreceptor afferents [primarily from the hypothalamus (47,213)] to the respiratory pacemaker cells in the medulla (454), (ii) type III and IV afferent potentiation from increased muscle temperature (18,202,240), and (iii) stimulation of the carotid body (44,139). With regards to the latter, resection of the carotid nerves in the cat attenuates the ventilatory increase to whole body heating (139), while perfusing warmed blood through the isolated carotid bifurcation of the dog increases ventilation (44). Of note, however, the environmental-related changes in ventilation are quite different from cats and dogs to humans.…”

Section: Arterial Blood Gasesmentioning

confidence: 99%

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

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“…There is evidence that ventilatory response to hypoxia depends upon body temperature [1,2]. The carotid chemoreceptor response to hypoxia or chemical stimuli in absolute terms is also suppressed by direct local cooling [3][4][5].Frappell et al [6], however, found that the VE normalized by VO 2 (VE/VO 2 ) does not decline during hypothermia and that a similar level of hypoxic hyperventilation in the hypothermic and normothermic conditions was seen in anesthetized rats. They suggested an important hypothesis that in relation to metabolic rate, respiratory "gain" to hypoxic stimulus is not depressed in hypothermic animals.…”

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confidence: 99%

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confidence: 99%

Ventilation- and Carotid Chemoreceptor Discharge-Response to Hypoxia during Induced Hypothermia in Halothane Anesthetized Rat.

Maruyama

Fukuda

2000

JJP

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Augmentation of ventilation in response to hypoxic arterial chemoreceptor stimulation is one of the important protective strategies against acute O 2 deficiency. However, O 2 "deficiency" is determined by a relative balance between O 2 supply and requirement. It seems, therefore, likely that ventilatory response to hypoxia should vary when O 2 requirement (or consumption) of the whole body is altered such as by artificial reduction in body temperature. There is evidence that ventilatory response to hypoxia depends upon body temperature [1,2]. The carotid chemoreceptor response to hypoxia or chemical stimuli in absolute terms is also suppressed by direct local cooling [3][4][5].Frappell et al. [6], however, found that the VE normalized by VO 2 (VE/VO 2 ) does not decline during hypothermia and that a similar level of hypoxic hyperventilation in the hypothermic and normothermic conditions was seen in anesthetized rats. They suggested an important hypothesis that in relation to metabolic rate, respiratory "gain" to hypoxic stimulus is not depressed in hypothermic animals. There has been, however, no direct evidence to support this hypothesis. Respiratory gain to acute hypoxic stimulus is deter-

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Respiratory and Vasomotor Effects of Variations in Carotid Body Temperature

Cited by 47 publications

References 0 publications

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Cerebral Vascular Control and Metabolism in Heat Stress

Ventilation- and Carotid Chemoreceptor Discharge-Response to Hypoxia during Induced Hypothermia in Halothane Anesthetized Rat.

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