Non-linear dependence of interstitial fluid pressure on joint cavity pressure and implications for interstitial resistance in rabbit knee

AIMS: Synovium retains lubricating fluid in the joint cavity. Synovial outflow resistance estimated as dPj/dQs (Pj, joint fluid pressure and Qs trans-synovial flow) is greater, however, than expected from interstitial glycosaminoglycan concentration. This study investigates whether subsynovial fluid pressure increases with intra-articular pressure, as this would reduce the estimated resistance estimate. METHODS: Interstitial fluid pressure (Pif) was measured as a function of distance from the joint cavity in knees of anaesthetized rabbits, using servo-null pressure-measuring micropipettes and using an external 'window'. Joint fluid pressure Pj was either endogenous (-2.4 +/- 0.4 cmH2O, mean +/- SEM) or held at approximately 4, 8 or 15.0 cmH2O by a continuous intra-articular saline infusion that matched the trans-synovial interstitial drainage rate. RESULTS: At endogenous Pj the peri-articular Pif was subatmospheric (-1.9 +/- 0.3 cmH2O, n = 19). At raised Pj the Pif values became positive. Gradient dPif /dx was approximately 20 times steeper across synovium than subsynovium. Pif close to the synovium-subsynovium border (Pif*) increased as a non-linear function of Pj to 1.4 +/- 0.2 cmH2O (n = 23) at Pj = 4.3 +/- 0.1 cmH2O : 2.3 +/- 0.2 cmH2O (n = 17) at Pj = 7.6 +/- 0.2 cmH2O: and 3.0 +/- 0.4 cmH2O (n = 26) at Pj = 15 +/- 0.2 cmH2O (P = 0.03, anova). CONCLUSIONS: Synovial resistivity is approximately 20x subsynovial resistivity. The increase in Pif*with Pj means that true synovial resistance d(Pj-Pif*)/dQs is overestimated 1.5x by dPj/dQs. This narrows but does not eliminate the gap between analysed glycosaminoglycan concentration, 4 mg ml(-1), and the net interstitial biopolymer concentration of 11.5 mg ml(-1) needed to generate the resistance.     

Comparison of microvascular filtration in human arms with and without postmastectomy oedema

Oedema is caused by impaired lymphatic drainage and/or increased microvascular filtration. To assess a postulated role for the latter in postmastectomy oedema, filtration was studied in the forearms of 14 healthy subjects and 22 patients with chronic, unilateral arm oedema caused by surgical and radiological treatment for breast cancer. A new non-contact optical device (the Perometer) and a conventional mercury strain gauge were used simultaneously to record forearm swelling rates caused by microvascular filtration during applied venous congestion. Filtration rate (FR) per 100 ml tissue was measured over 10-15 min at a venous pressure of 30 cmH2O, a pressure reached in the dependent forearm (FR30), and then at 60 cmH2O (FR60). Apparent filtration capacity of 100 ml soft tissue (CFCa) was calculated from FR60 - FR30/30, after adjustment for bone volume. The Perometer and strain gauge gave similar results in normal and oedematous arms. Mean CFCa in healthy subjects was (3.8+/-0.4) x 10(-3) ml (100 ml)-1 cmH2O-1 min-1, close to literature values. In the patients, FR30 was 47 % lower in the oedematous forearm than in the opposite, unaffected forearm (P = 0.04). FR60 showed a similar trend but did not reach significance (P = 0.15). The values of CFCa of (2.2+/-0.5) x 10(-3) ml (100 ml)-1 cmH2O-1 min-1 in the oedematous arm and (2.8+/-0.5) x 10(-3) ml (100 ml)-1 cmH2O-1 min-1 in the unaffected arm were not significantly different (P = 0.47). When differences in arm volume on the two sides were taken into account, the total fluid load on the lymphatic system of the oedematous forearm was (411.0+/-82.2) x 10(-3) ml min-1 at 30 cmH2O and (1168+/-235.6) x 10(-3) ml min-1 at 60 cmH2O, similar to the normal side, namely (503.7+/-109.3) 10(-3) ml min-1 and (1063+/-152.0) x 10(-3) ml min-1, respectively (P >/= 0.50). The filtration capacity of the entire oedematous forearm (CFCa scaled up by total soft tissue volume), (25.4+/-6.2) x 10(-3) ml cmH2O-1 min-1, was not significantly greater than that of the normal forearm, (18.3+/-2.6) x 10(-3) ml cmH2O-1 min-1 (P = 0.40). The results indicate that no major change occurs in the microvascular hydraulic permeability-area product of the forearm, or in the total filtration load on the lymph drainage system during dependency, in the arm with postmastectomy oedema compared with the normal arm. This argues against a significant haemodynamic contribution to postmastectomy oedema.     

A two-dimensional morphometry-based model of interstitial and transcapillary flow in rabbit synovium.

The synovial lining of a joint is a layer of specialized connective tissue, containing fenestrated capillaries, that regulates the volume and composition of fluid in the joint cavity. The hydraulic conductance of the synovial lining and of the plasma-to-cavity pathway is increased by high intra-articular pressures (IAP greater than 9 cmH2O) and this is accompanied by an increase in the interstitial pathway's area/pathlength ratio. In order to assess the contribution of the altered pathway geometry to the conductance changes, and also to evaluate the conductivity of the synovial interstitial matrix (Ki) and local flow patterns, a two-dimensional model of trans-synovial flow was developed from morphometric data at low IAP (5 cmH2O) and high IAP (25 cmH2O). Darcy's law was applied to finite elements within a 'unit cell' of synovium to compute a steady-state pressure field. Elements adjacent to limited discrete porous regions of the capillary wall were additionally subjected to the Starling principle. Appropriate values of Ki and capillary wall conductance were obtained by iteration to match the experimentally measured net conductances. The value of Ki that matched the data at low IAP was 1.4-2.1 x 10(-12) cm4 s-1 dyn-1 (1.4-2.1 x 10(-15) m4 s-1 N-1). This is in the range reported for some other fluid-confining tissues, namely scleral stroma and aortic wall. Comparison between a capillary model with localized porous regions and one with a uniformly distributed permeability showed that the uniformity assumption (commonly used in mathematical modelling) leads to severe underestimation of the local pericapillary pressure gradients. At high IAP, synovial deformation was found to account for 24-50% of the increased hydraulic conductances. To explain the remainder, it was necessary to postulate a rise in Ki, especially in the zone between the joint cavity and capillary wall. Possible mechanisms involving tissue hydration and/or glycosaminoglycan wash-out at high IAP are discussed. The model highlights a need for quantitative biochemical analysis.     

Pulmonary vascular pressure profile in adult ferrets: measurements in vivo and in isolated lungs

We have determined the vascular pressure profile in lungs of adult ferrets utilizing an anaesthetized open chested preparation and have compared the pressure profile in vivo with that in isolated, perfused lungs. Ten adult ferrets, mean body weight 980 +/- 108 g, were studied. For in vivo measurements, five ferrets were anaesthetized, mechanically ventilated and the left chest wall resected. Pressures were measured in the pulmonary artery, left atrium and by micropuncture, in 20-50 microns diameter subpleural arterioles and venules. During micropuncture, ventilation was stopped for 1-2 min and the lungs kept distended at an airway pressure of 6 cmH2O. Left atrial pressure was raised to approximately 8 cmH2O with saline infusion so that lungs were in Zone 3. Cardiac output was measured by thermodilution. Lungs of five other ferrets were isolated and perfused with a steady flow roller pump. In these lungs blood flow was adjusted so that pulmonary artery pressure was similar to that in anaesthetized ferrets, with airway and left atrial pressures at 6 and 8 cmH2O respectively (Zone 3). Blood haematocrit (35 +/- 7%) was similar in the two groups. In lungs of anaesthetized ferrets total arteriovenous pressure drop was 12.1 +/- 1.9 cmH2O, with cardiac output being 210 +/- 80 ml kg body weight-1 min-1. Fractional resistance in arteries was 37%, 37% in microvessels and 26% in veins. In isolated ferret lungs, though blood flow was only 48 +/- 10 ml kg body wt-1 min-1 for the same total arteriovenous pressure drop as in vivo, the longitudinal distribution of vascular resistance was similar to that in live ferrets.(ABSTRACT TRUNCATED AT 250 WORDS)     

Optimization of the artificial urinary sphincter: modelling and experimental validation

The artificial urinary sphincter should be long enough to prevent strangulation effects of the urethral tissue and short enough to avoid the improper dissection of the surrounding tissue. To optimize the sphincter length, the empirical three-parameter urethra compression model is proposed based on the mechanical properties of the urethra: wall pressure, tissue response rim force and sphincter periphery length. In vitro studies using explanted animal or human urethras and different artificial sphincters demonstrate its applicability. The pressure of the sphincter to close the urethra is shown to be a linear function of the bladder pressure. The force to close the urethra depends on the sphincter length linearly. Human urethras display the same dependences as the urethras of pig, dog, sheep and calf. Quantitatively, however, sow urethras resemble best the human ones. For the human urethras, the mean wall pressure corresponds to (-12.6 +/- 0.9) cmH2O and (-8.7 +/- 1.1) cmH2O, the rim length to (3.0 +/- 0.3) mm and (5.1 +/- 0.3) mm and the rim force to (60 +/- 20) mN and (100 +/- 20) mN for urethra opening and closing, respectively. Assuming an intravesical pressure of 40 cmH2O, and an external pressure on the urethra of 60 cmH2O, the model leads to the optimized sphincter length of (17.3 +/- 3.8) mm.     

Mucopolysaccharide osmotic pressure in the measurement of interstitial pressure.

Subatmospheric pressures were recorded from cotton wicks inserted into Wharton's jelly of human umbilical cords (mean=-7.6+/-5.0 (SD) cmH2O; n=10). Hyaluronate concentrations (mean=0.69+/-0.30 g/100 g) and wick pressures correlated negatively (r=-0.825; P less than 0.01) but calculated hyaluronate osmotic pressures (mean=4.0+/-2.7 cmH2O) were insufficient to explain the full wick pressure. In model systems composed of asbestos fibers (mean radius=0.5 micron) and 0.9% saline, subatmospheric pressures were recorded which varied with the volume of saline added. When hyaluronate (1 g/100 g) was substituted for saline, lower wick pressures were recorded at each volume. The pressure lowering effect of hyaluronate was not seen in a matrix of glass fibers (mean radius=1.0 micron). It is suggested that the effect of hyaluronate in asbestos fibers is due to its immobilization by the matrix and the consequent development of osmotic pressure recorded via the wick. In the coarser glass-fiber matrix, hyaluronate was not immobilized and therefore had no osmotic effect. These experiments support the hypothesis that subatmospheric interstitial pressures result from osmotic pressure of immobilized mucopolysaccharide macromolecules.     

The contribution of the pulmonary microvascular pressure in the maintenance of an open lung during mechanical ventilation

Changes in pulmonary hemodynamics modify the mechanical properties of the lungs. The effects of alterations in pulmonary capillary pressure (Pc) were investigated on the airway and lung tissue mechanics during positive-pressure ventilation and following lung recruitment maneuvers. Isolated, mechanically normoventilated (PEEP 2.5 cmH(2)O) rat lungs were perfused with Pc set to 0 (unperfused), 5, 10 or 15 mmHg, in random sequence. The pulmonary input impedance (ZL) was measured at end-expiration before and after a 10-min long ventilation. After inflation of the lung to 30 cmH(2)O during P-V curve recordings, another set of ZL was measured to evaluate the degree of recruitment. The PEEP was then decreased to 0.5 cmH(2)O and the sequence was repeated. Airway resistance and parenchymal damping and elastance (H) were estimated from ZL by model fitting. From the P-V curves, elastance (E) and hysteresis indices were determined. Mechanical ventilation at both PEEP levels resulted primarily in elevations in the tissue parameters, with the greatest increases at the 0 Pc level (H changes of 27.8+/-4.2 and 61.3+/-3.7% at 2.5 and 0.5 cmH(2)O PEEP, respectively). The maintenance of physiological Pc (10 mmHg) led to a significantly lower elevation in H (11.6+/-1.5% versus 31.4+/-3.6%). The changes in the oscillatory mechanics were also reflected in E and the hysteresis of the P-V curves. These findings indicate that pulmonary hypoperfusion during mechanical ventilation forecasts a parenchymal mechanical deterioration. Physiological pressure in the pulmonary capillaries is therefore an important mechanical factor promoting maintenance of the stability of the alveolar architecture during positive-pressure mechanical ventilation.     

Effects of hydrogen peroxide on the guinea-pig tracheobronchial mucosa in vivo.

Lumenal entry of plasma (mucosal exudation) is a key feature of airway inflammation. In airways challenged with histamine-type mediators and allergen the mucosal exudation response occurs without causing epithelial derangement and without increased airway absorption. In contrast, reactive oxygen metabolites may cause mucosal damage. In this study, involving guinea-pig airways, we have examined effects of H2O2 on airway exudation and absorption in vivo. Vehicle or H2O2 (0.1 and 0.5 M) was superfused onto the tracheobronchial mucosal surface through an oro-tracheal catheter. 125I-albumin, given intravenously, was determined in tracheobronchial tissue and in lavage fluids 10 min after challenge as an index of mucosal exudation of plasma. The tracheobronchial mucosa was also examined by scanning electron microscopy. In separate animals, 99mTc-DTPA was superfused 20 min after vehicle or H2O2 (0.1 and 0.5 M) had been given. A gamma camera determined the disappearance rate of 99mTc-DTPA from the airways as an index of airway absorption. The high dose of H2O2 (0.5 M) produced epithelial damage, increased the absorption of 99mTc-DTPA (P < 0.001), and increased the exudation of plasma (P < 0.001). Notably, it appeared that all extravasated plasma had entered the airway lumen within 10 min. These data demonstrate that H2O2 differs from exudative autacoids such as histamine by causing both epithelial damage and plasma exudation responses. These data also agree with the view that the epithelial lining determines the rate of absorption and is responsible for the valve-like function that allows lumenal entry of extravasated bulk plasma without any increased inward perviousness.     

Applied pressures and net water flux across in vitro frog gastric mucosa.

The effects of hydrostatic pressure differences up to 0.4 atm/413 cmH2O were studied on frog gastric mucosa in vitro. Net water flux, transmucosal electrical potential difference, and acid secretion were measured. A significant correlation between hydrostatistic pressure difference and net water flow (r=0.77) was obtained. The intercept of the regression line, at zero hydrostatic pressure difference, is 9.3 +/- 0.5 microliter/cm2.h, and the slope 42.9 +/- 3.2 microliter/cm2.atm.h. No significant correlation was obtained between the hydrostatic pressure difference and the transmucosal potential difference (P greater than 0.20), the acid secretion (P greater than 0.20), or the nonacidic chloride transport, measured as short-circuit current (P greater than 0.20). Hydrostatic water flux is compared to osmotically induced flux previously reported. It is proposed that the difference between hydrostatic and osmotic induced water fluxes is due to the area of cells exposed to the pressures. Only part of surface cells are directly exposed to the osmotic pressure due to the presence of restricted extracellular compartments.     

Reevaluation of the needle method for measuring interstitial fluid pressure.

Inserting a needle into subcutaneous spaces should allow a subatmospheric pressure to be measured if interstitial fluid pressure is truly negative as measured by the capsule and wick techniques. Previous needle measurements of interstitial fluid pressure have produced a positive value, but in most instances fluid has been injected into the tissues prior to recording of pressure. Therefore, we measured subcutaneous needle pressure in anesthetized dogs without fluid injection into the tissues. Approximately 30 min are required for an equilibrium pressure after insertion of the needle. The mean 30-min pressure was 4.6 +/- 0.5 (SE) mmHg (n equals 41). With observable edema, interstitial fluid pressures as measured with the needle were always positive. However, the needle method for continuous recording of pressure lacks rapid sensitivity to changes in tissue fluid pressures. In order to develop a needle method that would follow changes in interstitial fluid pressure, 0.5-1 mul of saline was injected into or withdrawn from the tissue. With this method, pressure plateaued in 10-20 min. This plateau pressure increased with tissue hydration and decreased with dehydration.     

Interstitial pressure gradients around joints; location of chief resistance to fluid drainage from the rabbit knee

The hypothesis has been advanced that synovium offers the main resistance to fluid escape from joints, even though it is under 20 microm thick. To test this, fluid was infused into the knee joint cavity of anaesthetised rabbits to set up a pressure gradient, then the profile of periarticular interstitial fluid pressure (P(if)) was measured by advancing a micropipette, connected to a servo-null pressure recorder, in steps through a periarticular tissue 'window' until the joint cavity was entered. With intra-articular pressure (P(j)) raised to 15 cmH(2)O (the pressure of an acute joint effusion) the pressure gradient dP(if) /dx (where x is distance) across the synovial lining was 0.47 +/- 0.04 cmH(2)O microm(-1) (n = 10 joints). This was 23.5-fold greater than the gradient in the subsynovium (0.02 +/- 0.01 cmH(2)O microm(-1); P < 0.0001, Student's t test), indicating that the hydraulic resistivity of the subsynovium is 4 % of that of the synovium. The pressure profile was not altered by circulatory arrest. To test the hypothesis further, the effect of a stab perforation of the synovial lining on fluid drainage rate ((.Q(s)) was studied. Perforation raised both.Q(s) and the conductance term d.Q(s)/dP(j) more than 10-fold (n = 6 joints; P < 0.0001, ANOVA). The results thus support the view that, despite its thinness, the synovial lining offers the main hydraulic resistance to fluid drainage from a synovial joint.     

PEEP-induced changes in epithelial permeability in inbred mouse strains

Inbred mouse strains have demonstrated a range of susceptibilities to inhaled environmental irritants. C57Bl/6J mice are highly susceptible while C3H/HeJ mice are resistant to ozone exposures, as assessed by lavaged protein. However, lavaged protein reflects a loss of both the endothelial and epithelial barrier. To determine whether basal differences exist in the epithelial barrier, we measured soluble tracer ((99m)technetium-diethylenetriamine pentaacetic acid, (99m)Tc-DTPA) clearance from the lung in spontaneously breathing, anesthetized mice and mice ventilated with increased lung volume with applied positive end-expiratory pressure (PEEP; 1, 6, or 10cmH(2)O). Both strains showed more rapid clearance during ventilation with 10cmH(2)O PEEP compared with other ventilation pressures (p<0.001). There was a substantial difference in clearance between the two strains during ventilation with 10cmH(2)O PEEP (mean half time for C57Bl/6J mice=19+/-4min versus 34+/-3min for C3H/HeJ mice; p<0.001). Thus, when lung volume is increased, the susceptible C57Bl/6J strain shows a greater change in epithelial barrier than the resistant C3H/HeJ strain. These results may reflect fundamental differences in lung architecture.     

A practical protocol for titrating "optimal" PEEP in acute lung injury: recruitment maneuver and PEEP decrement

This study was conducted to evaluate the effectiveness and safety of a practical protocol for titrating positive end-expiratory pressure (PEEP) involving recruitment maneuver (RM) and decremental PEEP. Seventeen consecutive patients with acute lung injury who underwent PEEP titration were included in the analysis. After baseline ventilation, RM (continuous positive airway pressure, 35 cm H2O for 45 sec) was performed and PEEP was increased to 20 cmH2O or the highest PEEP guaranteeing the minimal tidal volume of 5 mL/kg. Then PEEP was decreased every 20 min in 2 cmH2O decrements. The "optimal" PEEP was defined as the lowest PEEP attainable without causing a significant drop (>10%) in PaO2. The "optimal PEEP" was 14.5 +/- 3.8 cmH2O. PaO2 /FI O2 ratio was 154.8 +/- 63.3 mmHg at baseline and improved to 290.0 +/- 96.4 mmHg at highest PEEP and 302.7 +/- 94.2 mmHg at "optimal PEEP", both significantly higher than baseline (p<0.05). Static compliance was significantly higher at "optimal" PEEP (27.2 +/- 10.4 mL/ cmH2O) compared to highest PEEP (22.3 +/- 7.7 mL/cmH2O) (p<0.05). Three patients experienced transient hypotension and one patient experienced atrial premature contractions. No patient had gross barotrauma. PEEP titration protocol involving RM and PEEP decrement was effective in improving oxygenation and was generally well-tolerated.     

Colonic absorption of bacterially synthesized vitamin K2 in the rat.

Colonic absorption of bacterially synthesized vitamin K2 ([3H]menaquinone-9) was studied with everted rat colonic sacs in vitro. The mean +/- SE rate of absorption of the vitamin by the colon was 20 +/- 1.45 pmol/min per 100 mg tissue at 300 nM mucosal concentration of the vitamin. The rate of absorption did not change (P greater than 0.10) with the addition of 2,4-dinitrophenol, Na azide, or KCN to the mucosal incubation medium. No evidence for transmural transport of the vitamin was detectable. When the concentration of the vitamin was increased in a stepwise fashion up to 900 nM, the absorption rate remained linear with respect to the mucosal fluid concentration (r = 0.98). Autoradiography indicated that the vitamin accumulated in the mucosal and submucosal layers of the large bowel. Absorption of the vitamin by the large bowel takes place via a passive, nonsaturable process that shows no evidence of energy dependence or carrier mediation. It was concluded that vitamin K2 (bacterial origin) is absorbable by the rat colon in amounts sufficient to meet the daily requirement of the animal and may explain the lack of bleeding problems in the face of episodic lack of dietary vitamin K.     

Tissue osmolality in intestinal villi during luminal perfusion with isotonic electrolyte solutions

A cryoscoptic technique has been developed that makes it possible to determine tissue osmolality in the core of the intestinal villi. During absorption from an isotonic electrolyte solution containing glucose an osmolality gradient was demonstrated from tip to base of the villi in both the jejunum and the ileum. The tissue osmolality at the villous tips was measured to 1 000-1 200 mOsm/kg H2O while the osmolality at the villous base was approximately isotonic with plasma. Increasing intestinal blood flow by i.a. administration of a vasodilator drug, or making the intestine ischemic by clamping the intestinal vascular supply while supplying the mucosa with oxygen, markedly decreased tissue osmolality. Substituting all sodium ions with choline in the luminal perfusate abolished almost completely the tissue hyperosmolality and the intestine became a secretory organ. These observations are consistent with the view that the observed villous tissue hyperosmolality was created by a countercurrent multiplication of sodium chloride. The physiological implications of this mechanism is discussed and it is, among other things, proposed that the hyperosmolar region represents the hyperosmotic compartment necessary for explaining intestinal water absorption.     

Mouth pressure twitches induced by cervical magnetic stimulation to assess inspiratory muscle fatigue

This study aimed at determining whether twitch mouth pressure (TwPmo) induced by cervical magnetic stimulation (CMS) was sensitive to inspiratory muscle fatigue produced by whole body exercise (WBE) in normal subjects. Twenty subjects performed one or two of the following protocols: (i). cycling at 85% V(O(2),max) until exhaustion; (ii). inspiratory resistive load (IRL) breathing at 62% of maximal inspiratory pressure until task failure. In eight subjects, oesophageal (TwPoes), gastric (TwPga) and transdiaphragmatic (TwPdi) pressures were recorded. The TwPmo was significantly reduced (P<0.05) 20 min after both WBE and IRL, from 17.5+/-4.4 to 15.9+/-3.9 cmH(2)O and from 19.4+/-4.9 to 17.7+/-4.5 cmH(2)O, respectively. Subsequently to IRL, the TwPdi decrease was associated with a reduction in TwPoes/TwPga ratio; not after WBE. Independently of the mode of ventilatory loading, inspiratory muscle fatigue was detected. Thus, inspiratory muscle fatigue after WBE can be assessed in normal subjects with a noninvasive technique.     

Constant mean airway pressure with different patterns of positive pressure breathing during the adult respiratory distress syndrome

Twenty-one ARDS patients were divided into two groups of severity according to FIO2 and PEEP required to maintain an adequate gas exchange. The 10 most severe patients (group A) underwent continuous positive pressure ventilation (CPPV) (I/E 3:1) with the mean airway pressure maintained at 21 +/- 6.2 cmH2O. The PEEP values were 12.6 +/- 4.3 cmH2O during CPPV and 6.5 +/- 3.7 cmH2O during IRV (p less than 0.01). Eleven less severe ARDS patients (group B) underwent CPPV and positive pressure spontaneous breathing (CPAP) at constant mean airway pressure of 14.3 +/- 3.8 cmH2O. The PEEP was 7 +/- 2.5 cmH2O during CPPV and 14.9 +/- 4.3 cmH2O during CPAP (p less than 0.001). In five patients of each group, the SF6 shunt was measured as representative of true shunt. The results showed that gas exchange, including true shunt, and haemodynamics did not change between CPPV and IRV and between CPPV and CPAP tests. Taken with previous work on mean airway pressure, our results further support the concept that the main determinant of oxygenation and haemodynamics is the mean airway pressure, irrespective of the PEEP level and of the mode of ventilation.     

Responses of bronchial C-fiber afferents of the rabbit to changes in lung compliance

Rapidly adapting receptors (RAR) in the lung are stimulated when the lung compliance is reduced. The present investigation was undertaken to determine whether bronchial C-fibers are also activated when lung compliance is decreased since both RAR and bronchial C-fibers are influenced by extra-vascular fluid in the airways. Action potentials (AP) were recorded from bronchial C, pulmonary C, RAR and slowly adapting receptor (SAR) afferents in the cervical vagus in open chest New Zealand White rabbits ventilated at a constant rate and tidal volume. AP were recorded during (a) positive end-expiratory pressure (PEEP) of 2-3 cmH2O (control), (b) zero end-expiratory pressure (ZEEP), (c) negative end-expiratory pressure (NEEP) of -4 cmH2O, (d) restoration of PEEP and (e) final control after hyper-inflation. Both RAR and bronchial C-fiber activity increased significantly compared with control when lung compliance was decreased (bronchial C-fibers: 35 +/- 5 vs. 66 +/- 13 impulses per 30 sec and RAR: 3 +/- 1 vs. 94 +/- 14 impulses per 30 sec).     

Evaluation of respiratory mechanics and lung histology in a model of atelectasis

To develop a reproducible model of atelectasis, 15 mechanically ventilated Wistar rats were wrapped around the thorax/abdomen with a sphygmomanometer. The cuff was inflated to transpulmonary pressures (PL) of -4 cmH2O (group A) and -8 cmH2O (group B) for 5 sec. Group C was not compressed. Airflow, volume, tracheal and oesophageal pressures were registered. Respiratory system (rs), lung (L), and chest wall resistive (DeltaP1), viscoelastic/inhomogeneous pressures (DeltaP2), DeltaPtot (=DeltaP1 + DeltaP2), static (Est) and dynamic (Edyn) elastances, and DeltaE (=Edyn - Est) were determined before and after compression. In A, respiratory mechanics remained unaltered. In B, Est,rs (+99%), Est,L (+111%), DeltaE,rs (+41%), DeltaE,L (+73%), DeltaP1,rs (+45%), DeltaP1,L (+44%), DeltaP2,rs (+41%), DeltaP2,L (+69%), DeltaPtot,rs (+40%), and DeltaPtot,L (+58%) increased after compression. Mean alveolar diameter and bronchiolar lumen decreased in A, and were even smaller in B. In conclusion, chest wall compression with PL of -8 cmH2O yielded a reproducible alveolar collapse, which resulted in increased elastic, resistive and viscoelastic/inhomogeneous pressures.     

Tissue osmolality in intestinal villi of four mammals in vivo and in vitro.

Using a freezing point depression method osmolality in the intestinal tissue of four mammals (gerbils, guinea-pigs, rabbits and rats) was estimated in vivo, during fluid transport from an isotonic electrolyte-glucose solution. Net fluid transport was also measured. In gerbils, guinea-pigs and rabbits tissue osmolality was also estimated during in vitro conditions. A marked hyperosmolality was observed in vivo in the upper parts of the villi of all four mammals studied. The tissue osmolality was significantly higher than that seen in the same species during in vitro conditions. A villus hyperosmolality was observed also in species which exhibited a net fluid secretion (guinea-pig, rabbit ileum), indicating that the fluid secretion emanated from the intestinal crypts. Based on the results of the present experiments and on observations made in earlier experiments performed on the cat, it is proposed that the villus hyperosmolality is created by a countercurrent multiplier present in the intestinal villus. The hyperosmolar compartment in the villus tissue creates the force that drives fluid from lumen to tissue.