Interleukin-6 is a multifunctional cytokine that has been shown to be increased in some pathological conditions involving the respiratory system such as those experimentally induced in animals or spontaneously occurring in humans. Experimental data demonstrating that interleukin-6 plays a significant role in commonly occurring respiratory system inflammatory diseases are reviewed here. Those diseases, i.e. asthma and chronic obstructive pulmonary disease, are characterised by mechanical derangements of the respiratory system, for the most part due to increased elastance and airway resistance. Recent findings showing that interleukin-6 has a causative role in determining an increase in airway resistance are reviewed. The end-inflation occlusion method was used to study the mechanical properties of the respiratory system before and after interleukin-6 administration. The cytokine was shown to induce significant, dose-dependent increments in both the resistive pressure dissipation due to frictional forces opposing the airflow in the airway (ohmic resistance) and the additional resistive pressure dissipation due to the visco-elastic properties of the system, i.e. stress relaxation (visco-elastic resistance). There were no alterations in respiratory system elastance. Even when administered to healthy mammals, interleukin-6 determines a significant effect on respiratory system resistance causing an increase in the mechanical work of breathing during inspiration. IL-6 hypothetically plays an active role in the pathogenesis of respiratory system diseases and the mechanisms that may be involved are discussed here.

Purpose: To describe the consequences of the cranial displacement of the diaphgram occurring during pneumoperitoneum (Pnp) and/or Trendelenburg (Tnd) position on respiratory mechanics. Possible addictive effects and the changes of the viscoelastic respiratory system resistance were studied, which were not extensively described before. Methods: The end-inflation occlusion method was applied on eight rats. It allows us to determine mechanical parameters such as respiratory system static elastance, the ohmic resistance due to frictional forces in the airways, and the additional viscoelastic impedance due to tissues deformation. Measurements during mechanical ventilation were taken in controls (supine position), after 20-25° head-down tilting (Tnd), after abdominal air insufflation up to 12 mmHg abdominal pressure in the supine position (Pnp), and combining Tnd + Pnp. Tnd and Pnp modalities were similar to those commonly applied during surgical procedures in humans. Results: We confirmed the previously described detrimental effects on respiratory mechanics due to the diaphgram displacement during both Pnp and Tnd. The increment in the total resistive pressure dissipation was found to depend primarily on the effects on the viscoelastic characteristics of the respiratory system. Data suggesting greater effects of Pnp compared to those of Tnd were obtained. Conclusion: The cranial displacement of the diaphgram occurring as a consequence of Pnp and/or Tnd, for example during laparoscopic surgical procedures, causes an increment of respiratory system elastance and viscoelastic resistance. The analysis of addictive effects show that these are more likely to occur when Pnp + Tnd are compared to isolated Tnd rather than to isolated Pnp.

Backgrounds: The effects of acute blood volume expansion (BVE) on the respiratory mechanics of normal animals have been not extensively studied. The subject is of both theoretical and practical interest since BVE is a frequent medical intervention, and the associated increase in cardiac output may occur in different physiopathological situations. Objectives: To describe the changes in the parameters of respiratory mechanics occurring as an effect of acute BVE and the related increase in cardiac output. Methods: We applied the end-inflation occlusion method in normal, positive pressure-ventilated rats to measure the respiratory mechanics under control and BVE conditions. Results: Under BVE conditions, we found a statistically significant increase in static respiratory system elastance (Est,rs), ohmic airway resistance plus resistance of respiratory system tissues to movement (Rmin,rs), and overall resistance including pendelluft and stress relaxation effects (Rmax,rs). Under BVE conditions, the resistive component due to sole stress relaxation and pendelluft (Rvisc,rs) increased almost significantly while a significant increment in mean respiratory system hysteresis surface area (Hyrs) was also found. Conclusions: Increasing pulmonary blood flow by BVE increases the mechanical work of breathing because of the effects on Est,rs, Rmin,rs and Rmax,rs, and because of the increase in Hyrs.