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Biomedical subjects

E Agostoni

Publications and source records attributed to E Agostoni.

At least 55 records · Page 3Linked to original sources
PubMed1991

Starling forces and lymphatic drainage in pleural liquid and protein exchanges.

Pleural liquid volume and protein concentration (C) were determined in rabbits 60 min after a 2 ml hydrothorax with various albumin concentrations in Ringer, homologous serum or plasma. The absorption rate of the hydrothorax decreased with the increase in colloid osmotic pressure of the pleural liquid (pi), being 0.56 +/- 0.03, 0.32 +/- 0.02 and 0.17 +/- 0.05 ml/h with Ringer, 1.1 and 3 g% albumin, respectively, and nil with 5% albumin, serum or plasma. C increased with Ringer and 1.1% albumin, did not change with 3% albumin, and decreased with 5% albumin, serum or plasma. The protein content in the pleural liquid increased with Ringer, did not change with 1.1% albumin, and decreased with the other hydrothoraces. These findings indicate that with hydrothoraces of this size: (1) the Starling forces plus the solute-coupled liquid absorption [Agostoni and Zocchi (1990) Respir. Physiol. 81: 19-28] provide most of the pleural liquid absorption when pi is less than or equal to physiological; (2) the lymphatic drainage increases with pi, providing most of the liquid outflow when pi is similar to that of plasma. This increase in lymphatic drainage, however, does not compensate for the effects of the changes in Starling forces produced by the increased pi.

Absorption↗
PubMed1991

Pleural liquid pressure.

The knowledge of pleural liquid pressure (Pliq) is essential for understanding the mechanical coupling between lung and chest wall and the liquid exchanges of the pleural space. In the last decade, research in this field contributed new ideas and stimulating controversies but also caused some confusion. These aspects, along with the older contributions, are considered in this review, which is divided into three sections. The topics of the first section are 1) measurements of Pliq with different techniques in various mammals and various regions of the pleural space, 2) comparison of Pliq with the pressure exerted by the lung recoil (Ppl), and 3) vertical gradient of Pliq and downward flow of pleural liquid. In the second section the mechanisms absorbing liquid from the pleural space are analyzed: 1) Starling forces of the visceral pleura, 2) lymphatic drainage through the stomata of the parietal pleura, and 3) active transport of solutes. The third section deals with 1) measurements of pleural liquid thickness with two approaches in the costal region of various mammals and 2) mechanisms preventing a complete removal of pleural liquid and, thus, ensuring the lubrication.

Animals↗
PubMed1990

Solute-coupled liquid absorption from the pleural space.

The occurrence of a solute-coupled absorption of liquid from the pleural space was studied by measuring in anesthetized rabbits the volume of liquid of the right pleural space 1 h after injecting into it 2 ml of Ringer solution or of Ringer with an inhibitor of a Na(+)-Cl- coupled transport or of the Na+/K+ pump. Volume collected after Ringer was 1.56 +/- 0.08 ml. Initial volume being 2.2 ml, net absorption rate was 0.64 ml/h. Volume collected after disulfonic stilbene (0.1 mM) or bumetanide (0.1 mM) was 2.01 +/- 0.06 and 2.01 +/- 0.05 ml, respectively; net absorption rate was reduced to 0.19 ml/h. This suggests the occurrence of Na(+)-Cl- coupled transports. Volume collected after ouabain (0.5 mM) was 2.08 +/- 0.08 ml; net absorption rate was reduced to 0.12 ml/h. This suggests the occurrence of the Na+/K+ pump. The marked reduction in the hydrothorax absorption produced by the inhibitors shows the occurrence of a solute-coupled liquid absorption from the pleural space. Liquid absorbed through the visceral pleura by the solute-coupled transport should be removed by the Starling forces of pulmonary capillaries. Solute-coupled absorption of liquid through the parietal pleura should oppose the filtration caused by the Starling forces.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1989

Pleural liquid pressure in the zone of apposition and in the lung zone.

Pleural liquid pressure in zone of apposition (Pliq,ap) and in lung zone (Pliq,L) was measured simultaneously through liquid filled cannulas in anesthetized dogs in lateral posture. At top Pliq,ap and Pliq,L at iso-height were -9.7 +/- 0.4 and -11.9 +/- 0.3 cm H2O, respectively, at end expiration (eE; P of delta less than 0.01; 11 dogs); -9.6 +/- 0.7 and -19.8 +/- 0.7 cm H2O at end inspiration (eI). At bottom they were -0.6 +/- 0.2 and -2.4 +/- 0.4 cm H2O, respectively, at eE (P of delta less than 0.05; 4 dogs); -1.5 +/- 0.3 and -8.5 +/- 1.0 cm H2O at eI. Vertical gradient of Pliq,ap was -0.97 +/- 0.02 cm H2O/cm. A 132% increase in ventilation (after 10 min dead space breathing) did not change eE and eI Pliq,ap, and eE Pliq,L, but decreased eI Pliq,L. These results imply: (1) no transmission to zone of apposition of tidal changes in Pliq,L; (2) a liquid flow from zone of apposition to lung zone; (3) a net filtration into zone of apposition. They suggest that absorption pressure of capillaries of visceral pleura is greater than that of lymphatics of zone of apposition. Lymphatic role in setting Pliq,L is discussed.

Animals↗
PubMed1989

Pleural pressure from abdominal to pulmonary rib cage: sweep of the lung border.

Pleural pressure was measured by a capsule placed in the superior part of right 8th or 9th intercostal space of dogs in left lateral posture. Transit of lung border was observed through endothoracic fascia at sides of the capsule. During inspiration the capsule membrane faced sequentially: diaphragm, lung border, lung; vice versa during expiration. Pressure on the diaphragm at end expiration was -5.3 +/- 0.5 cm H2O, reflecting outward recoil of the rib cage. At transit of lung border during inspiration (bor. I) a marked negative pressure spike occurred; a smaller spike occurred at expiratory transit (bor. E). These spikes should reflect pleural liquid pressure at lung border. At bor. I lung volume and radial displacement of rib 9 or 10 were greater during active than passive ventilation, whereas at bor. E they were similar under both conditions. Hence, during spontaneous inspiration displacement of lung border lags behind lung and rib expansion. Speed of lung border (assessed from duration of negative spike) ranged from 0.8 to 2.3 cm/sec during spontaneous breathing. On average it was similar at bor. I and bor. E, while air flow was greater at bor. I.

Animals↗
PubMed1989

Pleural liquid pressure at the caudal border of the lung.

Model simulation indicates that pressure recorded through a capsule, when lung border is under it, is essentially equal to pressure of pleural liquid (Pliq) surrounding lung border, though only a strip of capsule membrane is exposed to this liquid (the rest is facing diaphragm and lung). At the top of the right 8th or 9th intercostal space of dogs in left lateral posture Pliq recorded through a capsule at transit of lung border during inspiration (bor. I) or expiration (bor. E) was -19.7 +/- 1.1 and -11.2 +/- 0.3 cm H2O, respectively. Pliq recorded simultaneously through a cannula on the flat surface of lung in 5th or 6th intercostal space (corrected for 1 cm lower height) was -18.7 +/- 1.4 and -12.4 +/- 0.8 cm H2O. Similar values of Pliq on lung border and on flat surface of lung, despite different kinds of deformation and different measuring devices, provide further evidence that Pliq is more subatmospheric than pleural surface pressure. Seventy percent of difference in Pliq between bor. I and bor. E was accounted for by: (a) corresponding difference in pleural surface pressure, and (b) greater tidal change of liquid than surface pressure. Possible factors accounting for the remaining 30% are discussed.

Animals↗
PubMed1989

Lung border sweep upon phrenic stimulation: dynamic fall in pleural liquid pressure.

Pleural pressure was measured by a capsule in 9th or 10th intercostal space (ics) of dogs during tetanic stimulation of phrenic nerves (PS). When lung border passed under capsule (bor.I) a marked negative spike occurred, reflecting pleural liquid pressure (Pliq). In 9th ics spike was briefer than during spontaneous breathing (SB), speed of lung border being 4.6 times greater. During PS spike was greater and longer in 10th than in 9th ics, lung volume at bor.I being 228 ml greater. Lung volume at bor.I was smaller during PS than passive inflation because of chest wall deformation. Dynamic fall in Pliq at bor.I has been estimated about 4 cm H2O during SB, and at least 12 and 16 cm H2O (in 9th and 10th ics, respectively) during PS. Dynamic fall in Pliq seems essentially a viscous loss: it increased with thinning of pleural liquid (increase in lung volume), and with speed and displacement of lung border. Results suggest that at ordinary lung volume viscous loss of pleural liquid in this region is about 2 cm H2O per cm displacement at a speed of 1 cm/sec.

Animals↗
PubMed1988

Pleural pressure between diaphragm and rib cage during inspiratory muscle activity.

We measured the changes in pleural surface pressure (delta Ppl) in the area of apposition of the rib cage to the diaphragm (Aap) in anesthetized dogs during spontaneous breathing, inspiratory efforts after airway occlusion at functional residual capacity, and phrenic stimulation. Intact dogs were in supine or lateral posture; partially eviscerated dogs were in lateral posture. delta Ppl,ap often differed significantly from changes in abdominal pressure (delta Pab); sometimes they differed in sign (except during phrenic stimulation). Changes in transdiaphragmatic pressure in Aap (delta Pdi,ap) could be positive or negative and were less in eviscerated than in intact dogs. delta Pdi,ap could differ in sign among respiratory maneuvers and over different parts of Aap. Hence average delta Pdi,ap should be closer to zero than delta Pdi,ap at a given site. Since delta Ppl,ap = delta Prc,ap, where Prc,ap represents rib cage pressure in Aap, delta Pdi,ap = delta Pab - delta Prc,ap. Hence, considering that delta Pab and delta Prc depend on different factors, delta Pdi,ap may differ from zero. This pressure difference seems related to the interaction between two semisolid structures (contracted diaphragm and rib cage in Aap) constrained to the same shape and position.

Animals↗
PubMed1988

Transdiaphragmatic pressure and rib motion in area of apposition during paralysis.

Changes in pleural surface pressure in area of apposition of diaphragm to rib cage (delta Ppl,ap), changes in abdominal pressure (delta Pab), and redial displacement of the 11th rib have been recorded in anesthetized, paralyzed dogs during lung inflation or deflation. Above functional residual capacity (FRC) changes in transdiaphragmatic pressure in area of apposition (delta Pdi,ap) were essentially nil in intact (INT) dogs either in lateral or supine posture, and in partially eviscerated (EVS) dogs in lateral posture, either in the 10th or 11th intercostal space. Below FRC delta Pdi,ap could be positive (INT lateral and EVS), nil (EVS), or negative (INT supine and EVS); it could be different in the 10th and 11th intercostal spaces. Hence, with stretched (like with contracted) diaphragm, delta Ppl,ap measured at one site often differs from delta Pab and is not representative of average pressure acting on area of apposition. With volume increase above FRC, the 11th rib moved slightly in and then out in EVS and linearly out in INT. With volume decrease below FRC it moved out progressively in EVS, and it moved in and eventually reversed in INT. In paralyzed dogs in lateral posture the factor having the greatest influence on displacement of the abdominal rib cage is Pab. Mechanical linkage with pulmonary rib cage becomes relevant at large volume, whereas insertional traction of diaphragm becomes relevant at low volume.

Animals↗
PubMed1987

Effects of stretch receptors of bronchi or trachea on genioglossus muscle activity.

Activity of genioglossus muscle (GG) was recorded in anesthetized rabbits at control and under SO2 block of slowly adapting stretch receptors in thoracic airways (T) or in bronchi alone (B). At control peak activity occurred at 10% of inspiratory time, followed by a slight and a marked decrease. T and, particularly, B delayed onset and slowed rise of GG activity; then, this increased slightly under T and more under B, becoming greater than at control. During inspiratory efforts at end-expiratory volume GG activity at control was equal to that during open inspirations up to its peak, then progressively greater; during inspiratory efforts GG activity under T and B was equally smaller than at control. These findings indicate that bronchial input facilitates GG activity at end-expiratory volume and inhibits it at larger volumes: these effects are greater than those previously detected on diaphragm. Moreover, tracheal input inhibits onset and development of GG activity. Under all conditions end of inspiratory activity was simultaneous in GG and in diaphragm. Time to peak inspiratory flow correlated with time to early peak in GG activity.

Adaptation, Physiological↗
PubMed1987

Postinspiratory-ramp activity of diaphragm under inspiratory resistive load.

Inspiratory ramp activity, postramp activity (PRA) of diaphragm and respiratory flow were studied in anesthetized rabbits and conscious humans under inspiratory resistive load. Under load with chloralose-urethane anesthesia neural inspiration lasted 124 +/- 12 msec more than under control conditions and end of mechanical inspiration lagged behind that of neural inspiration by 114 +/- 4 msec. With pentobarbital-urethane anesthesia corresponding changes under load were 67 +/- 18 msec and 44 +/- 6 msec; after SO2 block of slowly adapting stretch receptors in bronchi corresponding changes under load were nil and 65 +/- 7 msec. In humans corresponding changes under load were about 192 and 127 msec. Both in rabbits and humans time course of PRA under load was essentially unchanged. Hence, under load a considerable part of PRA (or all of it under pentobarbital-urethane anesthesia without SO2 block) occurred during inspiration and that occurring during expiration was smaller than under control conditions. Consequently, under load braking of expiratory flow was smaller and peak expiratory flow occurred earlier than under control conditions.

Adult↗
PubMed1986

Discontinuity between inspiratory and postinspiratory diaphragm activity in man and rabbit.

Diaphragm activity (Edi, 20 Hz low cutoff) was recorded with great time resolution to ascertain whether there is a discontinuity between its inspiratory and postinspiratory periods in humans. We first determined in anesthetized rabbits that gaps or notches in Edi occurred within 80 msec before and after the end of mechanical inspiration in 70% of the analysable breaths in the esophageal lead and in 77% in direct leads. We then determined from the esophageal lead of 4 conscious subjects that gaps or notches in Edi occurred during the above-defined period in 45% of 682 analysable breaths. In each subject mean of moving average Edi (12 msec averaging interval) was computed out of 14-24 breaths, free of ECG artifacts within 200-250 msec before and after end inspiration. A deep indentation occurred near end-inspiration despite the lack of gaps or notches in 1/2 to 4/5 of these breaths. These results suggest that also in humans postinspiratory diaphragm activity does not represent the decay of inspiratory ramp.

Adult↗
PubMed1985

Breathing pattern and diaphragm EMG after SO2 in rabbit intra- or extrathoracic airways.

In anesthetized rabbits under SO2 block of slowly adapting stretch receptors (SAR) in intrathoracic airways TI increased by 49.7 +/- 6.9% and VT by 19.5 +/- 3.7%. TE decreased for small increases of TI and vice versa. Slope of moving average of diaphragm EMG (M.A.) decreased by 16.7 +/- 4.1% from 0 to 30% TI control, and increased by 26.3 +/- 8.1% from 30 to 70%. Considering that discharge from intrathoracic SAR increases during inspiration, these changes of M.A. indicate that their input facilitates inspiration at its beginning, but inhibits it later on, in line with previous conclusions based on SAR block which included 2/3 of extrathoracic trachea (ETT). Neither SO2 nor pressures from -40 to +40 cm H2O in ETT changed breathing pattern or M.A.. Hence, SAR of ETT do not affect parameters studied in rabbits. When extrathoracic airways were exposed to SO2 TI increased by 30.5 +/- 8.2%, TE by 37.9 +/- 5.1%, VT did not change. Hence, some receptors rostral to trachea, involved in respiratory control, are affected by SO2.

Animals↗
PubMed1985

Reflex partitioning of inputs from stretch receptors of bronchi and thoracic trachea.

A selective block of slowly adapting stretch receptors in anesthetized rabbits was induced by exposing to SO2 all thoracic airways (T) or the carina and bronchi alone (B). Increment of inspiratory time (TI) relative to control was 61% greater under B than T. The reverse would have happened if input responsible for Breuer-Hering inflation reflex originated from both bronchi and trachea. Hence, bronchial input activates inspiratory off-switch, while tracheal input delays its activation. During single inspiratory efforts with airways closed at end expiration diaphragm activity (Adi) decreased and TI0 increased relative to control equally under B and T. Hence, the input facilitating central inspiratory activity at end expiratory volume does not stem from trachea. At end of inspiratory ramp Adi stopped within 43 msec at control and 57 msec under B and T. Hence, bronchial input speeds up off-switching of inspiration. Postinspiratory Adi was greater under B than T, and nearly nil at control. Hence, bronchial input inhibits postinspiratory Adi, while tracheal input facilitates it. Inspiratory and expiratory flows were more damped under B than T, and under T than at control.

Animals↗
PubMed1985

Sulphur dioxide block of laryngeal receptors in rabbits.

In 6 rabbits moving average of activity of superior laryngeal nerve(SLN) increased when pressure in upper airways (Pua) was positive and decreased when it was negative. After SO2 exposure of upper airways SLN activity at Pua = 0 decreased to 40% and was no longer affected by changes in Pua. Activity of 67 fibers of SLN was recorded in 11 rabbits: 35 came from 'pressure' receptors, 27 from 'drive', and 5 from 'flow'. Thirty-three pressure receptors discharged at Pua = 0: 32 increased their firing rate with positive Pua and decreased it with negative Pua, one did the reverse. One pressure receptor silent at Pua = 0 fired with positive Pua, the other with negative Pua. Pressure receptors were slowly adapting. SO2 blocked within 3-9 min 84% of pressure receptors, 56% of drive receptors, and 4 out of 5 flow receptors. The receptors recovered control activity within 5-10 min after SO2 removal. SO2 block of laryngeal receptors may represent a convenient experimental tool for studies of laryngeal reflexes.

Animals↗
PubMed1985

Reflex effects on breathing of laryngeal denervation, negative pressure and SO2 in upper airways.

Respiratory reflex effects of laryngeal denervation, negative pressure and SO2 in upper airways were studied in anesthetized rabbits. Inspiratory efforts with nasal occlusion had longer duration (TIo) and smaller diaphragm activity (Adi) than with tracheal occlusion. After section of superior laryngeal nerves (SLN) these differences disappeared: values with tracheal occlusion became similar to those with nasal occlusion before denervation. This suggests that laryngeal pressure receptors, firing at zero pressure and decreasing their discharge with negative pressures, increase central inspiratory activity. After SO2 TIo, both with tracheal and nasal occlusion, increased even after laryngeal denervation, provided SO2 flowed through nasal pathway. Hence, nose and/or rhinopharynx contain receptors affected by SO2. After laryngeal denervation and SO2 TIo was shorter with nasal than with tracheal occlusion, despite equal Adi. This, combined with the above findings, suggests two groups of pressure receptors in nose and/or rhinopharynx with opposite effects on inspiratory off-switch: one unaffected and the other probably blocked by SO2. During nose breathing section of SLN produced only a slight decrease in mean inspiratory flow.

Animals↗