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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study the pathogenesis of the pulmonary damage following infusion of thrombin in combination with a fibrinolysis inhibitor, AMCA, in the dog was elucidated. An important mechanism in the development of the pulmonary damage following infusion of thrombin and AMCA seems to be an increased vascular permeability in the pulmonary microvasculature leading to pulmonary oedema. The question whether this pulmonary damage can be prevented by antihistamine (mepyramine maleate), antiserotonins (methysergide, reserpine) antiprostaglandins (acetylsalicylic acid, indomethacin, polyphloretin phosphate), 'anti-inflammatory agents' (methylprednisolone, calcium) or an anti-adrenergic agent (phenoxybenzamine) was investigated. None of these agents did prevent the lung damage following thrombin and AMCA. In order to study the possible role of bronchoconstriction, the complement system and the kinin system for this damage dogs were also artificially ventilated with an increased end-expiratory pressure, decomplemented with cobra venom factor or treated with Trasylol respectively. Neither were these treatments effective in preventing the pulmonary damage. The findings of the present study suggest that the permeability increasing substance involved in the pathogenesis of the pulmonary damage following thrombin and AMCA is not histamine, serotonin, prostaglandins or bradykinin. Therefore another, still unknown factor, may be of greater importance for this damage.
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PMID:Pulmonary damage following pulmonary microembolism in the dog. Effect of various types of treatment. 126 37

Determination of protein transfer across the endothelial barrier or the entire alveolar capillary membrane is critical for investigation of mechanisms leading to pulmonary edema. The purpose of this study was to evaluate Evans blue dye for determination of protein clearance across cultured bovine pulmonary artery endothelial cell monolayers and as a quantitative marker for albumin leakage to the air spaces in isolated perfused rat lungs. Evans blue dye bound tightly to albumin (EBA) as determined by lack of transfer through dialysis membranes and specific elution with albumin from a molecular exclusion column. EBA was equivalent to 125I-labeled albumin for calculation of albumin clearance rates (Calb) across intact and challenged monolayers [Calb (+ vehicle) = 0.12 microliters/min; Calb (+10 nM alpha-thrombin) = 0.47 microliters/min; Calb (+5 mg/ml trypsin) = 1.29 microliters/min]. Transfer of EBA was linear with time in both the endothelial cell monolayer model and the perfused lung. EBA was a sensitive marker for early edema in the perfused lung (before detectable weight gain) as well as for severe edema in the oxidant-injured lung (marked EBA accumulation in lavage fluid) and was a more specific marker for protein transfer than lavage fluid protein. EBA transfer is a convenient, reproducible, and accurate means to assess alterations in vascular permeability.
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PMID:Evans blue dye as a marker of albumin clearance in cultured endothelial monolayer and isolated lung. 144 23

Paraquat is a herbicide known to cause pulmonary edema in its acute toxic phase. Many investigators showed that paraquat induces morphological changes of alveolar epithelial cells even in its early phase. Controversy still exists, however, as to whether pulmonary vascular endothelial cells are also morphologically vulnerable to paraquat. To test the direct toxicity and metabolic changes of pulmonary vascular endothelial cells after paraquat addition, porcine pulmonary artery endothelial cells (PPAEC) were cultured. Thrombin- or bradykinin-stimulated PGI2 production was enhanced significantly, and the angiotensin converting enzyme (ACE) activity of cell lysate of PPAEC was significantly suppressed after a 24-hour incubation with 10(-4) M of paraquat. No further thrombin-induced enhancement of PGI2 production was noted after a 48-hour incubation. The alterations in arachidonic acid metabolism and ACE activity mentioned above did not result from cytotoxicity of paraquat because LDH release into culture medium was not increased during 72 hours of incubation with paraquat. Longer incubation more than 48 hours, in turn, induces obvious toxic effects on PPAEC.
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PMID:[Arachidonic acid metabolism and angiotensin converting enzyme activity by cultured porcine pulmonary artery endothelial cells are affected with paraquat]. 166 45

The rapid development of pulmonary edema that may occur in the rabbit after the intracisternal injection of a mixture of fibrinogen and thrombin has classically been considered to result from a vagally mediated increase in vascular permeability (G. R. Cameron and S. N. De, J. Pathol. Bacteriol 61: 375, 1949) and to not be dependent on hemodynamic mechanisms. We tested this hypothesis by evaluating the relationship between the degree of pulmonary hypertension and postmortem extravascular lung water content (EVLW) in both nonvagotomized (n = 10) and vagotomized (n = 7) rabbits administered thrombin (0.1 ml, 500 U/ml) and fibrinogen (1 ml, 27 mg/ml) intracisternally. No increase in EVLW was observed in either group unless pulmonary arterial pressure (Ppa) exceeded 25 Torr, and large increases in EVLW were only observed at higher Ppa's. These results thus indicate that some degree of pulmonary hypertension is required for the development of this form of edema. Because the vascular pressure required to produce edema in this model approaches that required to increase pulmonary vascular permeability in the rabbit, a pressure-dependent increase in permeability may be a common characteristic of neurogenic pulmonary edema in this species. Vagotomy had no protective effect but instead appeared to increase the amount of edema development for a given degree of pulmonary hypertension.
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PMID:Role of hemodynamics and vagus nerves in development of fibrin-induced pulmonary edema. 207 21

This study was undertaken to evaluate the role of vagal nerves in the development of neurogenic pulmonary edema. We injected fibrinogen and thrombin into the cisterna magna of rats, a model of neurogenic pulmonary edema. When the vagal nerves were left intact, pulmonary edema occurred (fibrin-induced pulmonary edema) at a rate of 33%. Vagotomy at the midcervical portion increased the incidence of pulmonary edema to a rate of 100%, whereas pretreatment with atropine did not affect the incidence. These results suggested that vagal afferent nerves or nonadrenergic-noncholinergic efferent nerves played an important role in inhibiting the development of fibrin-induced pulmonary edema. Furthermore, in vagotomized and vagal nerve-intact rats pretreated with capsaicin, the incidence of pulmonary edema was 100%. Pretreatment with a substance P antagonist, [D-Pro2, D-Trp7,9]-SP, also increased the incidence to 100% in the vagal nerve-intact rats. On the other hand, intravenous administration of some neuropeptides that may be released from the capsaicin-sensitive nerves (e.g., substance P or calcitonin gene-related peptide) inhibited the development of pulmonary edema in vagotomized rats. We concluded that the vagal capsaicin-sensitive nerves exerted an inhibitory effect on the development of fibrin-induced pulmonary edema.
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PMID:Capsaicin-sensitive nerves exert an inhibitory effect on the development of fibrin-induced pulmonary edema in rats. 247 55

Effects of depth of anesthesia, pH of fibrinogen and thrombin, and interventions in the vagus nerves on the development of fibrin-induced pulmonary edema were examined in the rat. Rats were anesthetized with an intraperitoneal injection of pentobarbital sodium, 25 or 50 mg/kg. Solutions of fibrinogen and thrombin at the same pH were separately injected into the cisterna magna. The pH values were adjusted to 6.5 or 8.5 with Tris buffer. Interventions in the vagus nerves, which consisted of atropine administration at a dose of 1 mg/kg, i.v. or bilateral vagotomy, were performed before the intracisternal injection of fibrinogen and thrombin. Animals in which no interventions in the vagus nerve was performed were designated as intact rats. Lung-water ratio was calculated as a ratio of the difference between wet and dry lung weight to dry lung weight. Incidences of pulmonary edema and lung-water ratios were lower under deep anesthesia than under light anesthesia. Both parameters were low in the vagotomized rats treated under deep anesthesia with fibrinogen and thrombin at a pH of 8.5, as compared to those treated similarly at pH 6.5. This phenomenon was not observed under light anesthesia. Interventions in the vagus nerves influenced the development of pulmonary edema to various degrees, depending on the pH values of the injected fibrinogen and thrombin. As suggested from these results, well-defined, specific conditions are required for investigating the mechanism triggering the development of fibrin-induced pulmonary edema.
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PMID:Factors influencing fibrin-induced pulmonary edema. 337 36

The effect of N-acetylcysteine (NAC), a free radical scavenger, was investigated in a microembolism rat model of adult respiratory distress syndrome (ARDS). Microembolism was induced by an intravenous injection of bovine thrombin and an intraperitoneal injection of a fibrinolysis inhibitor, trans-4-aminomethyl-cyclohexane-carboxylic acid (AMCA). NAC counteracted the experimentally induced increase in lung weight, the development of alveolar oedema, and the amount of fibrin in precapillary vessels. There was also a tendency to a decrease of the experimentally induced interstitial oedema caused by the NAC treatment, although it was not statistically significant. Surprisingly, NAC reduced plasma viscosity in both experimental and control animals. It also seemed to increase PaO2 in animals with pulmonary damage, but had a lowering effect on PaO2 in control animals. The results indicate that NAC has a significant preventive effect in this microembolism rat model of ARDS, and that this effect may be achieved through decreased deposition of fibrin, thus counteracting pulmonary oedema, and a decrease in plasma viscosity.
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PMID:Effect of N-acetylcysteine on pulmonary damage due to microembolism in the rat. 358 17

We have examined the mechanisms of lung vascular injury and pulmonary edema secondary to intravascular coagulation. Alpha-thrombin was infused intravenously to induce pulmonary intravascular coagulation. The results indicate that fibrin and neutrophils are essential requirements for lung vascular injury and pulmonary edema formation. The findings point to a fibrin-neutrophil interaction in inducing neutrophil adherence. Thrombin also has direct effects on endothelial permeability and can contribute to neutrophil sequestration in the lung by increasing endothelial adhesivity. Complement activation can explain only a part of the response. Lipid-derived mediators (e.g., LTB4 and mono HETEs) may be particularly important in the pathophysiology of lung vascular injury and pulmonary edema.
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PMID:Mechanisms of thrombin-induced lung vascular injury and edema. 361 10

We examined the direct effects of thrombin on pulmonary vasomotor tone in isolated guinea pig lungs perfused with Ringer albumin (0.5% g/100 ml). The injection of alpha-thrombin (the native enzyme) resulted in rapid dose-dependent increases in pulmonary arterial pressure (Ppa) and pulmonary capillary pressure (Ppc), which were associated with an increase in the lung effluent thromboxane B2 concentration. The Ppa and Ppc responses decreased with time but then increased again within 40 min after thrombin injection. The increases in Ppc were primarily the result of postcapillary vasoconstriction. Pulmonary edema as evidenced by marked increases (60% from base line) in lung weight occurred within 90 min after thrombin injection. Injection of modified thrombins (i.e., gamma-thrombin lacking the fibrinogen recognition site or i-Pr2P-alpha-thrombin lacking the serine proteolytic site) was not associated with pulmonary hemodynamic or weight changes nor did they block the effects of alpha-thrombin. Indomethacin (a cyclooxygenase inhibitor), dazoxiben (a thromboxane synthase inhibitor), or hirudin (a thrombin antagonist) inhibited the thrombin-induced pulmonary vasoconstriction, as well as the pulmonary edema. We conclude that thrombin-induced pulmonary vasoconstriction is primarily the result of constriction of postcapillary vessels, and the response is mediated by generation of cyclooxygenase-derived metabolites. The edema formation is also dependent on activation of the cyclooxygenase pathway. The proteolytic site of alpha-thrombin is required for the pulmonary vasoconstrictor and edemogenic responses.
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PMID:Alpha-thrombin-induced pulmonary vasoconstriction. 369 33

Computed chest tomography was performed in 13 rats with pulmonary damage due to microembolism, caused by injection of thrombin (500 NIH/kg body weight) and tranexamic acid, a fibrinolytic inhibitor (200 mg/kg body weight), and in 9 control rats. The purpose of the investigation was to perform attenuation measurements at two levels of the right lung, each with three regions of interest (anterior, mid and posterior). Alterations in attenuation, compared with controls, were correlated with lung weight. Compared with controls, the attenuation was significantly increased in the anterior and posterior regions at both levels in animals with pulmonary damage, but not in the mid regions. There was a statistically significant correlation between increasing attenuation and increasing lung weight. A significant difference was found between damaged and control lungs regarding the microscopic grade of interstitial oedema, alveolar oedema and fibrin. Histograms of attenuation values in computed tomograms might be of value in detecting alveolar oedema. It is concluded that computed chest tomography is a good method for detecting pulmonary oedema at an early stage of experimental microembolism in the rat.
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PMID:Computed chest tomography in rats with pulmonary damage due to microembolism. 381 23


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