Pulmonary Vascular Hemodynamics Research Articles

Fontan track症例の肺循環に対する扁桃摘出の効果

Fontan track症例の肺循環に対する扁桃摘出の効果

Retracted: Mice lacking the Raf‐1 kinase inhibitor protein exhibit exaggerated hypoxia‐induced pulmonary hypertension

Increased pulmonary vascular remodelling, pulmonary arterial pressure and pulmonary vascular resistance characterize the development of pulmonary arterial hypertension (PAH). Activation of the Raf/mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK)1/2 is thought to play an important role in PAH and Raf-1 kinase inhibitor protein (RKIP), negatively regulates this pathway. This study investigated whether genetic deletion of RKIP (and hence ERK1/2 up-regulation) resulted in a pulmonary hypertensive phenotype in mice and investigated a role for RKIP in mitogen-regulated proliferative responses in lung fibroblasts. Pulmonary vascular haemodynamics and remodelling were assessed in mice genetically deficient in RKIP (RKIP-/-) after 2 weeks of either normoxia or hypoxia. Immunoblotting and immunohistochemistry were used to examine phosphorylation of Raf-1, RKIP and ERK1/2 in mouse pulmonary arteries. In vitro, RKIP inhibition of mitogen signalling was analysed in CCL39 hamster lung fibroblasts. RKIP-/- mice demonstrated elevated indices of PAH and ERK1/2 phosphorylation compared with wild-type (WT) mice. Hypoxic RKIP-/- mice exhibited exaggerated PAH indices. Hypoxia increased phosphorylation of Raf-1, RKIP and ERK1/2 in WT mouse pulmonary arteries and Raf-1 phosphorylation in RKIP-/- mouse pulmonary arteries. In CCL39 cells, inhibition of RKIP potentiated mitogen-induced proliferation and phosphorylation of RKIP, and Raf-1. The lack of RKIP protein resulted in a pulmonary hypertensive phenotype, exaggerated in hypoxia. Hypoxia induced phosphorylation of RKIP signalling elements in WT pulmonary arteries. RKIP inhibition potentiated mitogen-induced proliferation in lung fibroblasts. These results provide evidence for the involvement of RKIP in suppressing the development of hypoxia-induced PAH in mice.

Short term effects of exercise training on exercise capacity and quality of life in patients with pulmonary arterial hypertension: protocol for a randomised controlled trial.

BackgroundAdvances in the understanding and management of pulmonary arterial hypertension have enabled earlier diagnosis and improved prognosis. However, despite best available therapy, symptoms of exertional dyspnoea and fatigue are commonly reported and result in a reduced capacity to perform daily activities and impaired quality of life. Exercise training has demonstrated efficacy in individuals with other respiratory and cardiovascular diseases. Historically, however, exercise training has not been utilised as a form of therapy in pulmonary arterial hypertension due to the perceived risk of sudden cardiac death and the theoretical possibility that exercise would lead to worsening pulmonary vascular haemodynamics and deterioration in right heart function. Now, with the advances in pharmaceutical management, determining the safety and benefits of exercise training in this population has become more relevant. Only three studies of supervised exercise training in pulmonary arterial hypertension have been published. These studies demonstrated improvements in exercise capacity and quality of life, in the absence of adverse events or clinical deterioration. However, these studies have not utilised an outpatient-based, whole body exercise training program, the most common format for exercise programs within Australia. It is uncertain whether this form of training is beneficial and capable of producing sustained benefits in exercise capacity and quality of life in this population.Design/MethodsThis randomised controlled trial will determine whether a 12 week, outpatient-based, supervised, whole body exercise training program, followed by a home-based exercise program, is safe and improves exercise capacity and quality of life in individuals with pulmonary arterial hypertension. This study aims to recruit 34 subjects who will be randomly allocated to the exercise group (supervised exercise training 3 times a week for 12 weeks, followed by 3 sessions per week of home exercise for 12 weeks) or the control group (usual medical care). Subjects will be assessed at baseline, 12 weeks and 24 weeks.DiscussionThis study will determine whether outpatient-based, whole body exercise training is beneficial and safe in individuals with pulmonary arterial hypertension. Additionally, this study will contribute to clinical practice guidelines for this patient population.Trial registrationAustralia and New Zealand Clinical Trials Register (ANZCTR): ACTRN12609000502235

Cell-based therapies in pulmonary hypertension: who, what, and when?

pulmonary hypertension (PH), diagnosed when mean pulmonary arterial pressure exceeds the upper limits of normal (i.e., >25 mmHg) at rest (2), occurs in a variety of clinical situations and is associated with a broad spectrum of histological patterns and abnormalities. PH is currently classified into five distinct World Health Organization (WHO) groups, based on common clinical parameters, potential etiological mechanisms, and responses to treatment (22). Although any form of PH can contribute to increased patient morbidity and mortality, pulmonary arterial hypertension (PAH) (WHO group 1) is a particularly severe and progressive form associated with right heart failure and premature death (1). At present, therapeutic approaches to stabilize or reverse this debilitating condition involve treatment with one or a combination of up to three specific classes of agents, including prostacyclin analogs, endothelin-1 receptor antagonists, and/or phosphodiesterase-5 inhibitors. Retrospective (meta)analyses of these therapeutic strategies have demonstrated a reduction in mortality with their use (7, 12); however, many experts believe that current PAH treatment is inadequate given the persistently high mortality rate and functional hemodynamic impairment in many patients. These observations have led to continued intensive investigation into pathogenetic mechanisms and many proposals for additional alternative new therapies (20, 24). Among the potential new therapies, increasing interest in the role of endothelial progenitor cells (EPCs) as a cell-based therapy has emerged. However, issues remain regarding what group of PH patients are most likely to benefit from treatment, at what point in the disease is treatment most likely to be successful, and what types of cells should be utilized for therapy.

Effects of stent implantation for peripheral pulmonary artery stenosis on pulmonary vascular hemodynamics and right ventricular function in a patient with repaired tetralogy of Fallot

Stent implantation is an effective alternative to surgery and balloon angioplasty for the treatment of stenotic vascular lesions. However, there is concern about the hemodynamic consequences related to the loss of vascular elasticity caused by the non-compliant property of the implanted stent. Here we report data for pulmonary vascular impedance and right ventricular performance after implantation of balloon-expanded stents for peripheral pulmonary stenosis in a 13-year-old girl with repaired pulmonary atresia and ventricular septal defect. Stent implantation reduced total vascular resistance, low-frequency impedance and wave reflection, and improved right ventricular contractile performance measured by the pressure-area relationship. However, pulmonary vascular wall stiffness remained elevated after stenting, and it was suggested that stent implantation resulted in a net increase in vascular wall stiffness. The long-term effects of implanted stents on vascular and ventricular hemodynamics need to be clarified.

Pulmonary Complications of Cirrhosis

Pulmonary vascular complications of liver disease comprise two distinct clinical entities: hepatopulmonary syndrome (HPS-microvascular dilatation and angiogenesis) and portopulmonary hypertension (POPH-vasoconstriction and remodeling in resistance vessels). These complications occur in similar pathophysiologic environments and may share pathogenic mechanisms. HPS is found in 15% to 30% of patients with cirrhosis and its presence increases mortality and the risks of liver transplantation, particularly when hypoxemia is present. Contrast echocardiography and arterial blood gas analysis are required to establish the diagnosis. No medical therapies are available, although liver transplantation is effective in reversing the syndrome. POPH is found in 4% to 8% of patients undergoing liver transplantation evaluation, and the presence of moderate to severe disease significantly increases perioperative transplant mortality. Transthoracic echocardiography is recommended for screening and right-heart catheterization is required to establish the diagnosis. Medical therapies are increasingly effective in improving pulmonary vascular hemodynamics in POPH and may result in better perioperative outcomes.

Progressive Dilatation of the Main Pulmonary Artery Is a Characteristic of Pulmonary Arterial Hypertension and Is Not Related to Changes in Pressure

Pulmonary artery (PA) dilatation is one of the consequences of pulmonary arterial hypertension (PAH) and is used for noninvasive detection. However, it is unclear how the size of the PA behaves over time and whether it is related to pressure changes. The aim of this study was to evaluate PA size during follow-up in treated patients with PAH and whether it reflects pulmonary vascular hemodynamics. Fifty-one patients with PAH who underwent at least two right-sided heart catheterizations (RHCs) together with cardiac MRI (CMR) were included in this study. Another 18 patients who had normal pressure at RHC were included for comparison at baseline. From RHC, we derived PA pressures and cardiac output. From the CMR images we derived PA diameter (PAD) and the ratio of the PAD and ascending aorta diameter. The PAD was significantly larger in patients with PAH than in patients without PAH (P < .001). A ratio of the PAD and ascending aorta diameter > 1 had a positive predictive value of 92% for PAH. Mean follow-up time was 942 days, and there was a significant dilatation during this period (P < .001). The change of the PAD did not correlate with the changes in pressure or cardiac output. A moderate correlation with follow-up time was found (r = 0.56; P < .001). A dilatated PA is useful for identifying patients with PAH. However, during patient follow-up, progressive dilatation of the PA is independent of the change in PA pressure and cardiac output and might become independent from hemodynamics.

Changes in right ventricular function with unilateral pulmonary artery occlusion test for pre-operative evaluation prior to lung resection

We measured the right ventricular ejection fraction (RVEF) before and during unilateral pulmonary artery occlusion test (UPAO) by thermodilution method. We also measured the right ventricular end-diastolic volume index (RVEDVI), right ventricular end-systolic volume index (RVESVI), and right ventricular stroke volume index (RVSVI). RVEF and RVSVI were significantly decreased by UPAO (p less than 0.05), but there were no obvious changes in RVEDVI and RVESVI. Some cases showed only a small decrease in RVEF by UPAO, even though their total pulmonary vascular resistance indices were over 700 dyne.sec.cm-5/m2 during UPAO. On the other hand, some cases had a decreased in RVEF of more than 10% by UPAO, even though their total pulmonary vascular resistance indices were under 400 dyne.sec.cm-5/m2 during UPAO. We consider that it is important to measure right ventricular functions such as RVEF together with pulmonary vascular hemodynamics in the pre-operative evaluation of cases of lung resection.

Variable prevalence of pulmonary hypertension in patients with advanced interstitial pneumonia

Pulmonary hypertension may occur in patients with interstitial pneumonia and is associated with increased mortality. We sought to determine the prevalence of pulmonary hypertension in sub-groups of patients with interstitial pneumonia and to investigate possible associations between pulmonary vascular hemodynamics and pulmonary function. The presence or absence of pulmonary hypertension was assessed in 70 patients with advanced interstitial pneumonia who underwent right heart catheterization. The associations of pulmonary hypertension with clinical characteristics and pulmonary function tests were analyzed. The prevalence of pulmonary hypertension in patients with idiopathic interstitial pneumonia was 29% vs 64% in patients with connective tissue disease-interstitial pneumonia (p = 0.013). African American patients had a significantly higher prevalence of pulmonary hypertension in the entire study population (81% vs 22%, p < 0.001) and in the idiopathic interstitial pneumonia group (70% vs 19%, p < 0.01). Regression analyses revealed no association between mean pulmonary artery pressure (mPAP) and forced vital capacity or mPAP and diffusion capacity of the lung for carbon monoxide in the entire cohort or in sub-groups of patients. African American patients and patients with connective tissue disease-interstitial pneumonia had a high prevalence of pulmonary hypertension. Non-African American patients with advanced idiopathic interstitial pneumonia (including idiopathic pulmonary fibrosis) had a low prevalence of pulmonary hypertension.

On the diagnosis of acute respiratory distress syndrome in nosocomial pneumonias

Clinical practice deals highly frequently with patients presenting a concomitant occurrence of acute respiratory distress syndrome (ARDS) and nosocomial pneumonia (NPn). Timely diagnosis of ARDS and NPn in such circumstances is problematic, but it provides a possibility of differential treatment. The aim of the investigation was to elucidate the value of the oxygenation index (OI), extravascular lung water index (EVLWI), pulmonary vascular permeability index (PVPI) and central hemodynamics indexes in the diagnosis of ARDS in NPn.

Time Course of Changes in Extravascular Lung Water Index, Intracranial and Cerebral Perfusion Pressures in Acute Cerebral Circulatory Disorders

Objective: to study the time course of changes in extravascular lung water index (ELWI) and intracranial and cerebral perfusion pressures (ICP and CPP) and to determine their possible relationships in acute cerebral circulatory disorders (ACCD). Subject and methods. ELWI, pulmonary vascular permeability index (PVPI), ICP, CPP, and central hemodynamics were studied by transpulmonary thermodilution and current X-ray studies were conducted in 18 patients on days 1, 3, 5, and 7 of ACCD. Results. Examinations revealed a supratentorial dislocation of the brain in 6 persons; its subtento-rial dislocation was found in 1 case; supra- and subtentorial dislocations were seen in 6. In patients, ELWI and PVPI increased from days 1 and 5, respectively. The high baseline ICP increased over time. CPP remained unchanged. Preserved left ventricular contractility, enhanced myocardial one, a significant direct correlation between ELWI and PVPI, as well as their increase confirmed that the noncardiogenic genesis was responsible for increased ELWI. A direct significant correlation was found between ICP and ELWI, ICP and PVPI. Against this background, acute respiratory distress syndrome developed in 14 patients with pneumonia evolving in its presence in 7 patients. Conclusion. In ACCD, ELWI increases in the first 24 hours of the acute period. One of its causes is, along with others, primary and/or secondary damage to the brainstem structures with elevated ICP and progressive brain dislocation. The determination of ICP, unlike CPP, is crucial in the diagnosis and treatment of primary/secondary brain injuries and in prognosis. Key words: acute cerebral circulatory disorder, extravascular lung fluid, pulmonary vascular permeability, intracranial pressure, cerebral perfusion pressure, acute respiratory distress syndrome.

What to expect after tricuspid valve replacement? Long-term results

Current knowledge in long-term results of tricuspid valve replacement is limited. Present study reviews our experience from a consecutive series. Forty-two patients (16 male, 26 female; mean age: 33+/-15) underwent tricuspid valve replacement between March 1987 and December 2004. The etiology was rheumatic in 64%, Ebstein's anomaly in 31%, and endocarditis in 5%. Nineteen patients were in New York Heart Association (NYHA) Class III functional capacity (45%), and 13 in class IV (31%). Twenty patients (48%) underwent isolated tricuspid valve replacement. The remaining underwent combined (mitral and/or aortic) valve replacements. Tricuspid replacement device was mechanical in 31% and bioimplant in 69%. Hospital mortality was 26%. Rheumatic etiology, reoperation and elevated pulmonary artery pressure were associated with higher early mortality. The patients with decreased functional capacity (NYHA Class III/IV), congestive symptoms and rheumatic origin were more prone to low cardiac output development. The Kaplan-Meier survivals were 37% at 10 years and 30% at 15 years. The 10-year event-free survival was 31%. Elevated pulmonary artery pressure and rheumatic etiology unfavorably affected the long-term results. The average functional capacity in survivors improved significantly after operation. Any tricuspid disease not amenable to repair thus necessitating replacement is an unfortunate situation since both the short and long-term results of valve replacement are suboptimal in regard to those of left-sided valve replacements, probably due to different structural and geometrical characteristics of right ventricle and the low-pressure venous system hemodynamics. Etiology, clinical presentation and pulmonary vascular hemodynamics are major determinants of the outcome.

Effects of Intravenous Nesiritide on Pulmonary Vascular Hemodynamics in Pulmonary Hypertension

Background Nesiritide is effective in the treatment of decompensated heart failure (HF). We evaluated the acute hemodynamic effects of nesiritide, a recombinant B-type natriuretic peptide, in patients with HF and pulmonary hypertension (PH). Methods and Results Twenty patients with HF and PH (mean pulmonary arterial [PA] pressure >25 mm Hg) were enrolled: 10 with postpulmonary capillary wedge (PCW) >15 mm Hg and 10 with precapillary PH (PCW) ≤15. The pulmonary and systemic hemodynamics were determined by right heart catheterization at baseline and at 15 and 30 minutes after an intravenous nesiritide infusion (2 mcg/kg bolus and 0.01 mcg·kg·min). For the patients with postcapillary PH, the mean left ventricular ejection fraction was 28 ± 15%. After the 30-minute nesiritide infusion, right atrial (RA) pressure decreased 48% ( P < .0001), mean PA pressure decreased 29% ( P < .0001), PCW pressure decreased 40% ( P < .0001), cardiac index (CI) increased 35% ( P = .009), pulmonary vascular resistance index (PVRI) decreased 35% ( P = .01), and arteriovenous oxygen difference (AVDO 2) decreased 27% ( P = .0003). For precapillary PH patients, there was no change in RA, PA, or PCW pressure, nor any change in CI, PVRI, or AVDO 2. Conclusions Nesiritide acutely and significantly reduced PA pressure, PVRI, and biventricular filling pressures in patients with postcapillary PH. However, for patients with precapillary PH, nesiritide had no significant acute hemodynamic effect on the pulmonary hemodynamics. The lack of acute beneficial effects of nesiritide in patients with advanced precapillary PH may be related to their relatively fixed remodeling of the pulmonary vasculature.

Correlation between pulmonary vascular change and hemodynamics in patients with complete atrioventricular septal defect.

The study of the pulmonary vasculature in Taiwanese with atrioventricular septal defect has not been reported previously. This study investigated the correlation between pulmonary vascular change and hemodynamics in these patients. Ten children with complete atrioventricular defect, 8 of whom had Down syndrome, underwent open lung biopsy. Their age ranged from 8 months to 6 years (mean, 2 years 7 months). Cardiac catheterization was performed and the systolic pressures of pulmonary and systemic arteries were measured immediately before cardiopulmonary bypass (CPB) and immediately after cardiac repair in 9 patients, and expressed as a ratio of pulmonary to systemic systolic pressure (Pp/Ps). Medial hypertrophy and intimal proliferation were prominent in 7 patients with pulmonary hypertension. The alveolar wall muscular arteries and percent arterial medial thickness increased significantly with increasing post-repair Pp/Ps, preoperative Pp/Ps, pulmonary arteriolar resistance index and pre-CPB Pp/Ps (p < 0.02). The arteries present per 100 alveoli were inversely correlated with the above mentioned hemodynamic parameters (p < 0.02). The results of qualitative and quantitative analyses of the pulmonary vasculature in patients with complete atrioventricular defect correlated well with pre-and postoperative pulmonary arterial pressure and can be used to predict the postoperative pulmonary arterial pressure.

The effects of carbon dioxide on oxygenation and systemic, cerebral, and pulmonary vascular hemodynamics after the bidirectional superior cavopulmonary anastomosis

The effects of carbon dioxide on oxygenation and systemic, cerebral, and pulmonary vascular hemodynamics after the bidirectional superior cavopulmonary anastomosis

The effects of carbon dioxide on oxygenation and systemic, cerebral, and pulmonary vascular hemodynamics after the bidirectional superior cavopulmonary anastomosis

We investigated the effects of different CO(2) tensions on oxygenation, pulmonary blood flow (Qp), cerebral blood flow, and systemic blood flow (Qs) after the bidirectional superior cavopulmonary anastomosis (BCPA). Hypoxemia refractory to management of a high pulmonary vascular resistance index (PVRI) may complicate recovery from the BCPA. After BCPA, CO(2) was added to the inspired gas of mechanically ventilated patients. The Qp, Qs, PVRI, and systemic vascular resistance index (SVRI) were calculated from oxygen consumption, intravascular pressures, and oxygen saturations. Cerebral blood flow was estimated by near infrared spectroscopy and transcranial Doppler. In nine patients (median age 7.1, range 2 to 23 months), arterial oxygen tension increased significantly (p < 0.005) from 36 +/- 6 mm Hg to 44 +/- 6 to 50 +/- 7 mm Hg at arterial carbon dioxide tensions (PaCO(2)) of 35, 45, and 55 mm Hg, respectively and decreased to 40 +/- 8 mm Hg at PaCO(2) 40 mm Hg. At a PaCO(2) of 55 and 45 compared with 35 mm Hg, Qp, cerebral blood flow, and Qs increased significantly, PVRI, Qp/Qs, and the ratio of Qp to inferior vena caval blood flow were unchanged, but SVRI decreased. We have demonstrated that after the BCPA, systemic oxygenation, Qp, Qs, and cerebral blood flow increased and SVRI decreased at CO(2) tensions of 45 and 55 mm Hg compared with 35 mm Hg. We suggest that hypoxemia after the BCPA is ameliorated by a higher PaCO(2) and that low PaCO(2) or alkalosis may be detrimental. Hypercarbic management strategies may allow earlier progression to the BCPA, which may contribute to reducing the interval morbidity in patients with a functional single ventricle.

The effect of 100 % oxygen on the pulmonary vascular hemodynamics in pulmonary arterial hypertension

The effect of 100 % oxygen on the pulmonary vascular hemodynamics in pulmonary arterial hypertension

Pre-operative pulmonary vascular hemodynamics: relation to serial clinical and hemodynamic outcomes up to 1 year post cardiac transplantation

Severe pre-operative pulmonary hypertension has been associated with sub-optimal outcomes following heart transplantation. In this retrospective review, serial clinical and hemodynamic outcomes were evaluated in a consecutive series of 442 cardiac transplants performed between 1981 and 2001. We examined PVR (<2, 2-5, >=5), TPG (<10, 10-15, >=15) and PA sys (<50, 50-70, and >=70 mmHg) pre, 1 week, 3 months, and 1 year post transplantation. Increasing PVR and PA sys were similarly associated with higher mortality post transplantation, whereas TPG was not. ∗p<0.05 vs PVR <5.

Superoxide possibly produced in endothelial cells mediates the neutrophil-induced lung injury

Background. The mechanism by which stimulated neutrophils (polymorphonuclear leukocytes [PMNs]) damage pulmonary vascular endothelium was investigated.Methods. The ability of unstimulated and mechanically stimulated PMNs to adhere to pulmonary endothelial cells and, thereby, alter pulmonary vascular permeability was tested. Each series was conducted on 6 rats. To stimulate PMNs, they were agitated gently in a glass vial for 10 seconds.Results. Perfusing lungs with the stimulated PMNs elicited a fivefold increase in permeability compared with lungs perfused with the unstimulated cells. This increase in permeability was blocked completely by preincubation of stimulated PMNs with CD18 monoclonal antibody. This increase in permeability was also blocked completely by superoxide dismutase (SOD) or the xanthine oxidase (XO) inhibitor allopurinol. Pulmonary vascular hemodynamics were unaffected by any treatment protocol. The accumulation of stimulated PMNs within the lungs was not inhibited by SOD but was partially blocked by allopurinol.Conclusions. These findings suggest that stimulated PMN-induced increases in pulmonary vascular filtration resulted from endothelial cell injury caused by superoxide anion possibly generated by XO, exclusively present in the endothelial cells.

Gut-Derived Mesenteric Lymph

Previously, we showed that mesenteric lymph generated following hemorrhagic shock increases endothelial cell permeability and contributes to lung injury. It has also been shown that lymph produced at the site of burn injury plays a role in altering pulmonary vascular hemodynamics. In addition, previous experimental work has suggested that organs and tissues distant from the injury site may contribute to pulmonary dysfunction. One explanation would be that gut-derived inflammatory factors (in addition to those produced locally at the site of injury) are reaching the pulmonary circulation, where they exert their effects via the gut lymphatics. The 2 hypotheses herein were that (1) gut-derived factors carried in the mesenteric lymph of rats generated following thermal injury will contribute to lung injury and (2) intestinal bacterial overgrowth will potentiate the degree of burn-induced lung injury. These hypotheses were tested by examining the effect of mesenteric lymph flow interruption prior to thermal injury on burn-induced lung injury in rats with a normal intestinal bacterial flora and in rats with intestinal Escherichia coli overgrowth. These rats were termed E. coli-monoassociated rats. Normal intestinal bacterial flora and monoassociated male Sprague-Dawley rats were subjected to sham burn, 40% total body surface area burn, or lymphatic division plus burn. After 3 hours, 10 mg of Evans blue was injected to measure lung permeability. After the rats were killed, a bronchoalveolar lavage was performed and the fluid analyzed spectrophotometrically. Bronchoalveolar lavage fluid protein content, pulmonary myeloperoxidase activity, and alveolar apoptosis served to further quantitate lung injury. Both normal intestinal bacterial flora and monoassociated-burned rats exhibited significant increases in lung permeability, bronchoalveolar lavage fluid protein content, myeloperoxidase activity, and alveolar apoptosis. The combination of monoassociation and thermal injury resulted in even further increases in lung injury over thermal injury alone. Lymphatic division prior to thermal injury ameliorated burn-induced increases in lung permeability, bronchoalveolar lavage fluid protein content, pulmonary myeloperoxidase accumulation, and alveolar apoptosis in both normal intestinal bacterial flora and monoassociated rats. The results of this study support the hypothesis that gut-derived factors carried in the mesenteric lymph contribute to burn-induced lung injury and may therefore play a role in postburn respiratory failure and suggest that intestinal bacterial overgrowth primes the host such that when animals are exposed to a second stimulus (such as thermal injury) an exaggerated response occurs.