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Abstract: We investigated the interaction between the central and peripheral chemoreflexes in humans using a temporal separation technique in three tests. In two tests hyperventilation was used to reduce central . In these tests the difference in the responses to the same step increases in to 45mmHg at normoxic and hypoxic O2 tensions provided a measure of the response to isocapnic hypoxia at a low central . In a third test the response to a hypoxic step during sustained isocapnia at 45mmHg provided a measure of the response to isocapnic hypoxia at a high central . The responses to isocapnic hypoxia at high and low central were not significantly different, confirming the conclusion of previous studies that central and peripheral chemoreflex signals interact additively. This finding contrasts with those from recent animal experiments and emphasizes the need for caution when using animal experiments to make conclusions about the physiology of the respiratory chemoreflexes in humans. [Copyright &y& Elsevier]

Abstract: We simultaneously measured respiratory, cerebrovascular and cardiovascular responses to 10-min of isoxic hypoxia at three constant CO2 tensions in 15 subjects. We observed four response patterns, some novel, for ventilation, middle cerebral artery blood flow velocity, heart rate and mean arterial blood pressure. The occurrence of the response patterns was correlated between some measures. Isoxic hyperoxic and hypoxic ventilatory sensitivities to CO2 derived from these responses were equivalent to those measured with modified (Duffin) rebreathing tests, but cerebrovascular sensitivities were not. We suggest the different ventilatory response patterns reflect the time course of carotid body afferent activity; in some individuals, carotid body function changes during hypoxia in more complex ways than previously thought. We concluded that isoxic hyperoxic and hypoxic ventilatory sensitivities to CO2 can be measured using multiple hypoxic ventilatory response tests only if care is taken choosing the isocapnic CO2 levels used, but a similar approach to measuring the cerebrovascular response to isocapnic hyperoxia and hypoxia is unfeasible. [Copyright &y& Elsevier]

Highlights: [•] The cerebrovascular reactivity to CO2 of the middle cerebral artery was measured with trans-cranial Doppler ultrasound. [•] Cerebrovascular reactivity differed from morning to evening, exhibiting a circadian rhythm. [•] Cerebrovascular reactivity did not differ from one day to the next, exhibiting excellent test–retest reliability. [ABSTRACT FROM AUTHOR]

Cerebrovascular reactivity (CVR) is often defined as the increase in cerebral blood flow (CBF) produced by an increase in carbon dioxide (CO 2 ) and may be used clinically to assess the health of the cerebrovasculature. When CBF is estimated using blood oxygen level dependent (BOLD) magnetic resonance imaging, CVR values for each voxel can be displayed using a color scale mapped onto the corresponding anatomical scan. While these CVR maps therefore show the distribution of cerebrovascular reactivity, they only provide an estimate of the magnitude of the cerebrovascular response, and do not indicate the time course of the response; whether rapid or slow. Here we describe transfer function analysis (TFA) of the BOLD response to CO 2 that provides not only the magnitude of the response (gain) but also the phase and coherence. The phase can be interpreted as indicating the speed of response and so can distinguish areas where the response is slowed. The coherence measures the fidelity with which the response follows the stimulus. The examples of gain, phase and coherence maps obtained from TFA of previously recorded test data from patients and healthy individuals demonstrate that these maps may enhance assessment of cerebrovascular pathophysiology by providing insight into the dynamics of cerebral blood flow control and distribution. [ABSTRACT FROM AUTHOR]

Abstract: Cerebrovascular reactivity (CVR) is the change in cerebral blood flow (CBF) in response to a change in a vasoactive stimulus. Paradoxical reductions in CBF in response to vasodilatory stimulation (‘steal’) are associated with vascular pathology. However, a pathophysiological interpretation of ‘steal’ requires a comprehensive conceptual model linking pathology and changes in blood flow. Herein, we extend a simple model explaining steal published in the late 1960s by incorporating concepts of CBF regulation from more recent studies to generate a comprehensive dynamic model. The main elements of the model are: (a) the relationship between changes in CBF and the arterial partial pressure of carbon dioxide (PaCO2) in healthy vascular regions is sigmoidal; (b) vascular regions vasodilate to compensate for decreased perfusion pressure, leading to (c) an encroachment on vasodilatory reserve and, reduced CVR; (d) a vasodilatory stimulus may increase CBF capacity above the flow capacity of major cerebral blood vessels; and (e) this limitation induces competitive intra-cerebral redistribution of flow from territories with low vasodilatory reserve to those with high reserve. We used CVR measurements generated by applying precise, computer-controlled changes in PaCO2 as the vasoactive stimulus, and measured blood oxygen level dependent (BOLD) MRI signals as high resolution surrogates of CBF to test predictions derived from this model. Subjects were 16 healthy adults and 16 patients with known cerebral steno-occlusive diseases. We observed regional sigmoidal PaCO2–BOLD response curves with a range of slopes; graded changes in PaCO2 resulted in redistributions of BOLD signal consistent with the known underlying vascular pathology and predictions of the model. We conclude that this model can be applied to provide a hemodynamic interpretation to BOLD signal changes in response to hypercapnia, and thereby aid in relating CVR maps to pathophysiological conditions. [Copyright &y& Elsevier]