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INFLUENCE OF BODY TEMPERATURE ON RESPONSES TO HYPOXIA AND HYPERCAPNIA: IMPLICATIONS FOR SIDS
Author(s) -
Maskrey Michael
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02061.x
Subject(s) - hypercapnia , hypothermia , hypoxia (environmental) , hyperthermia , anesthesia , medicine , respiratory system , thermoregulation , respiration , hypoxic pulmonary vasoconstriction , control of respiration , raphe , chemistry , acidosis , serotonin , oxygen , vasoconstriction , anatomy , serotonergic , organic chemistry , receptor
SUMMARY 1. This paper reviews current knowledge regarding interactions between body temperature and the respiratory responses to hypoxia and/or hypercapnia, with special emphasis on how these interactions might predispose towards sudden infant death syndrome (SIDS). 2. Use has been made of an adult rat model in which body core temperature is fixed by means of an intra‐abdominal heat exchanger. Initial studies indicated that hyperthermia (T b ∼ 41° C) enhanced the ventilatory response to hypercapnia, whereas hypothermia (T b ∼35°C) interacted with hypoxia to depress respiration. 3. Studies involving hypothalamic lesions in urethane‐anaesthetized rats have implicated the posterior hypothalamic area in the hypoxia/hypothermia interaction. Further studies are directed towards examining the role played by more caudal areas, including the raphe nuclei. 4. It has been shown that not only does the hypoxial hypothermia interaction depress breathing but it also reduces, or sometimes eliminates, the ventilatory response to hypercapnia, which under normal circumstances provides one of the most powerful excitatory inputs to the respiratory centres. This implies that an expected reversal of the respiratory depression by build up of CO 2 levels may not occur, which in turn has important implications for SIDS. 5. The literature dealing with the effects of hyperthermia on hypoxic and hypercapnic responses is also reviewed. It is concluded that environmental heat stress may only become a significant problem when it accompanies a febrile infection, under which circumstances it may seriously compromise thermo‐regulatory ability and alter breathing responses to chemical stimuli.