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Inhaled cigarette smoke selectively reverses human hypoxic vasoconstriction
P M Dupuy1, J P Lançon, M Françoise
1Department of Anaesthesiology and Intensive Care, Hôpital Universitaire Le Bocage, Dijon, France.
Intensive Care Medicine
|November 1, 1995
Summary
Cigarette smoke inhalation rapidly reverses acute hypoxic pulmonary vasoconstriction in humans. This effect, similar to nitric oxide (NO), is mediated by the NO-cGMP pathway without altering systemic arterial pressure.
Area of Science:
- Cardiovascular Physiology
- Respiratory Medicine
- Pharmacology
Background:
- Hypoxia induces pulmonary vasoconstriction, increasing pulmonary arterial pressure (PAP).
- Nitric oxide (NO) is a vasodilator that reduces PAP.
- The effects of cigarette smoke on pulmonary hemodynamics are not fully understood.
Purpose of the Study:
- To compare the acute effects of inhaled cigarette smoke and nitric oxide (NO) on pulmonary and systemic arterial pressures (PAP and SAP).
- To investigate the role of the NO-cGMP pathway in mediating these effects.
- To determine if cigarette smoke causes systemic vasodilation.
Main Methods:
- One healthy adult volunteer inhaled hypoxic gas (FIO2 0.12), nitric oxide (NO) at varying concentrations, and cigarette smoke.
- Pulmonary and systemic arterial pressures (PAP and SAP) were continuously monitored.
- Plasma arterial cyclic guanosine monophosphate (cGMP) levels were measured.
Main Results:
- Hypoxia induced stable pulmonary vasoconstriction.
- Inhaled NO caused a dose-dependent fall in PAP and increased plasma cGMP.
- Cigarette smoke inhalation also reduced PAP and elevated plasma cGMP, without affecting SAP.
- Neither NO nor cigarette smoke altered systemic arterial pressure (SAP).
Conclusions:
- Cigarette smoke selectively reverses acute hypoxic pulmonary vasoconstriction in humans.
- The effect of cigarette smoke is comparable to NO and likely involves the NO-cGMP pathway.
- Cigarette smoke inhalation does not induce systemic vasodilation in this context.