fibrin and Pulmonary-Edema

Neonatal respiratory distress syndrome (RDS) is an acute lung injury believed to result primarily from surfactant deficiency in the immature lung. Although surfactant replacement therapy has improved the outcome of this disease, RDS remains a major cause of neonatal mortality and morbidity. Preliminary experimental evidence suggests that unopposed intravascular thrombin activity may contribute to the progression of RDS by promoting high permeability pulmonary oedema and pulmonary hypertension. In the extravascular lung compartment, polymerizing fibrin may inhibit surfactant function. In addition, interstitial and alveolar thrombin formation and resulting fibrin deposition may contribute to the development of chronic lung disease through amplification of inflammation and fibrosis. There is good evidence that extravascular coagulation occurs during the course of RDS. Fibrin is a major component of the hyaline membranes, which are a hallmark of acute lung injury, and which can be regarded as locally produced clots. It has been less certain whether neonatal RDS is also associated with intravascular activation of the coagulation system. Although low levels of antithrombin III (AT III) have been reported in infants with RDS, direct evidence of increased intravascular thrombin formation has been lacking. However, recently, plasma concentrations of thrombin-antithrombin III (TAT) complexes have been measured in infants with RDS and correlated with RDS severity. TAT formation was significantly increased in severe neonatal RDS, while free AT III activity was decreased. These data are consistent with increased thrombin generation and resulting AT III consumption. Therefore, to regulate thrombin activity, infants with severe RDS may benefit from replacement therapy with AT III concentrate. This hypothesis has been strengthened by experiments that have demonstrated the efficacy of thrombin inhibition in several animal models of acute lung injury. However, controlled clinical trials will be required to determine whether thrombin is just a coincidental marker of neonatal RDS, or whether unopposed thrombin activity exacerbates the disease process.

Topics: Animals; Antithrombin III; Antithrombin III Deficiency; Clinical Trials as Topic; Fibrin; Fibrinolytic Agents; Humans; Hypertension, Pulmonary; Infant, Newborn; Pulmonary Edema; Respiratory Distress Syndrome, Newborn; Thrombin

Topics: Adult; Disseminated Intravascular Coagulation; Fibrin; Humans; Hyaline Membrane Disease; Infant, Newborn; Infant, Premature, Diseases; Lung; Organ Size; Pulmonary Atelectasis; Pulmonary Edema; Respiration, Artificial

Prosthetic heart valve obstruction is a severe and potentially fatal complication. We present a patient with a Bjork-Shiley prosthetic mitral and aortic valve implantation and recurrent pulmonary edema. Echocardiogram showed a rate-dependent "obstruction alternans" of the prosthetic mitral valve due to pannus formation.

Topics: Aged; Aortic Valve; Echocardiography, Doppler; Electrocardiography; Female; Fibrin; Heart Failure; Heart Rate; Heart Valve Prosthesis; Humans; Mitral Valve; Postoperative Complications; Prosthesis Design; Prosthesis Failure; Pulmonary Edema; Reoperation; Thrombosis

The alveolar compartment is a procoagulant antifibrinolytic environment in acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS). A study was undertaken to test the hypothesis that the alveolar epithelium can initiate intra-alveolar coagulation by expressing active tissue factor (TF).. Using an in vitro cell surface TF assay and TF ELISA, the activity and production of TF in cultured alveolar epithelial (A549) cells following exposure to cytomix (tumour necrosis factor alpha, interleukin 1beta and interferon gamma) was measured. TF gene transcription was measured by semi-quantitative reverse-transcription PCR. Immunohistochemistry for TF was performed on lung sections from patients with ARDS and controls. TF protein levels were measured by ELISA in undiluted pulmonary oedema fluid from patients with ALI/ARDS and compared with control patients with hydrostatic pulmonary oedema.. TF activity, mRNA and protein levels increased in A549 cells after stimulation with cytomix. Increased TF activity was also seen in A549 cells following incubation with pulmonary oedema fluid from patients with ALI/ARDS. Immunohistochemistry for TF in human lung tissue from patients with ARDS showed prominent TF staining in alveolar epithelial cells as well as intra-alveolar macrophages and hyaline membranes. TF antigen levels in oedema fluid (median 37 113 (IQR 14 956-73 525) pg/ml) were significantly higher than in plasma (median 336 (IQR 165-669) pg/ml, p<0.001) in patients with ALI/ARDS, and TF procoagulant activity in oedema fluid was much higher than in plasma of these patients. Higher plasma levels were associated with mortality.. The alveolar epithelium is capable of modulating intra-alveolar coagulation through upregulation of TF following exposure to inflammatory stimuli and may contribute to intra-alveolar fibrin deposition in ARDS.

Topics: Blood Coagulation; Cells, Cultured; Enzyme-Linked Immunosorbent Assay; Female; Fibrin; Gene Expression; Humans; Immunohistochemistry; Male; Polymerase Chain Reaction; Pulmonary Alveoli; Pulmonary Edema; Respiratory Mucosa; RNA, Messenger; Thromboplastin

Considerable confusion exists regarding the proper classification of idiopathic eosinophilic pneumonia (IEP). Furthermore, there are no reports describing the clinicopathological differences between the various forms of eosinophilic pneumonias.. The histological findings in acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP) were examined and the clinical and radiological features were contrasted with them.. Radiologically, ground glass opacity and interlobular septal thickening were characteristic of the AEP cases, while air space consolidation was seen in all CEP cases. Histologically, interstitial oedema and fibrin deposition were prominent in the AEP cases. Type II cells were detached from the alveolar walls, although the basal lamina was predominantly intact. In CEP, in addition to cellular infiltration, there was prominent intraluminal fibrosis. Disruption of the basal lamina was observed and nests of intraluminal fibrosis were directly adjacent and connected to the alveolar walls.. An essential histological difference between AEP and CEP is the severity of basal lamina damage and the amount of subsequent intraluminal fibrosis. In AEP particularly, these findings explain the radiographical findings, as well as the rapid and complete improvement noted in such cases.

Topics: Acute Disease; Adolescent; Adult; Aged; Basement Membrane; Biopsy; Bronchoalveolar Lavage; Chronic Disease; Female; Fibrin; Humans; Lung; Male; Middle Aged; Pulmonary Alveoli; Pulmonary Edema; Pulmonary Eosinophilia; Pulmonary Fibrosis; Radiography, Thoracic; Retrospective Studies; Tomography, X-Ray Computed

The present study was undertaken to evaluate possible roles of L-glutamate ionotropic receptors in neurogenic pulmonary edema. Perfusion of L-glutamate into the fourth ventricles of rats increased nitric oxide (NO) signals in the efflux solution concentration-dependently, significantly reducing both the occurrence and severity of neurogenic pulmonary edema. This effect was completely reversed by prior intracisternal injection of an NO synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), or an N-methyl-D-aspartate (NMDA) receptor antagonist, dizocilpine maleate (MK-801), and partially by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a 2-amino-3-hydroxy-5-methyl-4-isoxazol propionic acid (AMPA)/kainic acid receptor antagonist. Administration of MK-801 or CNQX alone, without L-glutamate, almost completely prevented neurogenic pulmonary edema development. These results suggest that endogenous L-glutamate may facilitate underlining disease process, whereas L-glutamate exogenously applied into the fourth ventricle may have an inhibitory action via release of NO, through ionotropic receptors.

Topics: 6-Cyano-7-nitroquinoxaline-2,3-dione; Animals; Blood Pressure; Blood Proteins; Body Fluids; Dizocilpine Maleate; Dose-Response Relationship, Drug; Excitatory Amino Acid Agonists; Excitatory Amino Acid Antagonists; Fibrin; Fourth Ventricle; Glutamic Acid; Heart Rate; Male; N-Methylaspartate; NG-Nitroarginine Methyl Ester; Nitric Oxide; Proteins; Pulmonary Edema; Rats; Rats, Wistar; Receptors, Glutamate; Vagus Nerve

The alveolar fibrinolytic system is altered in acute lung injury (ALI). Levels of the fibrinolytic protease inhibitor, plasminogen activator inhibitor-1 (PAI-1), are too low in bronchoalveolar lavage to address its prognostic significance. This study was performed to assess whether PAI-1 antigen in undiluted pulmonary edema fluid levels can identify patients with ALI and predict their outcome. PAI-1 antigen levels in both plasma and edema fluid were higher in ALI compared with hydrostatic edema, and edema fluid PAI-1 values identified those with ALI with high sensitivity and specificity. Both the high plasma and edema fluid PAI-1 antigen values were associated with a higher mortality rate and fewer days of unassisted ventilation in patients with ALI. Differences in PAI-1 activity were concordant with levels of PAI-1 antigen. Although the fibrin-derived alveolar D-dimer levels were strikingly similar in both groups, ALI patients had a higher relative proportion of D-monomer. In conclusion, PAI-1 levels in edema fluid and plasma identify those with ALI that have a poor prognosis. The data indicate that fibrin turnover in early ALI is a consequence of a rapid fibrinogen influx and fractional fibrinolytic inhibition.

Topics: Acute Disease; Adult; Aged; Enzyme-Linked Immunosorbent Assay; Extravascular Lung Water; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Humans; Hydrostatic Pressure; Male; Middle Aged; Plasminogen Activator Inhibitor 1; Predictive Value of Tests; Prognosis; Pulmonary Edema; Sepsis

In the course of investigations on mechanisms underlying development of neurogenic pulmonary edema (NPE), we have evaluated effects of nitric oxide (NO) in the central nervous system on incidence and severity in the fibrin-induced pulmonary edema model. Rats left-unilaterally vagotomized 1, 2 and 4 weeks before injections of fibrinogen and thrombin into the cisterna magna, after cutting the right vagus nerve, grouped as LVIW, LV2W or LV4W, respectively. The brain NO synthase (NOS) mRNA level in the left medulla oblongata was elevated in the LV2W group, compared to the control, but decreased in the LV4W rats. Incidences of pulmonary edema were 100% in the control group, decreasing to 78% in LV1W group, 17% in LV2W group, and back to 72% in LV4W group. The lung water ratio, a parameter of severity, demonstrated a similar pattern of change as the incidence. The lowered incidence and severity obtained in the LV2W group were reversed by intracisternal injection of N-nitro-L-arginine methyl ester (L-NAME). From these results, we propose that an increase in nitric oxide, possibly in the nucleus tractus solitarius 2 weeks after left vagotomy, may have an inhibitory action on the development of neurogenic pulmonary edema in rats.

Topics: Animals; Drug Administration Schedule; Fibrin; Injections, Intraperitoneal; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide Synthase; Pulmonary Edema; Rats; Rats, Wistar; RNA, Messenger; Severity of Illness Index; Solitary Nucleus; Vagotomy

In order to find some treatments for respiratory failure caused by pulmonary edema, we investigated the mechanism of neurogenic pulmonary edema. Previously, stimulation of sympathetic nerves caused an increase in pulmonary vascular permeability, possibly due to neuropeptide Y. Neuropeptide Y injected into the trachea increased lung vascular permeability dose-dependently, the ED50 of which was 0.3-1 nM. Such an effect remained even after treatment with reserpine, as well as in the presence of alpha- and beta-blockers. And norepinephrine enhanced the effect of neuropeptide Y on lung vascular permeability. These responses were almost similar to those obtained by stimulation of sympathetic nerves. Furthermore, neuropeptide Y, in fibrin-induced pulmonary edema, was localized in alveolar macrophages and alveolar spaces, amounting to approximately 200 nM in edema fluid. The value was significantly greater than that obtained in hydrostatic pulmonary edema by 10-30 times. Peptide YY, an analogue of neuropeptide Y, had no action on lung vascular permeability, whereas the effect of neuropeptide Y was inhibited by pretreatment with neuropeptide Y- 13-36, an antagonist for Y3-recetor subtype. These results suggested that neuropeptide Y enhances the lung vascular permeability via Y3-recetor subtype. Neuropeptide Y- 13-36, in fibrin-induced pulmonary edema, decreased a ratio of protein concentration in edema fluid to that in serum, indicating that neuropeptide Y actually acts a role in the development of neurogenic pulmonary edema, via an increase in lung vascular permeability.

Topics: Adrenergic alpha-Antagonists; Adrenergic beta-Antagonists; Adrenergic Uptake Inhibitors; Animals; Capillary Permeability; Dose-Response Relationship, Drug; Fibrin; Neuropeptide Y; Norepinephrine; Peptide YY; Pulmonary Circulation; Pulmonary Edema; Rats; Receptors, Neuropeptide; Reserpine; Respiratory Insufficiency

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.

Topics: Analysis of Variance; Animals; Blood Pressure; Capillary Permeability; Female; Fibrin; Fibrinogen; Hemodynamics; Hypertension, Pulmonary; Male; Pulmonary Edema; Rabbits; Thrombin; Vagotomy; Vagus Nerve

Experimental pneumonia caused by Pasteurella haemolytica was induced in 2-week-old gnotobiotic (n = 4) and conventional (n = 6) calves by endobronchial inoculation into the right caudal lung lobe of 7.9 x 10(10) +/- 0.6 x 10(10) (mean +/- SD) colony-forming units of P haemolytica in the 6-hour log phase of growth. The calves were studied for 24 hours or less. Regression lines for the relationship between clinical index and time for the gnotobiotic group and conventional group of calves were compared, and the clinical index was found to be significantly (P less than or equal to 0.005) more rapid in the gnotobiotic group. There was also a significant difference in the preinoculation, absolute segmented neutrophil count (P less than or equal to 0.05), and in the total serum protein, albumin, and globulin values (P less than or equal to 0.05). Comparison of the preinoculation and post inoculation blood cell and blood chemical values revealed a significant increase (P less than or equal to 0.05) in the numbers of band neutrophils and fibrinogen in conventional calves, and a significant decrease (P less than or equal to 0.05) in the total WBC count in gnotobiotic calves. Necropsy of both groups of calves revealed a circular to oblong lesion that was congested, edematous, and firm, and which occupied 20% to 100% of the right caudal lung lobe and involved the remaining lung lobes to a more minor degree. When mean lesion scores of the 2 groups of calves were compared, no significant difference (P less than or equal to 0.05) was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Cattle; Cattle Diseases; Female; Fibrin; Germ-Free Life; Lung Diseases; Male; Pasteurella; Pasteurellosis, Pneumonic; Pulmonary Edema; Time Factors

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.

Topics: Animals; Blood Pressure; Calcitonin Gene-Related Peptide; Capsaicin; Extracellular Space; Fibrin; Heart Rate; Lung; Male; Neuropeptides; Pulmonary Edema; Rats; Rats, Inbred Strains; Substance P; Vagotomy; Vagus Nerve

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.

Topics: Anesthesia; Animals; Body Water; Female; Fibrin; Hydrogen-Ion Concentration; Male; Proteins; Pulmonary Edema; Rats; Vagotomy; Vagus Nerve

Blood coagulation, fibrinolysis, and arterial blood gases were examined in 66 nonacclimatized mountaineers at 4,557 m. Subjects were classified according to a clinical score as healthy (n = 25), having mild acute mountain sickness (AMS) (n = 24), showing severe AMS (n = 13), and suffering from high-altitude pulmonary edema (HAPE) (n = 4). Coagulation times, euglobulin lysis time, and fibrin(ogen) fragment E were normal in all groups without significant changes. Fibrinopeptide A (FPA), a molecular marker of in vivo fibrin formation, was elevated in HAPE to 4.2 +/- 2.7 ng/ml (P less than 0.0001) compared with the other groups showing mean values between 1.6 +/- 0.4 and 1.8 +/- 0.7 ng/ml. FPA was normal in one patient with HAPE, however. Severe AMS was accompanied by a significant decrease in arterial PO2 due to an increase in alveolar-arterial O2 difference, whereas arterial PCO2 did not change significantly. We conclude that activation of blood coagulation is not involved in the pathogenesis of AMS and the impairment of gas exchange in this disease. Fibrin generation occurring in HAPE is probably an epiphenomenon of edema formation.

Topics: Adult; Altitude Sickness; Arteries; Blood Coagulation; Blood Gas Analysis; Female; Fibrin; Humans; Hypoxia; Male; Pulmonary Edema

We studied the effects of crystalloid (75 ml/kg of Ringer's lactate) or colloid (6% dextran-70, 6% hydroxyethyl starch, or 25 ml/kg of 5% human serum albumin) fluid infusions or no treatment (control) on the calculated lung capillary (Pc)-plasma oncotic pressure (pi c) gradient and pulmonary edema. Two sets of mongrel dogs were studied: uninjured (n = 25; 14 to 22 kg) and pulmonary fibrin-microembolized (n = 25; 15 to 23 kg). In both sets of experiments, left atrial pressure was controlled (15 mm Hg) throughout the 4-h plus experimental period. In the uninjured set, the Pc-pi c gradient averaged +1.0 and -0.2 mm Hg in the hydroxyethyl starch and dextran groups, +0.7 and +2.3 mm Hg in the human serum albumin and control groups, and +6.2 mm Hg in the Ringer's lactate group. In the fibrin-microembolized group, this gradient averaged 2.6, 2.4, 3.0, 5.3, and 9.5, respectively. The extravascular lung water to bloodless dry lung wet weight ratios in the no-fluid treatment group of the uninjured and microembolism groups with increased pressure (3.8 +/- 0.3 to 4.1 +/- 0.4 [SEM]; NS) are consistent with interstitial or perivascular edema. There were, however, no significant differences noted between the respective control groups or any fluid treatment group in either set of experiments. These data support the view that infusion of either colloid or crystalloid solutions in normal or pulmonary fibrin-microembolized lungs does not produce sufficient change in the Pc-pi c gradient to elevate edemagenesis when pulmonary capillary pressure is limited to 22 mm Hg in dogs.

Topics: Animals; Blood Gas Analysis; Body Water; Colloids; Crystallization; Dogs; Fibrin; Fluid Therapy; Hemodynamics; Isotonic Solutions; Lung; Pulmonary Artery; Pulmonary Edema; Pulmonary Embolism; Ringer's Lactate; Solutions

We perfused the isolated dog lung lobe with a 6% dextran (mol wt 60,000-90,000) balanced salt solution to determine the importance of blood components in lung fluid balance following injury with oleic acid (OA). The ventilated lower left lobe (LLL) was perfused at constant vascular pressure and weighed continuously as an index of transvascular fluid exchange. Each LLL was washed out with at least 600 ml of perfusate before recirculation started. All LLLs perfused with 6% dextran ion solution (group I) rapidly developed a permeability edema. The addition of 10% serum (vol/vol) from the lobe donor to the 6% dextran ion solution greatly improved LLL stability. One group of dextran-serum perfused LLLs (group II, n = 6, control) was infused with 2.0 ml normal saline; a second group (group III; n = 5) was given 45 microliters/kg body wt OA. Group II showed a linear rate of weight gain that averaged 7.9 g X h-1 X 100 g-1 over 3 h compared with an average rate of 249 g X h-1 X 100 g-1 in group III. In contrast to no change in group II, group III exhibited a decline in PO2 (P less than 0.05), and lobar compliance (P less than 0.05) and airway fluid was evident in all lobes by 0.5 h after infusion. The wet-to-dry weight ratio was higher in group III than group II. In the near absence of blood, massive edema developed rapidly following OA. Thus normal blood components, such as platelets, leukocytes, and fibrin do not appear to be essential mediators of OA-induced permeability edema. OA appears to increase vascular permeability either by injuring the lung directly or by releasing mediators endogenous to lung tissue.

Topics: Animals; Blood Platelets; Capillary Permeability; Dextrans; Dogs; Female; Fibrin; Leukocytes; Male; Oleic Acids; Perfusion; Pulmonary Edema; Sodium Chloride

Microembolic pulmonary oedema was induced by injection of thrombin (500 NIH units/kg body weight) i.v. in rats in which fibrinolysis had been inhibited by pretreatment with trans-4-aminomethyl-cyclohexanoid-carboxylic acid (AMCA). To evaluate the role of serotonin in this condition the effect of pretreatment with the antiserotonin compound methysergide (2.5 mg/kg body weight) on the amount of pulmonary oedema was studied. Pretreatment with methysergide resulted in a 20% decrease in lung weight in thrombin-treated rats. It caused a significant reduction of dilated lymph vessels, and of interstitial and alveolar oedema, as evaluated morphometrically. Methysergide pretreatment did not significantly alter the number of degranulated mast cells. Antiserotonin is thought to exert its effect by lowering the filtration pressure in the pulmonary microcirculation.

Topics: Animals; Fibrin; Male; Methysergide; Premedication; Pulmonary Edema; Rats; Rats, Inbred Strains; Serotonin Antagonists; Skin; Thrombin

Topics: Animals; Blood Pressure; Dogs; Fibrin; Humans; Models, Biological; Molecular Weight; Peptides; Pulmonary Edema; Pulmonary Embolism; Rats; Respiratory Insufficiency

Topics: Animals; Disseminated Intravascular Coagulation; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinolysis; Kallikreins; Kinins; Peptidyl-Dipeptidase A; Pulmonary Edema; Rats

Topics: Animals; Body Weight; Dogs; Fibrin; Hemodynamics; Iodine Radioisotopes; Lung; Organ Size; Pulmonary Edema; Pulmonary Embolism; Time Factors; Tranexamic Acid

The authors studied the pathological aspects of the lungs in an experimental study made in dogs submitted to fat embolism. The histological aspects were of hemorrhagic edema when the lungs were fixed in the classical way as well when they were fixed inflated. The alveolar microatelectasias were only seen in lungs fixed in the classical way but not were seen in lungs fixed when inflated.

Topics: Animals; Dogs; Embolism, Fat; Fatty Acids, Unsaturated; Fibrin; Lipids; Lung; Male; Oleic Acids; Pulmonary Alveoli; Pulmonary Edema; Triglycerides

Topics: Animals; Blood Coagulation; Brain; Disseminated Intravascular Coagulation; Fibrin; Haplorhini; Hematocrit; Kidney; Liver; Myocardium; Papio; Pulmonary Edema; Shock, Hemorrhagic; Shock, Septic; Spleen

Changes in the clotting system, as well as morphological and functional alterations corresponding to that of the pathologic phenomenon of disseminated intravascular coagulation (DIC) or consumption coagulopathy, were produced by thrombin infusion (550 NIH U X kg-1 X h-1) in rats and simultaneous inhibition of fibrinolysis by PAMBA (100 mg/kg). Changes in the fibrinogen level and platelet count as well as the appearances of fibrin monomers and the formation of microthrombi in several organs were evaluated. Simultaneously, the function of the respiratory system was investigated by continuous measurement of oxygen consumption as well as elasticity and water content of the lung. From the time course of the alterations in the several parameters, conclusions can be drawn for the pathogenesis and the possible therapeutic influence on DIC.

Topics: Aminobenzoates; Animals; Antifibrinolytic Agents; Blood Cell Count; Blood Platelets; Blood Vessels; Disease Models, Animal; Disseminated Intravascular Coagulation; Endothelium; Fibrin; Fibrinogen; Hemoglobins; Hemolysis; Lung; Lung Volume Measurements; Male; Pulmonary Edema; Rats; Respiration; Thrombin; Thrombosis

Administration of 0.5 mg bleomycin to mice twice weekly for 4 weeks induced pulmonary fibrosis. The initial site of injury was the intima of pulmonary arteries and veins where endothelial cells became edematous and were separated from the underlying basement membrane by large blebs. These lesions occurred after 2 weeks and were associated with infiltration of perivascular spaces by lymphocytes and plasma cells. Capillary endothelial blebbing and interstitial edema were observed after 4 weeks, when multifocal necrosis of type 1 alveolar epithelial cells was accompanied by fibrinous exudation into the alveoli. The process of repair was characterized by proliferation and metaplasia of type 2 epithelial cells, fibroblastic organization of alveolar fibrin and fibrosis of the interstitium within 8 to 12 weeks. The consistent induction of changes similar to those of diffuse pulmonary fibrosis or fibrosing alveolitis in man suggests that bleomycin-induced injury may provide a suitable model for the investigation of this ill-defined group of diseases.

Topics: Animals; Bleomycin; Capillaries; Disease Models, Animal; Endothelium; Epithelium; Exudates and Transudates; Fibrin; Fibroblasts; Lung; Lymphocytes; Metaplasia; Mice; Microscopy, Electron; Necrosis; Plasma Cells; Pulmonary Alveoli; Pulmonary Artery; Pulmonary Edema; Pulmonary Fibrosis; Pulmonary Veins

Topics: Administration, Oral; Animals; Constriction; Dyspnea; Female; Fibrin; Growth; Heart Ventricles; Hemorrhage; Hypertrophy; Inclusion Bodies; Injections, Intraperitoneal; Iron; Liver; Lung; Lymphocytes; Mast Cells; Muscle, Smooth; Organ Size; Pulmonary Artery; Pulmonary Edema; Pulmonary Veins; Pyrrolizidine Alkaloids; Rats; Time Factors

Topics: Animals; Burns; Fibrin; Fractures, Bone; Humans; Hypoxia; Lung; Microcirculation; Pulmonary Edema; Pulmonary Embolism; Wounds and Injuries

Topics: Adult; Basement Membrane; Biopsy; Collagen; Cytoplasm; Diagnosis, Differential; Epithelial Cells; Erythrocytes; Fibrin; Fluorescent Antibody Technique; Glycogen; Hemorrhage; Hemosiderin; Hemosiderosis; Humans; Leukocytes; Lung; Lung Diseases; Macrophages; Male; Microscopy, Electron; Pulmonary Alveoli; Pulmonary Edema

Topics: Animals; Biopsy; Bronchi; Cilia; Dogs; Epithelial Cells; Exudates and Transudates; Fibrin; Graft Rejection; Hemorrhage; Lung; Lung Transplantation; Methods; Microscopy, Electron; Microscopy, Electron, Scanning; Necrosis; Pulmonary Alveoli; Pulmonary Edema; Replantation; Time Factors; Transplantation, Homologous

Topics: Animals; Capillaries; Epithelium; Female; Fibrin; Lipidoses; Lung; Lymphatic System; Macrophages; Male; Necrosis; Phagocytosis; Pneumonia; Pulmonary Alveoli; Pulmonary Edema; Salmonella; Salmonella Infections; Salmonella Infections, Animal; Swine; Time Factors; Toxins, Biological

Topics: Alloxan; Animals; Autoradiography; Blood Pressure; Body Weight; Bronchi; Dogs; Exudates and Transudates; Fibrin; Heparin; Lung; Organ Size; Pulmonary Alveoli; Pulmonary Artery; Pulmonary Edema; Time Factors; Water

Topics: Animals; Biopsy; Blood Coagulation Tests; Bone and Bones; Collagen; Disease Models, Animal; Disseminated Intravascular Coagulation; Dogs; Embolism, Fat; Exudates and Transudates; Fibrin; Fractures, Bone; Hindlimb; Hypoxia; Leukocytes; Lung; Microscopy; Microscopy, Electron; Muscles; Musculoskeletal System; Pulmonary Edema; Pulmonary Embolism; Triolein

Topics: Animals; Biopsy; Dogs; Extracellular Space; Exudates and Transudates; Fibrin; Graft Rejection; Inclusion Bodies; Leukocytes; Lung; Lung Transplantation; Macrophages; Microscopy, Electron; Pulmonary Alveoli; Pulmonary Edema; Transplantation Immunology; Transplantation, Autologous; Transplantation, Homologous

Topics: Adult; Anti-Bacterial Agents; Autoimmune Diseases; Blood Viscosity; Capillaries; Cell Membrane; Fibrin; Gas Poisoning; Glucocorticoids; Humans; Hypoxia; Male; Nitrogen Dioxide; Pulmonary Edema; Shock

Topics: Adult; Biopsy; Extracellular Space; Exudates and Transudates; Female; Fibrin; Graft Rejection; Humans; Inclusion Bodies; Laparotomy; Leukocytes; Liver Neoplasms; Lung; Macrophages; Male; Microscopy, Electron; Middle Aged; Pulmonary Alveoli; Pulmonary Edema; Transplantation, Autologous; Transplantation, Homologous

Topics: Adolescent; Adult; Blood Coagulation Disorders; Bone Marrow; Brain; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Hemorrhage; Humans; Kidney Glomerulus; Leukemia, Myeloid, Acute; Liver; Lymph Nodes; Male; Middle Aged; Pulmonary Edema; Skin; Spleen

Topics: Animals; Epinephrine; Fibrin; Male; Naphthalenes; Pulmonary Alveoli; Pulmonary Edema; Rats; Rodenticides; Thiourea

Topics: Alkaloids; Animals; Basement Membrane; Capillaries; Cell Nucleus; Collagen; Cytoplasm; Cytoplasmic Granules; Endoplasmic Reticulum; Epithelium; Fibrin; Golgi Apparatus; Heterocyclic Compounds; Lipids; Lung; Macrophages; Male; Microscopy, Electron; Pulmonary Alveoli; Pulmonary Edema; Pyrroles; Rats; Ribosomes; Time Factors

Topics: Accidents, Traffic; Adolescent; Adult; Aged; Asphyxia Neonatorum; Brain Abscess; Capillaries; Child; Child, Preschool; Fibrin; Heart Arrest; Heart Failure; Humans; Infant; Infant, Newborn; Lung; Macrophages; Meningitis; Microcirculation; Middle Aged; Myocardial Infarction; Pancreatic Diseases; Postoperative Complications; Proteins; Pulmonary Alveoli; Pulmonary Atelectasis; Pulmonary Circulation; Pulmonary Edema; Respiration, Artificial; Respiratory Insufficiency; Shock, Traumatic; Suicide; Tetanus

Topics: Animals; Blood Proteins; Connective Tissue; Fibrin; Fibrinogen; Hypertension, Renal; Injections, Intraperitoneal; Kidney; Lung; Male; Nephrectomy; Pulmonary Edema; Rats; Renin; Sodium Chloride; Tissue Extracts

Rats were exposed to 98.5% oxygen at 765 torr for 6-72 hr. The pulmonary changes were investigated by electron microscopy and by morphometric methods. A progressive thickening of the air-blood barrier, from the normal 1.5 to 3 micro after 3 days, was due primarily to enlargement of the interstitial space by accumulation of edema which was replaced secondarily by cells and fibrin. This was accompanied by destruction of about 50% of the capillaries. Morphometric data allowed an estimate of the degree of impairment of lung function. The primary cellular damage was located in endothelial cells which underwent cytoplasmic changes and, finally, fragmentation. In contrast, the damage to the epithelial lining of alveoli was relatively scarce compared to the extensive endothelial changes. This pertained even to severely damaged lungs with 65% of the alveoli obliterated by a heterogeneous exudate. Possible causes for this apparently different reaction of epithelium (the first target cell) and endothelium to toxic oxygen effects are discussed.

Topics: Animals; Capillaries; Connective Tissue; Epithelium; Exudates and Transudates; Fibrin; Hyperbaric Oxygenation; Lung; Male; Microscopy, Electron; Pulmonary Alveoli; Pulmonary Edema; Rats

Topics: Animals; Blood Vessels; Carbon; Epinephrine; Fibrin; Pulmonary Edema; Quaternary Ammonium Compounds; Rats; Thiourea

Topics: Fibrin; Hypertension; Lung; Pressure; Pulmonary Edema; Thrombin; Vasoconstriction; Vasodilation

Topics: Fibrin; Humans; Lung; Lung Diseases; Pulmonary Edema; Sympathetic Nervous System