Changes In Pulmonary Vascular Permeability Research Articles

Re-Expansion Pulmonary Edema as a Life-Threatening Complication in Massive, Long-Standing Pneumothorax: A Case Series and Literature Review.

Re-expansion pulmonary edema is a rare and potentially life-threatening complication that can occur after the rapid re-expansion of a collapsed lung due to pneumothorax or pleural effusion. It has a multifactorial pathogenesis, and risk factors for re-expansion pulmonary edema, such as chronic lung collapse, rapid re-expansion, and changes in pulmonary vascular permeability, have been identified. Clinical manifestations vary, ranging from almost asymptomatic to a rapidly fatal condition, and its incidence may be more common and less fatal than previously believed. The literature emphasizes the importance of early recognition and management to ensure favorable outcomes. However, there is ongoing debate regarding the indications for ventilatory support and the timing of non-invasive or invasive ventilation. Herein, we report a case series of three paradigmatic examples of massive re-expansion pulmonary edema occurring over a period of 10 years in our institution among a population of 815 patients with spontaneous pneumothorax. We also conducted a literature review on re-expansion pulmonary edema, with a particular focus on diagnosis and management. In each case, despite initially normal clinical parameters, severe respiratory distress developed following the insertion of a thoracic drainage tube for a massive spontaneous pneumothorax. Two patients required High-Flow Nasal Oxygen, and one was addressed to intensive management, including CPAP. In all cases, the patient's outcome was optimal.

EXPERIMENTAL EVALUATION OF THE PULMONARY EDEMA INDUCED BY THE VENOM OF THE SCORPION TITYUS ASTHENES IN RATS

The species Tityus asthenes has been responsible for scorpion sting deaths in Panama. Pulmonary edema is one of the main causes of death registered by scorpionism. In the present work, we determined the capacity of the venom of the scorpion Tityus asthenes to induce pulmonary edema in rats. The ability of T. asthenes venom to induce acute pulmonary edema in rats was determined using four approaches: (1) the difference in wet weight using the lung index between treated and untreated lungs; (2) histological analysis; (3) changes in pulmonary vascular permeability; and (4) total leukocyte count obtained from bronchoalveolar lavage. We found that histological sections of venom-treated lungs showed moderate pulmonary edema, and an increase in total leukocyte count compared to control samples. However, the pulmonary index and the vascular permeability of venom-treated lungs were similar to those of control samples. We conclude that the venom of T. asthenes scorpions can induce moderate pulmonary edema in rats. The experimental model was validated for future studies on the pathophysiology of pulmonary edema caused by the venom of scorpions of the genus Tityus in Panama.

The effect of heparin on vascular endothelial cell injury induced by lipopolysaccharide in rats and the study of nuclear factor-κB, interleukin-1β, interleukin-6, tumor necrosis factor-α

Objective To investigate the effect of heparin on vascular endothelial cell injury induced by lipopolysaccharide in rats, and the changes of the levels of nuclear factor-κB (NF-κB), interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α. Methods 90 SD rats were randomly divided into three groups: LPS group, heparin group and control group, 30 rats in each group. Rats in the LPS group and heparin group were injected with 10 mg/kg by intraperitoneal injection of lipopolysaccharide solution to establish sepsis model. The heparin group was injected with 300 IU/kg heparin solution before 1H injection. Rats in control group were injected with NaCl solution by intraperitoneal injection in accordance with 10 mg/kg. The morphological changes of lung tissue in rats at 6 h were compared. The changes of NF-κB, IL-1β, IL-6, TNF-α in three groups were detected by enzyme linked immunosorbent assay. The pulmonary vascular permeability changes of rats were detected by Evans blue (EB). Results In Lipopolysaccharide group and heparin group 0 h to 6 h nf-kappa B significantly increased activity of lipopolysaccharide group by 0 h (2.51±0.49) U/L up to 6 h (18.85±2.97) U/L, heparin group by 0 h (2.39±0.34) U/L up to 6 h (3.37±0.82) U/L, lipopolysaccharide group nf-kappa B increased activity levels compared with heparin group is more significant (P=0.021); 6 to 12 h h two groups the nf-kappa B activity significantly decreased (P<0.05), of which the lipopolysaccharide group by 0 h (18.85±2.97) U/L fell to 6 h (13.47±2.19) U/L (P=0.022), heparin group by 0 h (3.37±0.82) U/L fell to 6 h (2.25±0.34) U/L (P=0.048), but it is still significantly higher than the control group, and 0 h level (P=0.000); 0 h three groups of blood beta, IL-6, IL-1β, TNF-α level difference was not significant (IL-1 beta: P=0.940; IL-6: P=0.626; TNF-α: P=0.948), and 0 h to 6 h, lipopolysaccharide group and heparin group rats each index in the blood rise rapidly (within the group, compared with 0 h, 6 h, lipopolysaccharide group, IL-1β: P=0.039; IL-6: P=0.018; TNF-α: P=0.000; heparin group, IL-1β: P=0.036; IL-6: P=0.036; TNF-α: P=0.012), the index level significantly dropped 12 h (comparison group, compared with 6 h, lipopolysaccharide group, IL-1 beta: P=0.042; IL-6: P=0.027; TNF-α: P=0.008; heparin group, IL-1β: P=0.047; IL-6: P=0.045; TNF-α: P=0.034). Lipopolysaccharide group 6 h and 12 h of the blood of rats beta, IL-6, IL-1 TNF-αlevel was significantly higher than that of heparin group (lipopolysaccharide group: heparin group, 6 h, IL-1β: P=0.031; IL-6: P=0.023; TNF-α: P=0.000; 12 h, IL-1β: P=0.046; IL-6: P=0.038; TNF-α: P=0.017). (3) the contents of rat lung EN heparin [(1.21±0.18) mg/ml], and significantly lower than the lipopolysaccharide group [(1.92±0.20) mg/ml] (t=-8.344, P=0.000). Conclusion The heparin can inhibit the damage of vascular endothelial cells by inhibiting the levels of NF-κB, IL-1β, IL-6 , TNF-α in sepsis rats, and thus play an anti-inflammatory role in sepsis. Key words: Heparin; Lipopolysaccharide; Sepsis; Vascular endothelial cell injury

Effect of prone position on pulmonary vascular permeability in acute respiratory distress syndrome

In early acute respiratory distress syndrome (ARDS), alteration in the pulmonary capillary permeability is associated with outcome [1]. Alteration in the relation of extravascular lung water to intrathoracic blood volume (EVLW/ITBV) derived from thermal-dye dilution curves indicates changes in the pulmonary vascular permeability. Prone positioning improves gas exchange in most patients with ARDS, however whether this improvement is related to effects on pulmonary vascular permeability has not been evaluated. This prospective pilot study was designed to investigate whether prone positioning would alter EVLW/ITBV as a measure of pulmonary vascular permeability. Patients with ARDS on inverse ratio pressure-controlled ventilation with PEEP > 10 cmH2O for at least 24 hours were recruited. Patients were turned prone for 18 hours. Except for FiO2, ventilatory settings remained unchanged during the study period. Values of EVLW and ITBV were obtained using a single transpulmonary arterial thermodilution technique with a 5F-fibreoptic thermistor femoral artery catheter. Measurements of EVLW and ITBV were taken at pre-prone, 1, 2, 6, 12 and 18 hours after proning and 1 hour after supine. EVLW/ITBV while prone was normalised to pre-prone values as a baseline to illustrate differences during prone and supine. Data were expressed as mean (SEM). Repeated measures ANOVA was used for statistical analysis. Twelve episodes of proning in 11 patients were studied. Although mean PaO2/FiO2 improved within 1 hour, it continued to improve during the period studied and only reached significance 12 hours after proning (17.9 ± 2.9 v 35.1 ± 4.2, P < 0.05). Mean EVLW/ITBV did not change significantly. At least 12 hours may be needed for maximal benefit with prone positioning. Changes in pulmonary vascular permeability in ARDS do not appear to be an important mechanism to account for the improvement in gas exchange seen following prone positioning. Table 1 Changes in EVLW/ITBV after prone positioning in ARDS

Modified Evans blue fluorimetry for determination of pulmonary vascular permeability in rats sustaining burns, and delayed fluid resuscitation of burn shock

The present experiment used modified Evans blue fluorimetry to determine changes in pulmonary vascular permeability using a delayed resuscitation model of burn shock in rats. The results showed that pulmonary vascular permeability in the immediate resuscitation (IR) group regressed to normal 12–24 h following the burn whereas it regressed slowly in the delayed resuscitation (DR) group. The study showed that Evans blue fluorimetery is a reliable and sensitive method for determining pulmonary vascular permeability, and dimethyl formamide is a preferable extracting solution which provides a quick and convenient means for scientific research.

LUNG INJURY FROM GUT ISCHEMIA

Gut ischemia/reperfusion (I/R) appears to produce pulmonary vascular injury through endotoxin release and cytokine activation. The ability of hepatic reticuloendothelial cells to clear bacterial products may also be impaired during I/R. To test this, diversion of the splanchnic blood flow from the liver into the systemic circulation was performed via a microsurgical portacaval transposition in anesthetized Sprague-Dawley rats (275-375 g). Shunted animals underwent portacaval transposition and were allowed to recover for 7-10 days; sham animals underwent exploration but no shunt was created. The I/R animals were subjected to 60 minutes of reperfusion. All shunts were patent at autopsy. Pulmonary vascular permeability was assessed by measuring tissue retention of Evans blue dye. Gut I/R produced significant increases in pulmonary vascular permeability (46.2% +/- 11.0% vs. 16.4% +/- 3.8% [I/R vs. control]; p < 0.05) regardless of the presence of hepatic bypass (32.7% +/- 9.0% vs. 10.0% +/- 1.4% [I/R vs. control]; p < 0.05). These data indicate that a mediator or mediators of gut origin are responsible for pulmonary vascular permeability changes following gut I/R and are not appreciably modulated by the liver.

Compounds that increase cAMP prevent ischemia-reperfusion pulmonary capillary injury.

This study evaluated the physiological effects of compounds that increase adenosine 3',5'-cyclic monophosphate (cAMP) on changes in pulmonary capillary permeability and vascular resistance induced by ischemia-reperfusion (I-R) in isolated blood-perfused rabbit lungs. cAMP was elevated by 1) beta-adrenergic stimulation with isoproterenol (ISO, 10(-5) M), 2) post-beta-receptor stimulation of adenylate cyclase with forskolin (FSK, 10(-5) M), 3) and dibutyryl cAMP (DBcAMP, 1 mM), a cAMP analogue. Vascular permeability was assessed by determining the capillary filtration coefficient (Kf,c), and capillary pressure was measured using the double occlusion technique. The total, arterial, and venous vascular resistances were calculated from measured pulmonary arterial, venous, and capillary pressures and blood flow. Reperfusion after 2 h of ischemia significantly (P less than 0.05) increased Kf,c (from 0.115 +/- 0.028 to 0.224 +/- 0.040 ml.min-1.cmH2O-1.100 g-1). These I-R-induced changes in capillary permeability were prevented when ISO, FSK, or DBcAMP was added to the perfusate at reperfusion (0.110 +/- 0.022 and 0.103 +/- 0.021, 0.123 +/- 0.029 and 0.164 +/- 0.024, and 0.153 +/- 0.030 and 0.170 +/- 0.027 ml.min-1.cmH2O-1.100 g-1, respectively). I-R significantly increased total, arterial, and venous vascular resistances. These increases in vascular resistance were also blocked by ISO, FSK, and DBcAMP. These data suggest that beta-adrenergic stimulation, post-beta-receptor activation of adenylate cyclase, and DBcAMP prevent the changes in pulmonary vascular permeability and vascular resistances caused by I-R in isolated rabbit lungs through a mechanism involving an increase in intracellular levels of cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Provocation of pulmonary vascular endothelial injury in rabbits by human recombinant interleukin-1 beta.

Interleukin-1 (IL-1) mediates components of the acute-phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied the effects of human recombinant IL-1 beta (rIL-1 beta) or rIL-1 alpha on circulating granulocytes, their sequestration within the pulmonary microvasculature, pulmonary edema formation, and changes in pulmonary vascular permeability to 125I-labeled albumin. rIL-1 beta administration induced significant (P less than 0.03) but transient granulocytopenia followed by significant (P less than 0.04) neutrophilia and significant (P less than 0.04) pulmonary leukostasis compared with saline-infused rabbits. Rabbits preinfused with 125I-labeled rabbit serum albumin and administered saline, rIL-1 beta, or rIL-1 alpha were sacrificed, and lung wet/dry weight ratios and bronchoalveolar lavage fluid and plasma 125I activities determined. Both rIL-1 beta and rIL-1 alpha increased lung wet/dry weight ratios (P less than 0.025 and P less than 0.01, respectively) compared with saline controls. rIL-1 beta increased bronchoalveolar lavage fluid/plasma 125I radioactivity ratios (P less than 0.025). Electron microscopic analysis of lung sections obtained from rIL-1 beta-infused animals demonstrated endothelial injury, perivascular edema, and extravasation of an ultrastructural permeability tracer. The observation that human rIL-1 can evoke acute pulmonary vascular endothelial injury and lung edema in rabbits supports the hypothesis that IL-1 may play a role in the pathogenesis of the adult respiratory distress syndrome.

Monokine-induced acute lung injury in rabbits.

Interleukin-1 (IL-1) mediates components of the acute phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied in unanesthetized rabbits the effects of intravenous divided dose infusions of a murine monokine preparation containing IL-1 activity, on circulating granulocytes, their sequestration within the pulmonary microvasculature, pulmonary edema formation, and changes in pulmonary vascular permeability. Monokine administration induced significant (P less than 0.01) granulocytopenia as well as a significant (P less than 0.001) increase in mean alveolar septal wall granulocytes per high power field (HPF) compared with saline-injected controls. Infusions of the monokine preparation significantly (P less than 0.005) increased lung wet-to-dry weight ratios as well as significantly (P less than 0.025) increased pulmonary extravasation of radiolabeled albumin. Electron microscopic analysis of lung sections obtained from monokine-infused animals demonstrated endothelial injury, perivascular edema, and extravasation of an ultrastructural tracer. We conclude that a monokine preparation containing IL-1 activity can induce profound granulocytopenia, pulmonary leukostasis, and acute pulmonary vascular endothelial injury.

Noninvasive Radioisotopic Assessment of Pulmonary Vascular Protein Leak: Experimental Studies and Potential Clinical Applications

Noninvasive, double-radioisotope measurement of pulmonary vascular protein leak is a specific and sensitive method for assessing pulmonary vascular permeability. It is sensitive enough to detect increases in vascular protein leak that are too small to produce detectable increases in gravimetric lung water. A simple method for calculating protein leak index reliably reflects expected changes in pulmonary vascular permeability in a broad range of lung injury conditions. This method of measurement may have significant experimental and clinical applications in the study of lung-injury-induced edema, and especially in the evaluation of levels of injury associated with increased permeability but not significant edema. In particular, this method may help to distinguish between increased-permeability edema, such as that which occurs in the adult respiratory distress syndrome, and other types of pulmonary edema in humans.

Increased pulmonary vascular permeability follows intracranial hypertension in sheep.

After reviewing the characteristics of neurogenic pulmonary edema, Theodore and Robin suggested that it was probably due to rupture of lung vessels by marked but transitory pulmonary hypertension. In this study, we have determined the effects of increased intracranial pressure in a sheep model in which we could measure the flow rate and protein content of lung lymph, and thus detect changes in pulmonary vascular permeability. We found that increasing intracranial pressure to amounts near systemic arterial pressure produced a 3-fold increase in the flow of protein-rich lymph, which indicates increased lung vascular permeability. The high permeability often developed, and always persisted, without extraordinary increases in pulmonary vascular pressure. We conclude that increased lung vascular permeability may follow intracranial hypertension and that extreme pulmonary hypertension is not a prerequisite. Our data do not permit us to exclude barotrauma to exchanging vessels as a cause of capillary damage, but do suggest that other factors, perhaps local release of permeability mediators, may be involved.

The sensitivity of the colloidal carbon technique in measuring pulmonary vascular permeability changes.

The sensitivity of the colloidal carbon technique in measuring pulmonary vascular permeability changes.