V Linardatou1, E Karatzanos2, N Panagopoulou2, D Delis2, C Kourek2, N Rovina3, S Nanas2, I Vasileiadis4. 1. Clinical Ergospirometry Exercise and Rehabilitation Laboratory, Evaggelismos Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece; Department of Oncology, General Hospital 'G. Gennimatas', Athens, Greece. 2. Clinical Ergospirometry Exercise and Rehabilitation Laboratory, Evaggelismos Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. 3. ICU, 1st Dept of Respiratory Medicine, 'Sotiria' Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. 4. ICU, 1st Dept of Respiratory Medicine, 'Sotiria' Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Electronic address: ivasileiadis@med.uoa.gr.
Abstract
OBJECTIVE: Acute effects of passive smoking on microcirculation have not been sufficiently studied. The aim of the present study was to detect microcirculatory alterations in healthy non-smokers after passive exposure to cigarette smoke, utilizing the Near Infrared Spectroscopy method combined with the vascular occlusion technique. METHODS: Sixteen (9 females, age: 34 ± 9 years) non-smoking, healthy volunteers were exposed to passive smoking for 30 min in a temperature-controlled environment. Smoke concentration was monitored with a real-time particle counter. The following microcirculatory parameters were estimated: baseline tissue oxygen saturation (StO2); StO2 decrement after vascular occlusion (indicating the oxygen consumption rate); StO2incremental response after vascular occlusion release (reperfusion rate); the time period where the StO2 signal returns to the baseline values after the hyperemic response. RESULTS: Baseline StO2 (79.6 ± 6.4 vs. 79 ± 8%, p = 0.53) as well as the time needed for StO2 to return to baseline levels (138.2 ± 26.5 vs. 142.1 ± 34.6 s, p = 0.64) did not significantly differ before vs. after passive smoking exposure. Oxygen consumption rate decreased after 30 min exposure to passive smoking (from 12.8 ± 4.2 to 11.3 ± 2.8%/min, p = 0.04); Reperfusion rate also significantly decreased (from 5.6 ± 1.8 to 5 ± 1.7%/s, p = 0.04). CONCLUSIONS: Our results suggest that acute exposure to passive smoking delays peripheral tissue oxygen consumption and adversely affects microcirculatory responsiveness after stagnant ischemia in healthy non-smokers.
OBJECTIVE: Acute effects of passive smoking on microcirculation have not been sufficiently studied. The aim of the present study was to detect microcirculatory alterations in healthy non-smokers after passive exposure to cigarette smoke, utilizing the Near Infrared Spectroscopy method combined with the vascular occlusion technique. METHODS: Sixteen (9 females, age: 34 ± 9 years) non-smoking, healthy volunteers were exposed to passive smoking for 30 min in a temperature-controlled environment. Smoke concentration was monitored with a real-time particle counter. The following microcirculatory parameters were estimated: baseline tissue oxygen saturation (StO2); StO2 decrement after vascular occlusion (indicating the oxygen consumption rate); StO2incremental response after vascular occlusion release (reperfusion rate); the time period where the StO2 signal returns to the baseline values after the hyperemic response. RESULTS: Baseline StO2 (79.6 ± 6.4 vs. 79 ± 8%, p = 0.53) as well as the time needed for StO2 to return to baseline levels (138.2 ± 26.5 vs. 142.1 ± 34.6 s, p = 0.64) did not significantly differ before vs. after passive smoking exposure. Oxygen consumption rate decreased after 30 min exposure to passive smoking (from 12.8 ± 4.2 to 11.3 ± 2.8%/min, p = 0.04); Reperfusion rate also significantly decreased (from 5.6 ± 1.8 to 5 ± 1.7%/s, p = 0.04). CONCLUSIONS: Our results suggest that acute exposure to passive smoking delays peripheral tissue oxygen consumption and adversely affects microcirculatory responsiveness after stagnant ischemia in healthy non-smokers.