Slide Presentations: Wednesday, November 3, 2010 |

Inhaled Albuterol Impairs Microcirculatory Responses to Induced Ischemia FREE TO VIEW

Bryon N. Johnson, DO; Larry P. Welder, BS; Kurt Trout, BS; Kevin Doerschug, MD
Author and Funding Information

University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA

Chest. 2010;138(4_MeetingAbstracts):907A. doi:10.1378/chest.10126
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PURPOSE: Impaired microvascular responses to ischemia are associated with organ failure and mortality in sepsis. Albuterol is absorbed into systemic circulation resulting in endothelium-dependent and independent vasodilation of the arterioles. We hypothesized that inhaled albuterol augments the microvascular response to ischemia.

METHODS: We studied 24 healthy subjects randomly assigned to receive either albuterol (540 mcg) or sham inhaler. Microvascular function was assessed before and after administration of albuterol or sham by methods previously validated. Stagnant forearm ischemia was induced with a vascular cuff at 250 mm Hg for five minutes. The percent oxygen saturation of microvascular hemoglobin (StO2) was measured in thenar tissue with Near Infrared Spectroscopy before, during, and after ischemia. The rate of tissue oxygen consumption (VO2tis) was defined as the change in THI*StO2 during ischemia. The reoxygenation rate was defined as the rate of increase of StO2 in the first 14 seconds of hyperemia. Following assessment of reoxygenation rates, subjects took 6 puffs from their assigned MDIs. The second ischemic period began 10 minutes following the end of the first. Post-inhalation microcirculatory values were calculated as a percent of baseline values. The effect of albuterol upon microcirculatory function was assessed by comparing post inhalation values between the groups.

RESULTS: Baseline reoxygenation rates in the two groups were similar (p=0.63). Following inhaler use, heart rates increased significantly in albuterol subjects (p<.0001) but not controls. During the second ischemic period, VO2tis remained unchanged in both groups. Following ischemia, reoxygenation rates were slower in albuterol subjects (93%) compared to controls (118 %; p = 0.007). Additionally, ischemic tissue in albuterol subjects reached peak StO2 slower than controls during the second hyperemic phase (p<.001).

CONCLUSION: In contrast to our hypothesis, albuterol impairs the microvascular response to ischemia in healthy subjects despite increased heart rates and no change in tissue oxygen consumption.

CLINICAL IMPLICATIONS: This response resembles the microvascular milieu related to poor outcomes among the critically ill. Further evaluation of albuterol's effects on microvascular function is needed in the critically ill.

DISCLOSURE: Bryon Johnson, No Financial Disclosure Information; No Product/Research Disclosure Information

2:15 PM - 3:45 PM




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