Journal of applied physiology
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Preliminary evidence supports an association between obstructive sleep apnea (OSA) and thoracic aortic dilatation, although potential causative mechanisms are incompletely understood; these may include an increase in aortic wall transmural pressures, induced by obstructive apneas and hypopneas. In patients undergoing cardiac catheterization, mean blood pressure (MBP) in the thoracic aorta and esophageal pressure was simultaneously recorded by an indwelling aortic pigtail catheter and a balloon-tipped esophageal catheter in randomized order during: normal breathing, simulated obstructive hypopnea (inspiration through a threshold load), simulated obstructive apnea (Mueller maneuver), and end-expiratory central apnea. Aortic transmural pressure (aortic MBP minus esophageal pressure) was calculated. ⋯ The difference between aortic MBP and esophageal pressure (and thus the extra aortic dilatory force) was median (quartiles) +9.3 (5.4, 18.6) mmHg, P = 0.02 during inspiration through a threshold load, +16.3 (12.8, 19.4) mmHg, P = 0.02 during the Mueller maneuver, and +0.4 (-4.5, 4.8) mmHg, P = 0.80 during end-expiratory central apnea. Simulated obstructive apnea and hypopnea increase aortic wall dilatory transmural pressures because intra-aortic pressures fall less than esophageal pressures. Thus OSA may mechanically promote thoracic aortic dilatation and should be further investigated as a risk factor for the development or accelerated progression of thoracic aortic aneurysms.
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We hypothesized that breathing hypoxic, hypercapnic, and CO-containing gases together reduces maximal aerobic capacity (Vo2max) as the sum of each gas' individual effect on Vo2max. To test this hypothesis, goats breathed combinations of inspired O2 fraction (FiO2) of 0.06-0.21 and inspired CO2 fraction of 0.00 or 0.05, with and without inspired CO that elevated carboxyhemoglobin fraction (FHbCO) to 0.02-0.45, while running on a treadmill at speeds eliciting Vo2max. Individually, hypoxia and elevated FHbCO decreased fractional Vo2max (FVo2max, fraction of a goat's Vo2max breathing air) in linear, dose-dependent manners; hypercapnia did not change Vo2max. ⋯ The FVo2max correlated highly with total cardiopulmonary O2 delivery, not peripheral diffusing capacity, and with arterial O2 concentration (CaO2), not cardiac output. Hypoxia and elevated FHbCO decreased CaO2 by different mechanisms: hypoxia decreased arterial O2 saturation (SaO2), whereas elevated FHbCO decreased O2 capacitance {concentration of hemoglobin (Hb) available to bind O2 ([Hbavail])}. When breathing hypoxic gas (FiO2 0.12), CaO2 did not change with increasing FHbCO up to 0.30 because higher SaO2 of Hbavail offset decreased [Hbavail] due to the following: 1) hyperventilation with hypoxia and/or elevated FHbCO; 2) increased Hb affinity for O2 due to both Bohr and direct carboxyhemoglobin effects; and 3) the sigmoid relationship between O2 saturation and partial pressure elevating SaO2 more with hypoxia than normoxia.
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Controlled mechanical ventilation (CMV) is known to result in rapid and severe diaphragmatic dysfunction, but the recovery response of the diaphragm to normal function after CMV is unknown. Therefore, we examined the time course of diaphragm function recovery in an animal model of CMV. Healthy rats were submitted to CMV for 24-27 h (n = 16), or to 24-h CMV followed by either 1 h (CMV + 1 h SB, n = 9), 2 h (CMV + 2 h SB, n = 9), 3 h (CMV + 3 h SB, n = 9), or 4-7 h (CMV + 4-7 h SB, n = 9) of spontaneous breathing (SB). ⋯ Finally, also the maximal specific force generation of skinned single diaphragm fibers was increased in the CMV + 4-7 h SB group compared with CMV (+45%, P < 0.05). In rats, reloading the diaphragm for 3 h after CMV is sufficient to improve diaphragm function, while complete recovery occurs after longer periods of reloading. Enhanced muscle fiber dimensions, increased protein synthesis, and improved intrinsic contractile properties of diaphragm muscle fibers may have contributed to diaphragm function recovery.
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In this study we used a rat model for prenatal nicotine exposure to test whether clinically relevant concentrations of brain nicotine and cotinine are passed from dams exposed to nicotine to her pups, whether this changes the trigeminocardiac reflex (TCR), and whether serotonergic function in the TCR brainstem circuitry is altered. Pregnant Sprague-Dawley dams were exposed to 6 mg·kg(-1)·day(-1) of nicotine via osmotic minipumps for the duration of pregnancy. Following birth dams and pups were killed, blood was collected, and brain nicotine and cotinine levels were measured. ⋯ Our data demonstrate that prenatal nicotine exposure significantly exaggerates both the TCR-evoked changes in heart rate in conscious unrestrained pups, and the excitatory neurotransmission to CVNs upon trigeminal afferent nerve stimulation within this brainstem reflex circuit. Application of the 5-HT1A receptor antagonist WAY 100635 (100 μM) and 5-HT2A/C receptor antagonist ketanserin (10 μM)significantly decreased neurotransmission, indicating an increased facilitation of 5-HT function in prenatal nicotine-exposed animals. Prenatal nicotine exposure enhances activation of 5-HT receptors and exaggerates the trigeminocardiac reflex.
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Neurovascular coupling (NVC) and dynamic cerebral autoregulation (dCA) are both impaired in the acute phase of ischemic stroke, but their reciprocal interactions are difficult to predict. To clarify these aspects, the present study explored NVC in a healthy volunteer population during a surrogate state of impaired dCA induced by hypercapnia. This study aimed to test whether hypercapnia leads to a depression of NVC through an impairment of dCA. ⋯ VRAP reflects myogenic activity in response to BP changes, whereas VCrCP is more indicative of metabolic control. The results revealed that hypercapnia significantly affected NVC, with significant reductions in the relative contribution of VCrCP to the paradigm-induced increase in CBFv. The present study suggests that hypercapnia impairs both dCA and NVC, probably acting through an impairment of the metabolic component of CBF control.