BackgroundFunctional cerebrovascular regulatory mechanisms are important for maintaining constant cerebral blood flow and oxygen supply in heathy individuals and are altered in heart failure. We aim to examine whether pulmonary arterial hypertension (PAH) is associated with abnormal cerebrovascular regulation and lower cerebral oxygenation and their physiological and clinical consequences.Methods and ResultsResting mean flow velocity in the middle cerebral artery mean flow velocity in the middle cerebral artery (MCAvmean); transcranial Doppler), cerebral pressure‐flow relationship (assessed at rest and during squat‐stand maneuvers; analyzed using transfer function analysis), cerebrovascular reactivity to CO 2, and central chemoreflex were assessed in 11 patients with PAH and 11 matched healthy controls. Both groups also completed an incremental ramp exercise protocol until exhaustion, during which MCAvmean, mean arterial pressure, cardiac output (photoplethysmography), end‐tidal partial pressure of CO 2, and cerebral oxygenation (near‐infrared spectroscopy) were measured. Patients were characterized by a significant decrease in resting MCAvmean (P<0.01) and higher transfer function gain at rest and during squat‐stand maneuvers (both P<0.05). Cerebrovascular reactivity to CO 2 was reduced (P=0.03), whereas central chemoreceptor sensitivity was increased in PAH (P<0.01), the latter correlating with increased resting ventilation (R 2=0.47; P<0.05) and the exercise ventilation/CO2 production slope (trueV˙normalE/normalV˙CO2 slope; R 2=0.62; P<0.05) during exercise for patients. Exercise‐induced increases in MCAvmean were limited in PAH (P<0.05). Reduced MCAvmean contributed to impaired cerebral oxygen delivery and oxygenation (both P<0.05), the latter correlating with exercise capacity in patients with PAH (R 2=0.52; P=0.01).ConclusionsThese findings provide comprehensive evidence for physiologically and clinically relevant impairments in cerebral hemodynamic regulation and oxygenation in PAH.

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Facial fractures lead to functional and esthetical deficits if not treated properly. Appropriate acute management of facial fractures must be based on prompt and thorough evaluation. Some fractures are best treated in a delayed fashion; others represent real emergencies and need to be treated within 24 h of trauma. Different types of reduction and fixation exist depending on the age of the patient, the location and type of fracture, and on the surgeon's preference.

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The aim of this study was to examine the impact of well‐controlled uncomplicated type 2 diabetes (T2D) on exercise performance. Ten obese sedentary men with T2D and nine control participants without diabetes matched for age, sex, and body mass index were recruited. Anthropometric characteristics, blood samples, resting cardiac, and pulmonary functions and maximal oxygen uptake (VO2max) and ventilatory threshold were measured on a first visit. On the four subsequent visits, participants (diabetics: n = 6; controls: n = 7) performed step transitions (6 min) of moderate‐intensity exercise on an upright cycle ergometer from unloaded pedaling to 80% of ventilatory threshold. VO2 (τVO2) and HR (τ HR) kinetics were characterized with a mono‐exponential model. VO2max (27.0 ± 3.4 vs. 26.7 ± 5.0 mL kg−1 min−1; P = 0.85), τVO2 (43 ± 6 vs. 43 ± 10 sec; P = 0.73), and τ HR (42 ± 17 vs. 43 ± 13 sec; P = 0.94) were similar between diabetics and controls respectively. The remaining variables were also similar between groups, with the exception of lower maximal systolic blood pressure in diabetics (P = 0.047). These results suggest that well‐controlled T2D is not associated with a reduction in VO2max or slower τVO2 and τ HR.

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Background Patients with pulmonary arterial hypertension (PAH) have lower cerebral blood flow (CBF) and oxygenation compared to healthy sedentary subjects, the latter negatively correlating with exercise capacity during incremental cycling exercise. We hypothesized that patients would also exhibit altered CBF and oxygenation during endurance exercise, which would correlate with endurance time. Methods Resting and exercise cardiorespiratory parameters, blood velocity in the middle cerebral artery (MCAv; transcranial doppler) and cerebral oxygenation (relative changes in cerebral tissue oxygenation index (ΔcTOI) and cerebral deoxyhemoglobin (ΔcHHb); near‐infrared spectroscopy) were continuously monitored in nine PAH patients and 10 healthy‐matched controls throughout endurance exercise. Cardiac output (CO), systemic blood pressure (BP) and oxygen saturation (SpO2), ventilatory metrics and end‐tidal CO2 pressure (PETCO2) were also assessed noninvasively. Results Despite a lower workload and endurance oxygen consumption, similar CO and systemic BP, ΔcTOI was lower in PAH patients compared to controls (p < .01 for interaction). As expected during exercise, patients were characterized by an altered MCAv response to exercise, a lower PETCO2 and SpO2, as wells as a higher minute‐ventilation/CO2 production ratio (trueV˙normalE/V˙CO2 ratio). An uncoupling between changes in MCAv and PETCO2 during the cycling endurance exercise was also progressively apparent in PAH patients, but absent in healthy controls. Both cHHb and ΔcTOI correlated with trueV˙normalE/V˙CO2 ratio (r = 0.50 and r = −0.52; both p < .05 respectively), but not with endurance time. Conclusion PAH patients present an abnormal cerebrovascular profile during endurance exercise with a lower cerebral oxygenation that correlate with hyperventilation but not endurance exercise time. These findings complement the physiological characterization of the cerebral vascular responses to exercise in PAH patients.