Key result
Hypertension disturbed regional and total cerebrovascular and peripheral responses to isocapnic hypoxia, limiting oxygen supply to the brain and skeletal muscle.
Why the study?
Does hypertension impair isocapnic hypoxia-induced cerebral and skeletal muscle hyperaemia and oxygen supply in middle-aged men?
Observational (n=18)
Does hypertension impair isocapnic hypoxia-induced cerebral and skeletal muscle hyperaemia and oxygen supply in middle-aged men?
Hypertension impairs regional and total cerebrovascular and peripheral vasodilatory responses to hypoxia, limiting oxygen supply to the brain and skeletal muscle.
May impair hypoxic tissue oxygenation in middle-aged hypertensives; leaves open clinical relevance and need for prospective confirmation.
Key points Hypoxaemia evokes a repertoire of homeostatic adjustments that maintain oxygen supply to organs and tissues including the brain and skeletal muscles. Because hypertensive patients have impaired endothelial‐dependent vasodilatation and an increased sympathetic response to arterial oxygen desaturation, we investigated whether hypertension impairs isocapnic hypoxia‐induced cerebral and skeletal muscle hyperaemia to an extent that limits oxygen supply. In middle‐aged hypertensive men, vertebral and femoral artery blood flow do not increase in response to isocapnic hypoxia, limiting brain and peripheral hyperaemia and oxygen supply. Increased chemoreflex‐induced sympathetic activation impairs skeletal muscle perfusion and oxygen supply, whereas an attenuation of local vasodilatory signalling in the posterior cerebrovasculature reduced brain hyperperfusion of hypertensive middle‐aged men in response to isocapnic hypoxia. Abstract The present study investigated whether hypertension impairs isocapnic hypoxia (IH)‐induced cerebral and skeletal muscle hyperaemia to an extent that limits oxygen supply. Oxygen saturation (oxymetry), mean arterial pressure (photoplethysmography) and muscle sympathetic nerve activity (MSNA; microneugraphy), as well as femoral artery (FA), internal carotid artery and vertebral artery (VA) blood flow (BF; Doppler ultrasound), were quantified in nine normotensive (NT) (aged 40 ± 11 years, systolic pressure 119 ± 7 mmHg and diastolic pressure 73 ± 6 mmHg) and nine hypertensive men (HT) (aged 44 ± 12 years, systolic pressure 152 ± 11 mmHg and diastolic pressure 90 ± 9 mmHg) during 5 min of normoxia (21% O 2 ) and IH (10% O 2 ). Total cerebral blood flow (tCBF), brain (CDO 2 ) and leg (LDO 2 ) oxygen delivery were estimated. IH provoked similar oxygen desaturation without changing mean arterial pressure. Internal carotid artery perfusion increased in both groups during IH. However, VA and FA BF only increased in NT. Thus, IH‐induced increase in tCBF was smaller in HT. CDO 2 only increased in NT and LDO 2 decreased in HT. Furthermore, IH evoked a greater increase in HT MSNA. Changes in MSNA were inversely related to FA BF, LDO 2 and end‐tidal oxygen tension. In conclusion, hypertension disturbs regional and total cerebrovascular and peripheral responses to IH and consequently limits oxygen supply to the brain and skeletal muscle. Although increased chemoreflex‐induced sympathetic activation may explain impaired peripheral perfusion, attenuated vasodilatory signalling in the posterior cerebrovasculature appears to be responsible for the small increase in tCBF when HT were exposed to IH.
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Fernandes et al. (2018) conducted an observational in Hypertension (n=18). Isocapnic hypoxia vs. Normoxia (21% O2) was evaluated on Cerebral and skeletal muscle hyperaemia and oxygen supply (vertebral and femoral artery blood flow, total cerebral blood flow, brain and leg oxygen delivery). Hypertension disturbed regional and total cerebrovascular and peripheral responses to isocapnic hypoxia, limiting oxygen supply to the brain and skeletal muscle.
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