Bronchoscopy and lung lavage induced bilateral pulmonary neutrophil influx and blood leukocytosis in dogs and monkeys.

Investigators have previously determined that repetitive lung washes attract neutrophils to the lungs. They ascribed this attraction to the release of chemotactic factors. Our studies demonstrate that lavage of one lobe of a lung attracts neutrophhils to unwashed lobes as well; therefore, the attraction of neutrophils cannot be entirely due to the local release of chemotactic agents. Further experiments showed that influx of neutrophils also occurred after bronchoscopy without lung lavage but not after the anesthesia alone. These studies suggest that the lungs have mechanisms that regulate and control neutrophil influx both locally and contralaterally. It is not yet clear whether the controlling mechanisms represent an integrated system in the control of leukocyte traffic through the lungs. In addition, lung lavage and bronchoscopy without lung lavage cause an increase in the blood leukocyte count, with an increase in the number of young neutrophil forms. Lung wash concentrates cause a dramatic increase in the number of blood leukocytes when instilled into a bronchus. These data indicate that lungs contain a material that can stimulate the bone marrow to release leukocytes from its reserves.

Reduction of intercellular adhesiveness of chick heart cells by herpes simplex viruses 1 and 2.

Infection with herpes simplex viruses type 1 or 2 prevented the aggregation of 7-day-old chick heart cells into smooth, spheroidal, spontaneously beating aggregates. Virus infection also caused a loosening of peripheral cells in aggregates formed from initially uninfected cells. Measurements of rate of attachment of labelled single heart cells to a monolayer of like cells (homotypic), to HEp-2 cells (heterotypic), or to plastic substrata (nonspecific adhesion) indicated that virus infection caused a significant but differential loss of homotypic and nonspecific adhesiveness, but no alteration in heterotypic attachment rates. These observations indicate that those cells surface changes induced by viruses which are related to cell adhesion can be quantified by techniques measuring attachment rates.

Local regulation of collateral ventilation by oxygen and carbon dioxide.

The effects of changes in CO2 and O2 on the mechanics of collateral ventilation were studied in anesthetized paralyzed dogs. A doublelumen catheter was wedged into a peripheral airway obstructing a segment of lung distal to the catheter. Through one lumen of the catheter, air, 5% CO2 in air, 10% CO2 in air, 5% O2 in N2, or 5% CO2 in N2 was infused at a constant flow (V). Pressure (Ps) was monitored through the other lumen. At functional residual capacity the resistance to collateral flor Rcoll = Ps/V. When V was interrrupted , the time for Ps to fall 63% was defined as the time constant for collateral ventilation, Tcoll. The effective compliance (Cs') = Tcoll/Rcoll. When air was replaced by 5% CO2, Rcoll fell 46.3% (+/- SE 2.8) and Tcoll fell 41.5% (+/- SE 3.0). When the CO2 concentration was increased from 5% to 10%, Rcoll fell an additional 9.2% (+/- SE 2.2) and Tcoll fell an additional 5.1% (+/- SE 4.4). When air was replaced by 5% O2 in N2, Rcoll rose 36.6% (+/- SE 6.0) and Tcoll rose 13.6% (+/- SE 10.5). No significant changes in Cs' were noted. We conclude that varying concentrations of CO2 and O2 provide potent mechanisms for the control of collateral ventillation which may be of importance in the regulation of ventillation perfusion relationships at the local level.