Influence of cerebral blood flow on the ventilatory response to hypoxia in humans

Abstract

SUMMARYThe purpose of this study was to quantify the possible reduction in ventilation that could be attributed to changes in cerebral blood flow (CBF) with hypoxia to determine whether it could be of sufficient magnitude to underlie hypoxic ventilatory decline (HVD). Six subjects underwent 20 min of isocapnic hypoxia (end-tidal Po2, 50 mmHg). An index of CBF was obtained using transcranial Doppler ultrasound of the middle cerebral artery. The CBF sensitivities to hypoxia and hypercapnia were obtained from the percentage changes in CBF between the last 3 min of the hypoxic or hypercapnic exposure and the 3 min period prior to the exposure. The magnitude of HVD during hypoxia was estimated by fitting a simple model of the ventilatory response to the hypoxic stimulus. The predicted fall in expiratory ventilation (VE) due to a reduction in brain PCO, generated by the increase in CBF with hypoxia in all subjects was less than the measured magnitude of HVD (33 %). Thus, the results from this study suggest that, in awake humans, changes in CBF during acute isocapnic hypoxia are quantitatively insufficient to underlie HVD in humans.

Cerebrovascular and ventilatory responses to acute isocapnic hypoxia in healthy aging and lung disease: effect of vitamin C

“…By further considering the entire velocity spectrum (i.e., the intensity weighted mean velocity, V IWM) a computational index of flow can be calculated (P V IWM) as previously described (39,40). The findings of the present study and others (40,41) suggest that during isocapnic hypoxia (50 mmHg), the relative cross-sectional area of the MCA remains constant and that this approach is suitable for certain hemodynamic states. The theoretical approach of this flow index has been confirmed in previous studies utilizing flow phantoms (3,19); however, further work is needed to fully validate this approach in humans using MRI-based measurements.…”

Dynamic Ventilatory Response to Acute Isocapnic Hypoxia in Septuagenarians

“…Moreover, in older physically active men in the eighth decade, the hypoxic ventilatory decline is characterised by a similar onset, time course and general form as their younger counterparts. Based on this finding, one might speculate that in such an active group of older men, the cerebral haemodynamic response to sustained isocapnic hypoxia may well be similar to young healthy men, that is, small and quantitatively insufficient to underlie HVD (Poulin & Robbins, 1998), although this remains to be investigated.…”

Comparing and characterizing transient and steady‐state tests of the peripheral chemoreflex in humans

“…Poulin & Robbins, 1998;Narkiewicz et al 2006;Steinback et al 2009;Hoiland et al 2015a). Last, we aimed to compare and correlate the magnitude of the HVRs elicited from the TT-N 2 test and the steady-state tests.…”

“…Ainslie & Duffin, 2009;Hoiland et al 2015a). Thus, central chemoreceptor activity may be depressed during isocapnic hypoxia and also dampen the HVR or the subsequent HVD (Poulin & Robbins, 1998;Hoiland et al 2015a). Despite these possible confounders, steady-state tests using DEF have been widely adopted and are believed to isolate the peripheral chemoreceptors and the HVR (e.g.…”

“…hypoxic ventilatory decline; Powell et al 1998;Steinback & Poulin, 2007); (iii) concomitant cardiovascular and cerebrovascular responses (e.g. Poulin & Robbins, 1998;Steinback & Poulin, 2008;Ainslie & Duffin, 2009;Willie et al 2012;Hoiland et al 2015a); and (iv) the complex interactions between the central and peripheral chemoreceptors (Blain et al 2010;Cui et al 2012;Tin et al 2012;Duffin & Mateika, 2013;Teppema & Smith, 2013;Wilson & Day, 2013;Smith et al 2015).…”