Search

New Findings: What is the central question of this study?Coronary blood flow in healthy humans is controlled by both local metabolic signalling and adrenergic activity: does the integration of these signals during acute hypoxia and adrenergic activation differ between sexes?What are the main findings and its importance?Both males and females exhibit an increase in coronary blood velocity in response to acute hypoxia, a response that is constrained by adrenergic stimulation in males but not females. These findings suggest that coronary blood flow control differs between males and females. Coronary hyperaemia is mediated through multiple signalling pathways, including local metabolic messengers and adrenergic stimulation. This study aimed to determine whether the coronary vascular response to adrenergic stressors is different between sexes in normoxia and hypoxia. Young, healthy participants (n = 32; 16F) underwent three randomized trials of isometric handgrip exercise followed by post‐exercise circulatory occlusion (PECO) to activate the muscle metaboreflex. End‐tidal PO2 was controlled at (1) normoxic levels throughout the trial, (2) 50 mmHg for the duration of the trial (hypoxia trial), or (3) 50 mmHg only during PECO (mixed trial). Mean left anterior descending coronary artery velocity (LADVmean; transthoracic Doppler echocardiography), heart rate and blood pressure were assessed at baseline and during PECO. In normoxia, there was no change in LADVmean or cardiac workload induced by PECO in males and females. Acute hypoxia increased baseline LADVmean to a greater extent in males compared with females (P < 0.05), despite a similar increase in cardiac workload. The change in LADVmean induced by PECO was similar between sexes in normoxia (P = 0.31), greater in males during the mixed trial (male: 12.8 (7.7) cm/s vs. female: 8.1 (6.3) cm/s; P = 0.02) and reduced in males but not females in acute hypoxia (male: −4.8 (4.5) cm/s vs. female: 0.8 (6.2) cm/s; P = 0.006). In summary, sex differences in the coronary vasodilatory response to hypoxia were observed, and metaboreflex activation during hypoxia caused a paradoxical reduction in coronary blood velocity in males but not females. [ABSTRACT FROM AUTHOR]

The utility of transthoracic saline contrast echocardiography (TTSCE) to assess blood flow through intrapulmonary arteriovenous anastomoses (Q̇IPAVA) in humans is limited due to the potential destabilizing effects of the gas concentration gradients established in varied blood-gas environments. This study assessed the specific effect of a hyperoxic and mixed venous blood-gas environment on the stability of saline contrast. We hypothesized that the rate of contrast mass lost in hyperoxic blood would be similar to mixed venous due to the establishment of equal and opposing gas gradients (O2, N2, CO2) created when the partial pressure of dissolved gases is manipulated. Using an in vitro model of the pulmonary circulation perfused with defibrinated sheep blood and a membrane oxygenator to control blood gases, we assessed the percent contrast conserved (an index of contrast stability) between inflow and outflow sites at multiple flow rates (1.8, 2.8, 4.3, and 6.8 L/min) in a hyperoxic (Po2: 646 ± 16 mmHg; Pco2: 0 ± 0 mmHg) and a mixed venous blood gas condition (Po2: 35 ± 3 mmHg; Pco2: 40 ± 0 mmHg). We found significant contrast decay with time in both conditions, with slightly higher contrast conservation in the hyperoxia trials (64 ± 32%) versus the mixed venous trials (55 ± 21%). These findings suggest that contrast stability is not likely a factor affecting the interpretation of TTSCE performed in healthy humans breathing hyperoxia and lends support to the existence of a local O2-dependent mechanism contributing to the regulation of Q̇IPAVA. NEW & NOTEWORTHY Hyperoxic blood has a small stabilizing effect on agitated saline contrast compared with mixed venous blood, lending support to studies that show the reversal of exercise-induced blood flow through intrapulmonary arteriovenous anastomoses (Q̇IPAVA) with hyperoxia. These data support the possible presence of a local O2-dependent regulatory mechanism within the pulmonary vasculature that may play a role in Q̇IPAVA regulation. [ABSTRACT FROM AUTHOR]

Keywords: cerebral; compliance; humans; neurovascular coupling; vascular EN cerebral compliance humans neurovascular coupling vascular 1033 1034 2 02/17/21 20210215 NES 210215 Cerebral neurovascular coupling (NVC) describes the temporal interaction between pairing regional cerebral blood flow to increased neural metabolic demand and is primarily governed via signalling within the neurovascular unit. However, following a rapid peak compliance response, reductions in vascular compliance may occur with sustained PCA vasodilation. Thus, vascular compliance may not contribute, at least to a great extent, to feed-back NVC mechanisms contributing to the plateau phase of the response. [Extracted from the article]

Reducing the work of breathing during exercise improves locomotor muscle blood flow and reduces diaphragm and locomotor muscle fatigue and is thought to be the result of a sympathetically mediated reflex. Aim: The aim of this study was to assess muscle sympathetic nerve activity (MSNA) when the work of breathing is experimentally lowered during dynamic exercise. Methods: Healthy subjects (n = 12; age = 29 ± 9 years) performed semi‐recumbent cycling trials at 40%, 60%, and 80% of peak workload. Exercise trials consisted of spontaneous breathing, reduced work of breathing (proportional assist ventilator), followed by further spontaneous breathing (post‐ventilator). MSNA was recorded from the median nerve. Results: There was no difference in work of breathing between PAV and post‐PAV at 40% peak work. At 60% peak work, the ventilator significantly (P < 0.05) reduced work of breathing (103 ± 39 vs 144 ± 47 J min−1), sympathetic nerve activity (35 ± 5 vs 42 ± 8 burst min−1), and V˙O2 (2.4 ± 0.5 vs 2.6 ± 0.5 L min−1) without influencing ventilation (86 ± 9 vs 82 ± 10 L min−1; P > 0.05), for PAV and post‐PAV respectively. During 80% peak work (n = 8), the ventilator significantly (P < 0.05) reduced work of breathing (235 ± 110 vs. 361 ± 150 J min−1), MSNA (48 ± 7 vs 54 ± 11 burst min−1), and V˙O2 (2.9 ± 0.6 vs 3.2 ± 0.7 L min−1) but not ventilation (121 ± 20 vs 123 ± 20 L min−1; P > 0.05), for PAV and post‐PAV respectively. There was a significant relationship between MSNA and V˙O2 (P < 0.0001) with a significant interaction due to the ventilator (P < 0.05). Conclusion: Lowering the normally occurring work of breathing during exercise results in commensurate reductions in MSNA. Our findings provide evidence of a sympathetically mediated vasoconstrictor effect emanating from respiratory muscles during exercise. [ABSTRACT FROM AUTHOR]

The utility of transthoracic saline contrast echocardiography (TTSCE) to assess blood flow through intrapulmonary arteriovenous anastomoses (Q̇ IPAVA ) in humans is limited due to the potential destabilizing effects of the gas concentration gradients established in varied blood-gas environments. This study assessed the specific effect of a hyperoxic and mixed venous blood-gas environment on the stability of saline contrast. We hypothesized that the rate of contrast mass lost in hyperoxic blood would be similar to mixed venous due to the establishment of equal and opposing gas gradients (O 2 , N 2 , CO 2 ) created when the partial pressure of dissolved gases is manipulated. Using an in vitro model of the pulmonary circulation perfused with defibrinated sheep blood and a membrane oxygenator to control blood gases, we assessed the percent contrast conserved (an index of contrast stability) between inflow and outflow sites at multiple flow rates (1.8, 2.8, 4.3, and 6.8 L/min) in a hyperoxic (Po 2 : 646 ± 16 mmHg; Pco 2 : 0 ± 0 mmHg) and a mixed venous blood gas condition (Po 2 : 35 ± 3 mmHg; Pco 2 : 40 ± 0 mmHg). We found significant contrast decay with time in both conditions, with slightly higher contrast conservation in the hyperoxia trials (64 ± 32%) versus the mixed venous trials (55 ± 21%). These findings suggest that contrast stability is not likely a factor affecting the interpretation of TTSCE performed in healthy humans breathing hyperoxia and lends support to the existence of a local O 2 -dependent mechanism contributing to the regulation of Q̇ IPAVA . NEW & NOTEWORTHY Hyperoxic blood has a small stabilizing effect on agitated saline contrast compared with mixed venous blood, lending support to studies that show the reversal of exercise-induced blood flow through intrapulmonary arteriovenous anastomoses (Q̇ IPAVA ) with hyperoxia. These data support the possible presence of a local O 2 -dependent regulatory mechanism within the pulmonary vasculature that may play a role in Q̇ IPAVA regulation.