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Biomedical subjects

Virginia A Imadojemu

Publications and source records attributed to Virginia A Imadojemu.

5 recordsLinked to original sources
PubMed2005

Effects of intermittent hypoxia on sympathetic activity and blood pressure in humans.

Sympathetic nerve activity and arterial pressure are frequently elevated in patients with obstructive sleep apnea (OSA). The mechanisms responsible for chronic sympathetic activation and hypertension in OSA are unknown. To determine whether repetitive apneas raise sympathetic nerve activity and/or arterial pressure, awake and healthy young subjects performed voluntary end-expiratory apneas for 20 s per min for 30 min (room air apneas). To accentuate intermittent hypoxia, in a separate group of subjects, hypoxic gas (inspired O2 10%) was added to the inspiratory port for 20 s before each apnea (hypoxic apneas). Mean arterial pressure (MAP) and muscle sympathetic nerve activity (MSNA, peroneal microneurography) were determined before and up to 30 min following the repetitive apneas. Following 30 hypoxic apneas (O2 saturation nadir 83.1+/-1.2%), MSNA increased from 17.4+/-2.7 to 23.4+/-2.5 bursts/min and from 164+/-28 to 240+/-35 arbitrary units respectively (P<0.01 for both; n=10) and remained elevated while MAP increased transiently from 80.5+/-3.7 to 83.1+/-3.9 mm Hg (P<0.05; n=11). In contrast, in the subjects who performed repetitive apneas during room air exposure (O2 saturation nadir 95.1+/-0.8%), MAP and MSNA did not change (n=8). End-tidal CO2 post-apnea, an index of apnea-induced hypercapnia, was similar in the 2 groups. In a separate control group, no effect of time on MAP or MSNA was noted (n=7). Thus, repetitive hypoxic apneas result in sustained sympathetic activation and a transient elevation of blood pressure. These effects appear to be due to intermittent hypoxia and may play a role in the sympathetic activation and hypertension in OSA.

Adult↗
PubMed2004

Extracellular calcium and vascular responses after forearm ischemia.

BACKGROUND: The myogenic response is a phenomenon in which blood vessels respond to increases and decreases in transmural pressure with constriction and dilation, respectively. Despite intense investigation into the signaling mechanisms underlying this response, the precise mechanisms remain unclear. It has been suggested that the myogenic response occurs when pressure or stretch evokes increases in vessel wall tension that results in vessel smooth muscle cell depolarization. This causes Ca2+ entry through voltage-gated Ca2+ channels. Of note, in vitro studies demonstrate that the magnitude of the myogenic response is dependent on the extracellular Ca2+. We tested the hypothesis that in conscious humans, physiological changes in extracellular Ca2+ concentrations would be an important determinant of the myogenic response. METHODS AND RESULTS: Venous blood ionized calcium was used as an index of interstitial calcium and was measured 5, 15, and then every 15 seconds for 75 seconds, then every 30 seconds for 90 seconds, then finally at the 300-second mark. Forearm blood pressure and flow velocity were determined after 10 minutes of forearm ischemia. We found that the rate of change in serum calcium levels varied as a function of transmural pressure (r=0.96). Moreover, the calcium concentration was inversely proportional to forearm blood velocity (r=0.99). CONCLUSIONS: We hypothesize that muscle stretch caused by a rise in transmural pressure raises interstitial calcium by unknown mechanisms and this in turn acts to lower limb flow velocity.

Adult↗
PubMed2002

Impaired vasodilator responses in obstructive sleep apnea are improved with continuous positive airway pressure therapy.

Obstructive sleep apnea causes cardiovascular morbidity and premature death. Potential links between sleep apnea and cardiovascular complications are chronically elevated activity of the sympathetic nervous system and abnormal vascular function. To explore vascular function, we determined the reactive hyperemic blood flow (RHBF) responses to 10 minutes of forearm arterial occlusion (plethysmography), blood pressure, and muscle sympathetic nerve activity (MSNA, microneurography) in eight patients with sleep apnea and in nine nonapneic control subjects. Peak RHBF and vascular conductance were markedly attenuated in sleep apnea compared with control subjects (p < 0.05). Seven sleep apnea patients were retested after at least two weeks of continuous positive airway pressure (CPAP) therapy. MSNA decreased after CPAP therapy (p < 0.05, n = 6), whereas blood pressure did not change. After CPAP therapy, peak RHBF and vascular conductance were increased compared with before treatment (p < 0.05; n = 7). Thus, vascular function is abnormal in sleep apnea and is improved by CPAP therapy. Furthermore, effective CPAP therapy decreases sympathetic activity in sleep apnea. Thus, sympathoexcitation and abnormal vascular function in patients with sleep apnea appear to be linked to the repetitive nocturnal apneic events.

Adult↗
PubMed2002

Obstructive apnea during sleep is associated with peripheral vasoconstriction.

Obstructive apnea during sleep is associated with a substantial transient blood pressure elevation. The mechanism of this pressor response is unclear. In this study we measured muscle sympathetic nerve activity (MSNA), mean arterial pressure (Psa), and mean limb blood velocity as an index of blood flow (MBV, Doppler) and calculated changes in limb vascular resistance during and after apneas during both wakefulness and sleep in patients with the obstructive sleep apnea syndrome. Immediately postapnea during sleep Psa increased significantly compared with the earlier stages of apnea and this was preceded by a rise of MSNA (n = 5). In contrast to blood pressure, MBV remained unchanged. Because resistance = blood pressure/blood flow, limb vascular resistance increased by 29 +/- 8% from late apnea to postapnea (n = 7, p < 0.002). Voluntary breathhold maneuvers during room air exposure evoked similar responses (n = 10). Supplemental oxygen administered via nonrebreather face mask attenuated the MSNA and vasoconstrictor responses to obstructive (n = 2) and voluntary apneas (n = 10). Our data suggest that obstructive apneas in patients with the obstructive apnea syndrome are accompanied by transient limb vasoconstriction. This vasoconstrictor response appears to be, at least in part, mediated by the sympathetic nervous system and may be linked to hypoxia.

Adrenergic Fibers↗