Pulmonary circulation in experimental toxic edema of the lungs

By means of ultrasonic method used in acute experiments on cats with open chest under artificial lung ventilation the authors studied the blood flow in low-lobar pulmonary artery and the vein, the blood pressure in pulmonary artery as well as the balance between output of right and left ventricles in experimental pulmonary edemas caused by intravenous infusion of mixture fatty acids. It was shown, that acute injury of lungs vessels produces redistribution of blood flow to the lesser circulation, increases the pressure in pulmonary artery. The pattern of pulsating blood flow in lobar artery and vein changes. The authors assume that in situation, when lung vessels permeability is already deranged redistribution of the blood to the lesser circulation aggravates the degree of edema.     

Regulation of respiration and pulmonary blood circulation in experimental pneumonia

The experiments on anesthetized cats were carried out to determine the functional state of respiration centre (impulse activity of genuine respiration neurons and electrical activity of major and additional respiration muscles). Functional peculiarities of macro- and microcirculation of the lung tissue were also studied in the open and closed chest in normal subjects and in conditions of experimental pneumonia.     

Pulmonary circulation in experimental pulmonary edema during diverse artificial respiration regimes

In acute experiments on cats with closed chest by ultrasonic method the authors studied the blood flow in low-lobar pulmonary artery and the vein, the blood pressure in pulmonary artery, lung vessels resistance in experimental pulmonary edema caused by intravenous infusion of mixture fatty acids at artificial ventilation of increased frequencies or volumes, at was shown, that artificial ventilation of increased frequencies in pulmonary edema reduces the pressure increase in pulmonary artery, lung vessels resistance and increases the blood flow in pulmonary artery and vein. Artificial ventilation of increased volumes produces more intense pressure increase in pulmonary artery and lung vessels resistance than in initial ventilation but the blood flow was slightly changed. The authors assume that artificial ventilation of increased frequencies or volumes in pulmonary edema due to pulmonary circulation change reduces the pulmonary edema intensity at the beginning.     

Pulmonary circulation in embolic pulmonary edema

The ultrasonic method was used in acute experiments on cats with open chest under artificial lung ventilation to obtain blood flow in low-lobar pulmonary artery and vein, the blood pressure in pulmonary artery, as well as the left atrial pressure in fat (olive oil) and mechanical (Lycopodium spores) pulmonary embolism. It is shown that pulmonary embolism produces the decrease in the blood flow in pulmonary artery and vein, the increase of the pressure in pulmonary artery and left atria, the increase of lung vessels resistance. The decrease is observed of systemic arterial pressure, bradycardia, and extrasystole. After 5-10 min the restoration of arterial pressure and heart rhythm occur and partial restoration of blood flow in pulmonary artery and vein. In many experiments the blood flow in vein outdoes that in the artery--it allows to suppose the increase of the blood flow in bronchial artery. After 60-90 min there occur sudden decrease of systemic arterial pressure, the decrease of the blood flow in pulmonary artery and vein. The pressure in pulmonary artery and resistance of pulmonary vessels remain high. Pulmonary edema developed in all animals. The death occurs in 60-100 min after the beginning of embolism.     

Pulmonary circulation in different gaseous media

The ultrasonic method was used in acute experiments on cats with an open (under artificial lung ventilation) and closed chest to explore lung circulation in a changed gaseous medium. Moderate hypoxia (10% O2) and hypercapnia (5, 10% CO2) induce a 10-15% decrease in the lung blood flow in the inferolobular pulmonary artery in the presence of unchanged or slightly elevated minute volume of the heart. The higher hypoxia (5% O2) provokes inconclusive changes in the lung blood flow: biphasic response or increase. It is assumed that considerable elevation of blood pressure in the common pulmonary artery in all the cases points to vasoconstriction that occurs under the effect of hypoxia and hypercapnia.     

Carrageenin-induced experimental pneumonia in rats.

The authors verified the possibility of modelling pneumonia by the intratracheal administration of carrageenin solution into the lungs of rats. The most satisfactory dose was found to be 0.5 ml 0.7% carrageenin solution administered at 40 degrees C. The disease, evaluated by the morphological and functional signs, culminated after two days. Both macroscopically and histologically the lungs displayed typical signs of catarrhal suppurative aspiration bronchopneumonia. Functionally, marked tachypnoea (mean 180 cycles/min as against 110 c/min in the conscious controls) and raised functional residual capacity were found. A drop in the respiration rate and in FRC after bilateral cervical vagotomy indicated that a reflex component participates in the origin of the above two signs.     

Intrapulmonary oxygen consumption in experimental pneumococcal pneumonia

To test the hypothesis that lung affected by acute bacterial pneumonia consumes significant amounts of O2, whole-body O2 consumption (VO2) was measured simultaneously by collection of expired gas (VO2exp) and by the Fick principle (VO2Fick) in five dogs with acute experimental pneumococcal pneumonia and in five uninfected controls. This approach is based on the premise that VO2Fick will not detect lung VO2, whereas the expired gas measurement represents the true whole-body VO2, including the lung. In controls VO2 exp averaged 110 +/- 20 ml/min (4.78 +/- 0.78 ml.min-1.kg-1), and VO2Fick was nearly identical at 114 +/- 21 ml/min (4.96 +/- 0.79 ml.min-1.kg-1). The VO2Fick in the pneumonia group was 127 ml/min, similar to both control group values when indexed for body weight (4.91 +/- 1.17 ml.min-1.kg-1). VO2exp, however, was 146 +/- 46 ml/min (5.74 +/- 1.57 ml.min-1.kg-1), exceeding VO2Fick by an average of 20 +/- 9 ml/min (P less than 0.01). This between-method difference of 20 +/- 9 ml/min (or 24 ml/min if the difference in the control group is assumed to apply to the pneumonia group) amounted to 13-15% of whole-body VO2 and can be attributed to VO2 in the lung, presumably by cells involved in the acute inflammatory response. Implications include the potential for significant underestimate of whole-body VO2 by the Fick method when used in the presence of lung inflammation and overestimate of blood flow to shunting or low ventilation-perfusion ratio lung units by the O2 method of measuring venous admixture-like perfusion. This observation may also explain the disproportionate hypoxemia sometimes seen in patients with severe pneumonia.