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Editors Selection IGR 8-3
Blood Flow: Vascular response to blood gas variations
Comment by Selim Orgül on:
22327 Retinal arteriolar and middle cerebral artery responses to combined hypercarbic/hyperoxic stimuli, Kisilevsky M; Mardimae A; Slessarev M et al., Investigative Ophthalmology and Visual Science, 2008; 49: 5503-5509
In a well-designed approach assessing blood flow in one retinal arteriole with a method combining laser Doppler velocimetry and simultaneous vessel densitometry (Laser Blood Flowmeter device from Canon) and blood velocity in the middle cerebral artery with a Doppler ultrasound system, Kisilevski et al. (1384) investigated the blood flow response during hypercarbia in combination with normoxia or hyperoxia (500 and 300 mmHg). Their experimental setup allowed for remarkably reproducible respiratory and hemodynamic conditions. Retinal vessel diameter, retinal blood velocity and retinal blood flow highly correlated with end-tidal oxygen levels. The retinal vascular response to hypercarbia during normoxia did not show a change in diameter, but disclosed a constriction during hypercarbia combined with hyperoxia. Blood velocity increased in response to hypercarbia during normoxia, and decreased during hypercarbia combined with hyperoxia, but only with higher oxygen levels (500 mmHg).
Hyperoxia is likely to overpower the vasodilatory effect of hypercarbia and applying carbogen in retinal ischemic condition may be injudiciousCombining the effect on vascular diameter and on blood velocity allowed to calculate retinal blood flow, which increased in response to hypercarbia during normoxia and decreased when hyperoxia was added, but, again only with higher oxygen levels (500 mmHg). Blood velocity in the middle cerebral also increased during hypercarbia, but, in contrast to the retinal circulation, remained unchanged when hyperoxia was added. Furthermore, while hypercarbia increased blood velocity in the retinal vasculature by 17%, it increased blood velocity in the cerebral circulation increased by 45%. In this vascular bed, the strong correlation was observed between blood velocity end-tidal carbon dioxide. This study confirmed that oxygen has a stronger effect on the retinal vasculature than carbon dioxide, but, most importantly, it demonstrated that the vascular responses to blood gas variation differ profoundly between the retinal and the cerebral circulation. Pharmacological interventions, which would have allowed to understand the regulatory mechanisms and the differences between the two vascular beds were not performed, but some aspects of endothelial regulation may tempt to speculate about an increased responsiveness to endothelin in the retinal circulation. Although part of the differences may be attributed to the difference in diameter of the examined vessels, it is likely that some local specifics have the heavier bearing on the observed differences. An important clinical implication of this study is that hyperoxia is likely to overpower the vasodilatory effect of hypercarbia and that applying carbogen in retinal ischemic condition may be injudicious.
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