Vincenzo Catena

Effects of Acute Blood Volume Expansion on Respiratory Mechanics in the Rat

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.

Cardiac output measurement by the thermodilution method: An in vitro test of accuracy of three commercially available automatic cardiac output computers

ObjectiveTo describe the accuracy and the reproducibility of the thermodilution flow measurements obtained using 3 commercially available cardiac output computers commonly used in intensive care units.DesignAn experimental “in vitro” study. Twelve different values of control flow (Qctr) were measured (Qmsr) using 3 different cardiac output computers (Abbott Critical Care System, Oximetrix 3 SvO2/CO Computer, Baxter Oximeter/Cardiac Output Computer SAT-1TM; American Edwards Laboratories, 9520 A Cardiac Output Computer). Standard equipment and techniques were employed, taking account of the specific weight and heat of warm water relative to blood. In addition, separate sets of measurements were performed in order to investigate the effect on Qmsr of some variables which may influence the “indicator” loss (time for injection, depth of immersion of the catheter, temperature of the injected fluid).SettingOur laboratory, inside the intensive care unit.Measurements and resultsThe analysis of the linear regression of Qmsr versus Qctr (r values between 0.992 and 0.984; residual standard deviation values comprised between 0.24 and 0.49 l/min; intercepts and slopes not significantly different from identity line), the values of the percentage errors (PE=[Qctr−Qmsr]·100/Qctr; PE mean values 7.9, 5.0 and 13.1), and those of the coefficients of variability (CV=standard deviation mean value, %; CV mean values 5.4, 5.8 and 4.6), show a good level of accuracy and reproducibility of the measurements. Our data confirm previously reported results. Furthermore, the cumulative effect of variables capable of influencing the “indicator” loss, even if corrected according to the “calculation constant” the manufacturers provide, was found to result in statistically significant changes of Qmsr.ConclusionThe accuracy and reproducibility of the automatic cardiac computers tested is sufficient for practical clinical purpose. It may also depend on the modality of injection of the cooling bolus, which may significantly influence the effective “indicator” losses.

Effects of the pneumoperitoneum and Trendelenburg position on respiratory mechanics in the rats by the end-inflation occlusion method

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.

Erythropoietin acutely decreases airway resistance in the rat

While some experimental data suggest that erythropoietin (EPO) influences respiratory mechanics, reports on scientific trials are lacking. In the present work, respiratory mechanics were measured using the end-inflation occlusion method in control and EPO treated anaesthetised and positive-pressure ventilated rats. Causing an abrupt inspiratory flow arrest, the end-inflation occlusion method makes it possible to measure the ohmic airway resistance and the respiratory system elastance. It was found that EPO induces a significant decrement in the ohmic airway resistance, not noted in control animals, 20 and 30 min after intraperitoneal EPO injection. The elastic characteristics of the respiratory system did not vary. Hypotheses about the mechanism (s) explaining these results were addressed. In particular, additional experiments have indicated that the decrement in airway resistance could be related to an increase in nitric oxide production induced by EPO. Spontaneous increments in plasmatic erythropoietin levels, such as those that take place in association with hypoxia and/or blood loss, appear to be related to the decrement in airway resistance, allowing pulmonary ventilation to increase without altering respiratory mechanics leading to deleterious increments in energy dissipation during breathing.

Daily variations of spirometric indexes and maximum expiratory pressure in young healthy adults.

In order to document possible variations in the main spirometric indexes in young healthy adults due to the time of the day, we performed standard and complete spirometric measurements at three different hours of the same day (8 am, 4 pm and 12 am) in 33 healthy, non-smoking young volunteers of both sexes. An index of airway resistance was also calculated. We confirm a general worsening of spirometric indexes at night-time compared to daily hours. This result also includes the main effort-independent indexes which were not previously measured. Maximum expiratory pressure does not show daily variations, while an index of respiratory system resistance exhibits a progressive increase from morning to night.

The effects of nifedipine on respiratory mechanics investigated by theend-inflation occlusion method in the rat

Abstract Context: Calcium channel blockers may theoretically exhibit relaxing effects not only on vascular smooth muscle but also on airway smooth muscle. Objective: To investigate possible effects of nifedipine on respiratory mechanics in the rat. Methods: Respiratory system mechanical parameters were measured by the end-inflation occlusion method in the rat in vivo before and after the intraperitoneal administration of nifedipine. Results: We found that nifedipine affects respiratory mechanics, inducing a reduction of airway resistance and of respiratory system elastance, probably because of a relaxing action on airway and parenchimal smooth muscle cells. Conclusion: Should these results be further confirmed by human investigations, a possible role of nifedipine in pharmacological respiratory system’s diseases treatment may be suggested.

A REVIEW OF THE EFFECTS OF BODY TEMPERATURE VARIATIONS ON RESPIRATORY MECHANICS: MEASUREMENTS BY THE END-INFLATION OCCLUSION METHOD IN THE RAT

The temperature of body fluids is expected to affect tissues mechanical properties, including respiratory system tissues. This is because of the changes in airway smooth muscle tone and contractile properties, influencing airway frictional resistance to airflow, and because of the temperature effects on the stress–strain relationships of elastin and collagen, which determinates the elastic behavior of the lungs as reflected by their pressure–volume relationship. Alveolar surfactant biological and physical properties have also been shown to be affected by temperature changes, suggesting influences on the respiratory system hysteretic properties. Experimental works describing the effects of body temperature variations on respiratory mechanics are reviewed, including recent findings dealing with investigations on respiratory mechanics carried out by the end-inflation occlusion method in the rat. This method allows to determine, together with the elastance of the respiratory system, its resistive properties too. In particular, both the ohmic airway resistance due to frictional forces in the airway and the additional visco-elastic resistance exerted because of tissues stress-relaxation may be quantified. The effects of body temperature variations were assessed, and experimentally induced temperature increments and/or decrements allowed to conclude that respiratory system tissues stiffness, both the ohmic and the stress-relaxation linked resistances, and the hysteretic behavior of the respiratory system, decrease with temperature increments. The mechanisms responsible for these effects are analyzed.

The Effects of Erythropoietin on the Respiratory Function: Measurements of Respiratory Mechanics in the Rat

Data reported in the literature indicate that erythropoietin (EPO) influences mammals respiratory function, for example stimulating pulmonary ventilation. Direct experimentations about possible effects of EPO on respiratory mechanics are lacking. In the present report, the endinflation occlusion method was applied in control and EPO-treated anaesthetised and positive-pressure ventilated rats to assess respiratory mechanics. The method involves a sudden flow arrest after a constant flow inflation, and allows to measure the ohmic airway resistance and the respiratory system elastance. A significant decrement of the ohmic airway resistance after 20 and 30 minutes from i.p. EPO administration was observed in experimental animals, which was not seen in control animals. The elastic characteristics of the respiratory system did not change over time in both groups. Hypothesis about the mechanism(s) explaining the results and potential applications to humans are addressed. In particular, further data were obtained by performing additional experiments suggesting that the observed airway resistance decrement may be related to an EPO-induced increased nitric oxide production, a rather well known bronchodilator agent. Literature and present results indicate that the spontaneous increments of plasmatic EPO concentrations, such as those happening in hypoxia and/or blood loss, may be associated with airway resistance decrement. It is suggested that erythropoietin, beside the well known effect on haematopoiesis, may activate complex physiological responses including haematological, circulatory and respiratory adaptations to hypoxia in mammals.