Increased lung vascular permeability after arachidonic acid and hydrostatic challenge

Seeger, Werner; Walmrath, D.; Menger, Maximilian M.; Neuhof, H.

doi:10.1152/jappl.1986.61.5.1781

Cited by 69 publications

(41 citation statements)

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“…There was some predominance of the precapillary (Ra) over the postcapillary (Rv) vascular resistance, and the mean Kf,c value was 8.6±2.2 mL·s -1 ·cmH 2 O·g lung wet weight ×10 -5 . These data correspond to previous investigations in the perfused rabbit lung [19]. Baseline V '/Q ' measurements revealed unimodal, narrow distribution of perfusion and ventilation to midrange V'/Q' (0.1< V'/Q' <10) areas (table 2).…”

Section: Baseline Conditionssupporting

confidence: 91%

“…The perfused lung model has been described previously [19]. Briefly, rabbits of either sex weighing 2.5-3.1 kg were anaesthetized with intravenous pentobarbital (60-90 mg·kg -1 ) and anticoagulated with heparin (1,000 U·kg -1 ).…”

Section: Isolated Lung Modelmentioning

confidence: 99%

“…The change of vascular volume was measured indirectly as change in lung weight over time. The initial rapid change in weight over the first 2 min was used for calculation of the compliance [19,21].…”

Section: Gravimetric Estimation Of Capillary Filtration Coefficientmentioning

confidence: 99%

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Effects of inhaled versus intravenous vasodilators in experimental pulmonary hypertension

Walmrath

Schermuly²,

Pilch³

et al. 1997

Eur Respir J

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Inhaled nitric oxide (NO) causes selective pulmonary vasodilation and improves gas exchange in acute lung failure. In experimental pulmonary hypertension, we compared the influence of the aerosolized vasodilatory prostaglandins (PG) PGI 2 and PGE 1 on vascular tone and gas exchange to that of infused prostanoids (PGI 2 , PGE 1 ) and inhaled NO.An increase of pulmonary artery pressure (Ppa) from 8 to ~34 mmHg was provoked by continuous infusion of U-46619 (thromboxane A 2 (TxA 2 ) analogue) in blood-free perfused rabbit lungs. This was accompanied by formation of moderate lung oedema and severe ventilation-perfusion (V'/Q') mismatch, with predominance of shunt flow (>50%, assessed by the multiple inert gas elimination technique).When standardized to reduce the Ppa by ~10 mmHg, inhaled NO (200 ppm), aerosolized PGI 2 (4 ng·kg -1 ·min -1 ) and nebulized PGE 1 (8 ng·kg -1 ·min -1 ) all reduced both pre-and postcapillary vascular resistance, but did not affect formation of lung oedema. All inhalative agents improved the V '/Q ' mismatch and reduced shunt flow, the rank order of this capacity being NO > PGI 2 > PGE 1 . In contrast, lowering of Ppa by intravascular administration of PGI 2 and PGE 1 did not improve gas exchange. "Supratherapeutic" doses of inhaled vasodilators in control lungs (400 ppm NO, 30 ng·kg -1 ·min -1 of PGI 2 or PGE 1 ) did not provoke vascular leakage or affect the physiological V'/Q' matching.We conclude that aerosolization of prostaglandins I 2 and E 1 is as effective as inhalation of nitric oxide in relieving pulmonary hypertension. When administered via this route instead of being infused intravascularly, the prostanoids are capable of improving ventilation-perfusion matching, suggesting selective vasodilation in well-ventilated lung areas. Eur Respir J 1997; 10: 1084- Inhalation of nitric oxide (NO) has been shown to cause "selective" pulmonary vasodilation, in the absence of vasodilatory effects in the systemic circulation [1][2][3][4]. The different response of gas exchange to NO might be related to the underlying mechanism of ventilation perfusion (V '/Q ') imbalance. In patients with chronic obstructive pulmonary disease (COPD) with broad V '/Q ' heterogeneity, caused by low V '/Q ' ratios but negligible intrapulmonary shunt, NO may worsen gas exchange because of increased perfusion of poorly-ventilated areas [5]. By contrast, in patients with severe adult respiratory distress syndrome (ARDS), in whom shunt flow predominates, the pulmonary vasodilatory effect of inhaled NO was accompanied by an acute improvement of gas exchange [6][7][8]. Due to the transbronchial route, the vasodilatory property of this agent is apparently restricted to well-ventilated lung areas, effecting a redistribution of blood flow from nonventilated regions to these areas. This is considered a substantial progress compared to the intravenous use of vasodilators, such as prostaglandin (PG) I 2 and PGE 1 . These prostanoids provoke nonselective vasodilation both in pulmonary and systemic vessels, and w...

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Section: Baseline Conditionssupporting

confidence: 91%

Section: Isolated Lung Modelmentioning

confidence: 99%

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Effects of inhaled versus intravenous vasodilators in experimental pulmonary hypertension

Walmrath

Schermuly²,

Pilch³

et al. 1997

Eur Respir J

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“…The model has been described previously [17]. Briefly, rabbits of either sex (body weight (BW) 2.2-2.6 kg) were deeply anaesthetized and anticoagulated with heparin, 1,000 U·kg -1 BW.…”

Section: Isolated Lung Modelmentioning

confidence: 99%

“…The capillary filtration coefficient (Kfc, given in cm 3 ·s -1 ·mmHg -1 ·g -1 wet lung weight ×10 -4 ) and the total vascular compliance were determined gravimetrically from the slope induced by a 7.5 mmHg step elevation of the venous pressure for 8 min. The application of this method to the present model and the use of zero time extrapolation of the slope of weight gain for the calculation of Kfc have been described previously [17]. In lungs already displaying toxin-induced weight gain before onset of the hydrostatic challenge, the pressure step-induced rate of weight gain was corrected for this baseline rate of weight gain.…”

Section: Isolated Lung Modelmentioning

confidence: 99%

Differential role of actin in lung endothelial and epithelial barrier properties in perfused rabbit lungs

Ermert¹,

Rössig²,

Hansen³

et al. 1996

Eur Respir J

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D Di if ff fe er re en nt ti ia al l r ro ol le e o of f a ac ct ti in n i in n l lu un ng g e en nd do ot th he el li ia al l a an nd d e ep pi it th he el li ia al l b ba ar rr ri ie er r p pr ro op pe er rt ti ie es s i in n p pe er rf fu us se ed d r ra ab bb bi it t l lu un ng gs s L. Ermert* + , R. Rössig*, T. Hansen*, H. Schütte*, K. Aktories**, W. Seeger* ABSTRACT: Lung fluid balance is critically dependent on capillary endothelial and alveolar epithelial barrier properties, and cytoskeletal components have been implicated in these barrier functions. In an earlier study, we perfused Clostridium botulinum C 2 toxin, which effects selective loss of non-muscle F-actin, through isolated rabbit lungs: a severalfold increase in the capillary filtration coefficient (Kfc) was noted, together with attenuations and disruptions of endothelial cells upon electron microscopic examination. In this model we have investigated the influence of the C 2 toxin on alveolar epithelial barrier properties. Epithelial permeability was assessed by continuous monitoring of the transepithelial passage of technetiumlabelled diethylenetriamine penta-acetic acid ( 99m Tc-DTPA), offered to the alveolar surface by aerosol technique.Intravascular administration of hydrogen peroxide, used as control agent, was shown to provoke a four-to fivefold increase in the clearance rate of 99m Tc-DTPA under conditions of severe fluid leakage into the lung interstitial and alveolar space. Intravascular administration of C 2 toxin caused a dose-and time-dependent increase in Kfc values (8-15 fold), but the Tc-DTPA clearance rate was entirely unaffected. Moreover, transbronchial application of C 2 toxin again reproduced the manifold increase in Kfc data (about six fold), but the rate of transepithelial passage of the hydrophilic Tc-DTPA complex remained unchanged.We conclude that the barrier properties of the lung microvascular endothelial and epithelial layer are differentially regulated. It is suggested that the actin microfilament system plays a decisive role in the structural and functional integrity of the endothelial but not the epithelial barrier. Eur Respir J., 1996, 9, 93-99

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Alveolar Surfactant and ARDS

Seeger¹,

Günther²,

Walmrath³

1998

Update in Intensive Care and Emergency Medicine

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Increased lung vascular permeability after arachidonic acid and hydrostatic challenge

Cited by 69 publications

References 0 publications

Effects of inhaled versus intravenous vasodilators in experimental pulmonary hypertension

Effects of inhaled versus intravenous vasodilators in experimental pulmonary hypertension

Differential role of actin in lung endothelial and epithelial barrier properties in perfused rabbit lungs

Alveolar Surfactant and ARDS

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