rhythm in mammals Science 1991 254:726 9.Mitsuyasu H.et al.Ile50 Val variant of il-4R alpha upregulates IgE synthesis and associates with a 10.s Nature Genet,.198,19:119 way J and Fredberg JJ.Perhaps airway sn othscle dysfunction contributes to asthmatic bronchial hyperresponsiveness after all.Am J Respir cell Mol Biol.1997,17:144. Summary The gas exchange between the living body and is called respiration,which is an important sign of lie.It includes three processes:exteral respiration (pulmonary ventilation and gas exchange in lungs),gas transport in the blood and internal respiration. Pulmonary ventilation means the inflow and outflow of air between the lung alveolus and the environment.The force that drives pulmonary ventilation comes from respiration movement.The rhythmic conraction and relaxation of the respiratory muscles cause the expansion or reduction of the During inspiration,alveolar pressure is lower than the atmospheric pressure so air flows into the lung (inhalation).During expiration,opposite changes occur because the alveolar pressure is greater than the atmospheric pressure and so air flows out of the lung (exhalation).Therefore the original impetus of pulmonary ventilation is respiratory movement and the direct impetus is the pressure difference between ure and atmospherie pressure avr()very morn in thy yentistion Itmean the pressure in the pleural space and is made of two factors:alveolar pressure (AP)acting on alveola cell wall (namely visceral pleura)and recoil force (RF)of lung They can be expressed as follows: IP=AP-RF.Hence,the intrapleural pressure is a slightly negative pressure (compared with atmosphere dBa。 lungs in expansion and toenhance both venous retu and lymphati During the process of pulmonary ventilation,only when the driving force overcomes the resistance,can ventilation take place.There are two kinds of resistance to pulmonary ventilation.One is the elastic resistance and another is the non-elastic resistance in pulmonary ventilation. The elastic resistance of pulmonary ventilation can be classified into two categories:alveolar suface tensio index to reflect the elastic resistance of the lung is the compliance of lung.which is the inverseo resistance.Type II alveolar epithelial cells synthesize and secrete pulmonary surfactant (PS).The physiological functions of PS are to reduce the alveolar surface tension thereby allowing lung expansion easily:to stabilize the different sized alveoli in lungs:to prevent alveolar collapse and the infiltration of fluid into the alyeoli The non- lasti resistance of pulmonary ventilation includes airway resistance,inertia resistance and tissue viscosity resistance.The airway resistance is a major element of non-elastic resistance.Many factors can lead to contraction of bronchial smooth muscle and the reduction of the bronchi radius These changes can appear in asthma. How to evaluate the function of pulmonary ventilation,there are many indexes.Timed vital capacity,vital capacity and alveolar minute volume are good indexes for the nction of pulmonary ventilation and the efficiency of pulmonary ventilation respectively.Some indexes can be used to differentiate obstructive and restrictive pulmonary ventilation dysfunction. The exchange of gases between the alveoli and blood in the capillary vessels is called pulmonary gas exchange.The diffusion constant is proportionl to the difference in gas partial pressure,temperature. 12 12 rhythm in mammals. Science,1991,254:726. 9．Mitsuyasu H. et al.Ile50 Val variant of il-4R alpha upregulates IgE synthesis and associates with atropic asthma. Nature Genet,1998,19:119. 10. Solway J and Fredberg JJ. Perhaps airway smooth muscle dysfunction contributes to asthmatic bronchial hyperresponsiveness after all. Am J Respir cell Mol Biol.1997,17;144. Summary The gas exchange between the living body and its environment is called respiration，which is an important sign of life. It includes three processes: external respiration (pulmonary ventilation and gas exchange in lungs), gas transport in the blood and internal respiration. Pulmonary ventilation means the inflow and outflow of air between the lung alveolus and the environment. The force that drives pulmonary ventilation comes from respiration movement. The rhythmic contraction and relaxation of the respiratory muscles cause the expansion or reduction of the chest and lung, which results in the expansion or reduction of the alveoli to change the alveolar pressure. During inspiration, alveolar pressure is lower than the atmospheric pressure so air flows into the lung (inhalation). During expiration, opposite changes occur because the alveolar pressure is greater than the atmospheric pressure and so air flows out of the lung (exhalation). Therefore the original impetus of pulmonary ventilation is respiratory movement and the direct impetus is the pressure difference between alveolar pressure and atmospheric pressure. The intrapleural pressure (IP) is very important in the process of pulmonary ventilation. It means the pressure in the pleural space and is made of two factors: alveolar pressure (AP) acting on alveolar cell wall (namely visceral pleura) and recoil force (RF) of lung. They can be expressed as follows: IP=AP-RF. Hence, the intrapleural pressure is a slightly negative pressure（compared with atmosphere pressure）. The physiological significance of negative pressure in pleural space is that it is required to hold the lungs in expansion and to enhance both venous return and lymphatic return. During the process of pulmonary ventilation, only when the driving force overcomes the resistance, can ventilation take place. There are two kinds of resistance to pulmonary ventilation. One is the elastic resistance and another is the non-elastic resistance in pulmonary ventilation. The elastic resistance of pulmonary ventilation can be classified into two categories: alveolar surface tension and elastic recoil of the lung；alveolar surface tension is more important. The common index to reflect the elastic resistance of the lung is the compliance of lung, which is the inverse of elastic resistance. Type II alveolar epithelial cells synthesize and secrete pulmonary surfactant (PS). The physiological functions of PS are to reduce the alveolar surface tension thereby allowing lung expansion easily；to stabilize the different sized alveoli in lungs；to prevent alveolar collapse and the infiltration of fluid into the alveoli. The non-elastic resistance of pulmonary ventilation includes airway resistance, inertia resistance and tissue viscosity resistance. The airway resistance is a major element of non-elastic resistance. Many factors can lead to contraction of bronchial smooth muscle and the reduction of the bronchi radius. These changes can appear in asthma. How to evaluate the function of pulmonary ventilation, there are many indexes. Timed vital capacity，vital capacity and alveolar minute volume are good indexes for the function of pulmonary ventilation and the efficiency of pulmonary ventilation respectively. Some indexes can be used to differentiate obstructive and restrictive pulmonary ventilation dysfunction. The exchange of gases between the alveoli and blood in the capillary vessels is called pulmonary gas exchange. The diffusion constant is proportional to the difference in gas partial pressure, temperature