Venous air emboli in sheep: reversible increase in lung microvascular permeability

Ohkuda, Kazuhiro; Nakahara, K; Binder, Andreas; Staub, Norman C.

doi:10.1152/jappl.1981.51.4.887

Cited by 83 publications

(51 citation statements)

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“…Indeed, the increase in protein clearance produced by exercise is the same as observed after I h of air microembolization and the same as produced by acidosis and hypoxia (Fig. 4), which are insults believed to increase pulmonary vascular permeability (23,26). If there was an increase in vascular permeability, it would have to be rapidly reversible because the increased lymph flow secondary to exercise returned to base line within minutes of stopping the exercise in both normoxic and hypoxic animals.…”

Section: Discussionsupporting

confidence: 54%

Effects of exercise on lung lymph flow in sheep and goats during normoxia and hypoxia.

Coates¹,

O’Brodovich²,

Jefferies³

et al. 1984

J. Clin. Invest.

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As bstract. Vigorous exercise causes a marked increase in cardiac output with only a minimal increase in measureable pulmonary vascular pressures. These changes in pulmonary hemodynamics should affect lung water and solute movement.On nine occasions, we measured the effect of normoxic exercise on lung lymph flow in four sheep and two goats with chronic lymph fistulas (wt = 15-25 kg). In addition, lymph flow was also measured on five occasions in sheep during exercise at reduced barometric pressures (430 and 380 mmHg). During normobaria, the animals ran at 3-5 km/h with 0-10% elevation of the treadmill for 15 to 85 min. Exercise on average caused a 100% increase in cardiac output, a 140% increase in lung lymph flow, and a slight but significant reduction in lymph to plasma concentration ratio (l/p) for total protein and albumin (mol wt = 70,000). There was a significant linear correlation between lymph flow and cardiac output (r = 0.87, P < 0.01). There was no change in l/p for IgG (mol wt = 150,000) or IgM (mol wt = 900,000) and no significant change in mean pulmonary arterial (Ppa) or mean left atrial (Pla) pressures. Transition from normobaria to hypobaria caused an increase in Ppa but no change in Pla, cardiac output, or lymph flow. Exercise during hypobaria caused increases in lymph flow that were qualitatively similar to changes observed during normobaric exercise:These investigations were presented in part at

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Section: Discussionsupporting

confidence: 54%

Effects of exercise on lung lymph flow in sheep and goats during normoxia and hypoxia.

Coates¹,

O’Brodovich²,

Jefferies³

et al. 1984

J. Clin. Invest.

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“…14 Pulmonary oedema may occur rapidly, or several hours later, but usually only after multiple episodes of air trapping. 17 The oedema fluid is rich in protein because of the increase in pulmonary capillary permeability, t3 In our patient, the diagnosis of pulmonary oedema secondary to VAE was supported by the occurrence of multiple episodes of VAE, the development of pulmonary oedema near the conclusion of surgery and the high protein content of tracheal aspirates.…”

Section: Discussionmentioning

confidence: 50%

Severe pulmonary oedema after venous air embolism

1993

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We present a 59-yr-old Accepted for publication 23rd June, 1993. vestigation revealed a dumb-bell shaped cervical meningioma at the C2-3 level of the spinal cord. He had diabetes, well controlled by diet, and mild, untreated hypertension with evidence of left ventricular hypertrophy (LVH) and right bundle branch block (RBBB) on the electrocardiogram (ECG). Dexamethasone and ranitidine were started two days before the cervical laminectomy.No premedication was given. Anaesthesia was induced with thiopentone 125 mg, fentanyl 300 ~g and succinylcholine I00 mg. Following tracheal intubation, anaesthesia was maintained with nitrous oxide 70% and isoflurane 0.5-1% in oxygen, and an infusion of atracurium to maintain the post-tetanic twitch count less than five. t Monitoring consisted of ECG, pulse oximeter, central venous pressure (CVP), direct arterial pressure, oesophageal stethoscope, end-tidal carbon dioxide (PETCOz), and urinary catheter. The central venous catheter (Cavafix 375: B Braun, Melsungen, Germany) was inserted through the right basilic vein and its position at the right atrium was confirmed subsequently by chest x-ray (CXR). Elastic stockings were used to minimize venous pooling. The patient was moved gradually to the sitting position. Normal saline (NS) 500 ml and stable plasma protein solution (SPPS) 500 ml were infused to maintain haemodynamic stability. Three hours after the start of surgery, during dissection of the dura, the PETCO2 decreased from 34.5 mmHg to 28.5 mmHg over 30 sec without any change in arterial pressure, heart rate, minute volume or airway pressure. Bilateral neck compression was performed and the inspired oxygen fraction (FIOz) increased to 1.0. There was no air aspirated from the central line and no site of air entrainment could be found. The PETCO2 gradually returned to normal over five minutes and surgery continued. An FIO2 of 0.3 in nitrous oxide was reintroduced ten minutes later without decrease in oxygen saturation. A similar episode occurred one hour later with a decrease in PETCO2 from 33 mmHg to 21 mmHg over 30 sec but again no source of air entrainment was found. There was no change in arterial pressure, heart rate or oxygen saturation. A third decrease in PETCO2 from 34.5 mmHg to 15 mmHg (Figure 1) developed half an hour CAN J ANAESTH 1993 / 40:10 / pp964-7

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“…6). The sensitivity of the injured lung to hydrostatic pressure changes has been demonstrated previously in sheep treated with Pseudomonas (6), endotoxin (7), and intravenous air emboli (8); and in dogs treated with oleic acid (9,26), alpha napthyl thiourea (7), or acid aspiration (5 reduced the measured small vein pressure to the level of the wedge pressure. The larger the artery that is occluded during the wedge pressure measurement, the less likely it is that the wedge pressure will reflect changes in small vein pressure.…”

Section: Protocolmentioning

confidence: 65%

“…This increased permeability not only promotes edema formation by reducing the oncotic gradient that normally acts to keep fluid within the vascular compartment (1)(2)(3)(4)(5), but also causes a dramatic increase in the rate of transvascular fluid flux in response to increased hydrostatic pressure gradients (2)(3)(4)(5)(6)(7)(8). Thus, edema can be caused by much smaller increases in microvascular pressure in an injured lung than in a normal lung with intact permeability (1,2,(6)(7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Lung injury edema in dogs. Influence of sympathetic ablation.

Dauber¹,

Weil²

1983

J. Clin. Invest.

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A B S T R A C T Increased vascular permeability characterizes lung injury pulmonary edema and renders fluid balance in the injured lung especially sensitive to changes in hydrostatic pressure. Pulmonary edema is often associated with increased sympathetic nervous system activity which can lead to pulmonary venoconstriction. This postcapillary venoconstriction could raise microvascular pressure and might therefore increase edema in the injured lung. We produced lung injury edema in dogs with oleic acid and directly measured small (<2 mm) pulmonary vein pressure. We found that the small pulmonary vein pressure was increased from 9.8±0.5 mmHg to 12.6±0.5 mmHg (n = 10) by oleic acid injury edema. The increase was not due to a rise in left atrial pressure since the small pulmonary vein-left atrial pressure gradient also increased. To test if this increase in the postcapillary pressure gradient was sympathetically mediated, we either unilaterally ablated the stellate ganglion or produced unilateral alpha adrenergic blockade with phenoxybenzamine before giving oleic acid. Both of these "antisympathetic" interventions prevented the increase in pulmonary vein pressure caused by oleic acid edema in the protected lung but not in the intact contralateral lung. These interventions produced a 30±6.8% reduction in the amount of edema caused by oleic acid. Restoring the increase in small vein pressure by inflating a balloon in the left atrium of dogs with bilateral stellate ganglion ablations abolished the reduction in edema produced by antisympathetic treatment. However, the decrease in edema was not significantly correlated with the reduction in pulmonary vein pressure. Thus, the mechanism of the effects of these antisympathetic interventions remains unclear. We conclude that lung injury edema causes sympathetically mediated pul-

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Venous air emboli in sheep: reversible increase in lung microvascular permeability

Cited by 83 publications

References 0 publications

Effects of exercise on lung lymph flow in sheep and goats during normoxia and hypoxia.

Effects of exercise on lung lymph flow in sheep and goats during normoxia and hypoxia.

Severe pulmonary oedema after venous air embolism

Lung injury edema in dogs. Influence of sympathetic ablation.

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