IN FAVOR OF HAVING A COOL HEAD AND A HOT BODY
to the editor: With respect to the three mechanisms of human SBC (9), there is no disputing that CO2 tension has a potent influence on the patency of the cerebral blood vessels and on cerebral blood flow (CBF). The point that needs to be resolved is if the caliber of the major cerebral vessels are also affected, even mildly, by any changes in CO2 tension by elevations in their temperature or if these two factors interact in their influence on cerebral blood vessels. This is of importance when making conclusions on changes in CBF velocity when assessed by transcranial Doppler (TCD) sonography, especially in the middle cerebral artery (MCA). To recap (9), by Poiseuille's Law for resistance to flow in blood vessels (Q =ΔP·πr4/8ηl), a 5% increase in the radius of the MCA gives an apparent ∼20% decrease in the blood flow velocity when measured by TCD. For a typical size MCA, with a diameter of 1.25 mm (7), a 5% radius change is a tiny 0.0625 mm. From the scant evidence that exists on this topic of CO2 tension and temperature effects on CBF, during hypocapnia, normocapnia, and hypercapnia the induction of hyperthermia gave a global increase in CBF (by tracer infusion and scintillation counting) in normotensive dogs across a PaCO2 range from ∼18 to 60 mmHg (3). This study also illustrated greater sensitivity of CBF to CO2 in hyperthermia versus normothermia (3), supporting a progressively greater positive effect of hyperthermia on CBF at higher CO2 tensions. In humans, however, MCA velocity (1) is reduced during eucapnic hyperthermia and similarly cerebral vascular conductance (i.e., MCAV/Mean Arterial Pressure) was reduced during normothermia and hyperthermia (5); these latter results, however, rest on the to-be-verified assumption of constant cross sectional area of the MCA.
The focus of some recent studies (4, 8) has been on resolving the mechanisms of control of human breathing during hyperthermia. These studies that illustrate a hyperthermia-induced hyperventilation (4) or thermal hyperpnea (8) do not imply that heat loss from the upper airways is a preferred avenue of heat loss for resting human SBC. The relative contributions of three mechanisms of SBC, as described in this Point:Counterpoint debate (9), are reported by Rasch et al. (6) during rest and during moderate exercise in humans.
The counterpoint to SBC in hyperthermic humans (9) has changed from one that there is no possible way that this response occurs to one that argues it appears to occur, but the cooling strategies to demonstrate it, in some instances, appear to have been too intense and “un-physiological.” Possibly the debate will now shift to one of which methods of cranial cooling are or are not acceptable to employ when studying mechanisms of human SBC or cranial thermoregulation. Irrespective of which method or technology is employed, an important parallel outcome of understanding mechanisms of human cranial thermoregulation and SBC continues to be the excellent benefits of neuroprotection that are afforded by human cranial cooling after traumatic brain injury, cardiac arrest or stroke (2).
- Copyright © 2011 the American Physiological Society