ATS 2009 · San Diego
International Conference
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Abstract Number: 951804
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| Contact/Presenting Author: Bethany P. Kulczewski |
| Department/Institution: Pulmonary Research, Beth Israel Deaconess Medical Center |
| Address: 330 Brookline Ave |
| City/State/Zip/Country: Boston, MA, 02215, United States |
| Phone: 617-667-4126 Fax: 617-667-1604 E-mail: bkulczew@bidmc.harvard.edu |
| ATS member:
No Student or in training:
No |
| Funding Source:
NIH |
Abstract Category:
08.18 - Intermittent Hypoxia |
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Presentation format:
Poster Only
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Preview Disclosure
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Travel Award:
No |
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Publication of email address:
No I confirm that all authors listed on this abstract have knowledge of the abstract submission: Yes |
Title: Arterial and Microvascular Responses to Acute Isocapnic Hypoxia in Humans
B P Kulczewski, BA1, M E Lynch, BA1, G S Gilmartin, MD1 and J W Weiss, MD1. 1Beth Israel Deaconess Medical Center, Boston, MA, United States.
RATIONALE: Obstructive Sleep Apnea (OSA) is characterized by both intermittent arousal from sleep and intermittent hypoxia. OSA is independently associated with insulin resistance and sympathoexcitation. Although a complete picture of the source of this insulin resistant state has yet to be provided, alterations in the distribution of capillary blood flow and therefore glucose and insulin delivery are associated with insulin resistance. We conducted a prospective, experimental trial in normal volunteers to evaluate the impact of brief isocapnic hypoxia, one component of OSA, on capillary blood flow and muscle sympathetic nerve activity (MSNA). METHODS: 10 healthy subjects were exposed to isocapnic hypoxia (goal SaO2= 80%) for 60 minutes. Brachial arterial blood flow was evaluated by ultrasound. Capillary blood flow and blood volume was measured in the ipsilateral forearm using contrast enhanced ultrasound. MSNA was recorded from the peroneal nerve. All measurements were taken at baseline and during the final 10 minutes of the 60 minute exposure to isocapnic hypoxia. RESULTS: Brachial arterial blood flow increased significantly with isocapnic hypoxia. (Baseline: 16.7  1.1 ml/min; exposure: 24.8 1.5 ml/min, p<0.03). However, capillary blood volume and blood flow were unchanged. There was a decrease in MSNA after 35 minutes and after 55 minutes from baseline. (Baseline: 33.6 5.2 bursts/100hb; 35 min: 25.7 3.7 bursts/100hb, p<0.05; 55 min: 22.1 2.8 bursts/100hb, p<0.05). CONCLUSIONS: As expected, brief exposure to isocapnic hypoxia resulted in an increase in total forearm blood flow. However, there was no significant change in capillary blood flow or blood volume as measured by CEU. This would suggest that during acute hypoxia there may be an increase in non-nutritive capillary flow, rather than recruitment of nutritive capillaries.
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