Hypercapnic hypoxia

Boleza, K.A., L.E. Burnett and K.G. Burnett. Hypercapnic hypoxia compromises bactericidal activity of fish anterior kidney cells against opportunistic environmental pathogens. Fish Shellfish Immunol. 11 593-610, 2001. 

Brain oedema in humans may be a sequelae to a variety of conditions such as tumour, injuries, hypertension, infarct or hypercapnic hypoxia. In some instances there is overlapping of mechanisms, such as tumour causing increased intracranial pressure followed by haemorrhage. Brain oedema may be focal or diffuse, frequently occurring with exclusion of the arcuate fibres. It is now recognized by most authors that two types of brain oedema can be differentiated vasogenic and cytoxic [1]. Their chemical parameters can be elucidated better in experimental models and tend to differ with the type of the oedema. The term demyelination in this condition refers to the pallor of white matter seen in sections stedned for demonstration of myelin. 

Cytoxic oedema resulting from damage to the parenchymal cells in either grey or white matter is characterized by cellular swelling. Permeability of the vascular channels remains largely unimpaired, and the accumulated fluid resembles an ultrafiltrate of serum. Experimental models for this can be obtained by intravenous administration of distilled water, by hypercapnic hypoxia, or TET poisoning. Fluid, sodium and chloride are significantly increased but the BBB is intact, as indicated by tracer studies, and the extracellular space is of normal size [13]. LDH is increased in oedema produced by water intoxication, but not after triethyltin (TET) [12]. 

The effect of oral tramadol on the ventilatory response to acute isocapnic hypoxia has been studied in 20 healthy volunteers. Tramadol had a small but significant depressive effect on the hypercapnic ventilatory response but no effect on the hypoxic ventilatory response (36). This is in contrast to morphine, which causes 50-60% suppression of the hypoxic ventilatory response. 

Thus, it is obvious that calcium and subsequently the chemosensory responses to hypoxia were abolished, while the hypercapnic responses were neither abolished nor exaggerated. The mechanisms of hypoxic responses were different from those of hypercapnic responses. AU these illustrations show the dominance of the response to CO2/H+ in the absence of the response to hypoxia. 

Equation 11.11 follows from the steady-state solutions to the model Equation 11.3 to Equation 11.7 and Equation 11.12, provided that the effect of changes in cerebral blood flow may be neglected. The effects of hypoxia and hypoxic-hypercapnic interaction may be modeled in a similar fashion by a hyperbolic relation [Cunningham et al., 1986]. 

Dasso LL, Buckler KJ, Vaughan-Jones RD. Interactions between hypoxia and hypercapnic acidosis on calcium signaling in carotid body type I cells. Am J Physiol Lung Cell Mol Physiol 2000 279(1) L36-L42. 

Cantu RC, Nahas CG, Manger WC. Effect of hypercapnic acidosis and of hypoxia on adrenal catecholamine output of the spinal dog. Proc Soc Exp Biol Med 1966 122 433-437. 

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