To investigate whether the acute inflammatory response produced by acute cigarette smoke exposure is associated with alterations in pulmonary and cardiovascular function, using a respirator we exposed 8 guinea pigs to 350 ml of cigarette smoke diluted in 2,000 ml room air for 10 min. Lung volumes, pressure volume curves and flow volume curves were performed. Measurements of pulmonary artery pressure, systemic pressure, heart rate and cardiac output were taken at baseline, immediately after the smoke exposure, and 1.5 h after smoke exposure. Aliquots of peripheral blood for total white cell count and differential count were obtained. After animal sacrifice, the right lung was lavaged and white cell count and differential count performed. We found that acute exposure to cigarette smoke produced a peripheral blood neutrophilia which rose progressively from a baseline of 36.3 ± 8% to a maximum of 72.2 ± 7.7% at 1.5 h after exposure. There was pulmonary neutrophilia with 24.6 ± 6.3% neutrophils in the lavage fluid of the smoke-exposed animals compared to 8.4 ± 4.3% in the control animals. Immediately after smoke exposure, there was acute airflow obstruction with a decrease in the peak flow and forced expiratory flow between 25–75% vital capacity. This was associated with airtrapping, as shown by a transient increase in residual volume. There was a slight decrease in systemic blood pressure in the smoke-exposed animals associated with a nonsignificant decrease in the heart rate, and the cardiac output remained stable. After 1.5 h, there was still evidence of airflow obstruction in the smoke-exposed animals, and both groups showed a slight decrease in cardiac output. We conclude that acute cigarette smoke exposure in guinea pigs produces pulmonary functional abnormalities which may be related to acute bronchoconstriction and to the inflammatory response. Within the constraints of this animal model, we could not find evidence of significant vasospasm