Hemorrhagic Pulmonary Edema Research Articles

Participation of regional sympathetic outflows in the centrogenic pulmonary pathology.

In anesthetized and vagotomized rats, a mechanical cerebral compression (CC) evoked systemic arterial hypertension (SAH) and pulmonary venous hypertension (PVH) followed by massive pulmonary hemorrhagic edema (PHE). The hemodynamic and pulmonary changes induced by CC were more pronounced in the right heart bypass (RHB) preparation (venous return to reservoir and constant pulmonary inflow). Additional observations in RHB included a marked reduction in reservoir volume (RV) without significant change in pulmonary vascular resistance (PVR). In either natural circulation or RHB, an upper thoracic sympathectomy did not affect the SAH, RV reduction, and PVR change, but reduced the PVH and PHE by approximately one-third. Such effects were not attributed to cardiac denervation, because beta 1-adrenergic blockade (metaprolol) did not alter the CC-induced PHE. Splanchnic denervation greatly diminished the SAH and prevented the RV reduction, PVH, and PHE. The results suggest that the centrogenic PHE is initiated from an intense arteriolar constriction, principally in the splanchnic beds. The latter causes left heart failure leading to volume and pressure loading and blood loss in the lungs. Direct sympathetic impulses to the lungs do not affect the PVR and RV changes and are not essential for the genesis of PHE. However, they may alter the vascular compliance and thereby exacerbate the PVH and PHE when passive accumulation of blood is produced in the lungs.

Toxic effects in mouse and rat of rubescenslysin from Amanita rubescens

Rubescenslysin, a protein derived from the edible fungus Amanita rubescens (Persoon ex Fries) Gray, has a direct cytolytic action. When given i.v. it is highly toxic: the ld 50 was 153 (119–197) haemolytic units (HU)/kg for rats and 312 (281–326) HU/kg for mice, equivalent to approximately 0·15 or 0·31 mg protein/kg, respectively. Poisoning was characterized by intravascular haemolysis, massive exudation of plasma with alveolar obstruction due to an increase in vascular permeability, cardiotoxicity and central nervous effects. Which of these phenomena predominated depended on the survival time, i.e. the dose and the rate of administration of the toxin. After large doses (600 HU/kg mouse) death ensued in as short a time as 10–15 sec and was accompanied by seizures. Doses in the region of the ld 50 or somewhat higher (300–400 HU/kg mouse or 200 HU/kg rat) killed mice in 30 sec to 60 min and rats in 7–15 min. Massive haemolysis and plasma exudation dominated the clinical picture and determined the biochemical, macroscopic and histological findings. Death resulted from noncardiac, haemorrhagic pulmonary oedema. The cardiac effects were relatively inconspicuous. Sublethal doses caused intravascular haemolysis of mild degree; haematuria being the most striking symptom.

Toxic effects of methylcyclopentadienyl manganese tricarbonyl (MMT) in rats: Role of metabolism

The toxicity of methylcyclopentadienyl manganese tricarbonyl (MMT) has been investigated in relation to its in vivo biotransformation in the rat. The LD 50 dose of MMT was found to be 50 mg/kg for oral administration and 23 mg/kg for ip administration. Death appeared to be caused by severe pulmonary hemorrhagic edema. Histological studies of MMT-treated animals revealed pathologic changes in lungs, liver, and kidney. Phenobarbital pretreatment protected rats from the lethal effects of 2.5 times the LD 50 dose of MMT, it shifted the site of tissue injury from the lungs to the liver, and it caused a doubling of the rate of biliary excretion of MMT metabolites. The possibility is discussed that MMT per se is toxic without bioactivation, and that the protective effect of phenobarbital pretreatment is due to a first-pass effect preventing toxic concentrations of orally administered MMT from reaching the systemic circulation.

Centrogenic pulmonary hemorrhagic edema induced by cerebral compression in rats. Mechanism of volume and pressure loading in the pulmonary circulation.

rats. Mechanism of volume and pressure loading in the pulmonary circulation Centrogenic pulmonary hemorrhagic edema induced by cerebral compression in 1524-4571 Copyright © 1980 American Heart Association. All rights reserved. Print ISSN: 0009-7330. Online ISSN: TX 72514 Circulation Research is published by the American Heart Association. 7272 Greenville Avenue, Dallas, 1980, 47:366-373 Circulation Research http://circres.ahajournals.org/content/47/3/366.citation located on the World Wide Web at: The online version of this article, along with updated information and services, is

Influence of cardiac output on intrapulmonary shunt

The effect of changing cardiac output on intrapulmonary shunt was studied in the setting of hemorrhagic pulmonary edema induced by intravenous oleic acid in 17 alpha-chloralose-anesthetized dogs. The dogs were mechanically ventilated and cardiac output was alternately depressed and augmented using either pharmacologic means or mechanical alteration of venous return. Following oleic acid, the measured ventilation-perfusion distributions, as measured by the multiple inert gas elimination technique, demonstrated a two-compartment blood flow distribution consisting of shunt and normal units. Changes in cardiac output were not associated with change in the shape of the distributions but there was a significant linear correlation between the level of cardiac output and the shunt fraction. The shunt fraction also varied directly with the mixed venous partial oxygen pressure and inversely with the pulmonary vascular resistance. These data suggest that shunt and nonshunt vessels behave differently in response to alterations of blood flow and emphasize that any interpretation of changes in shunt in the setting of diffuse lung injury must be interpreted in light of changes in cardiac output.

EFFECTS OF POSITIVE END-EXPIRATORY PRESSURE ON GAS EXCHANGE IN DOGS WITH NORMAL AND EDEMATOUS LUNGS

The effects of positive end-expiratory pressure (PEEP) at 5, 10, 15, and 20 cm H2O on the distribution of ventilation-perfusion (VA/Q) ratios was determined in four normal dogs and in ten with oleic acid-induced acute hemorrhagic pulmonary edema. Tidal volume and frequency were held constant at all times with mechanical ventilation during intravenous pentobarbital and gallamine anesthesia. Normal dogs had little or no shunt, and no areas of low (less than 0.1) or high VA/Q (greater than 10.0) at zero end-expiratory pressure (intermittent positive-pressure breathing). In these animals increasing PEEP caused progressive depression of cardiac output, associated with an increase in ventilation to both high VA/Q and unperfused regions. PEEP greater than or equal to 10 cm H2O resulted in a reduction in Pao2 and an increase in PaCO2. In dogs with pulmonary edema, PEEP's of 5 and 10 cm H2O resulted in dramatic reductions in shunt, virtual obliteration of low VA/Q regions, and market improvement in Pao2. However, at 15 and 20 cm H2O PEEP's high VA/Q and dead space ventilation with CO2 retention again developed in all but the most severely affected (shunt greater than 40%) dogs.

Continuous positive pressure ventilation in children with bronchopneumonia

The application of a small end-expiratory pressure of 5 cmH2O to the assisted ventilation of nineteen children (mean age 19 months) with bronchopneumonia was compared with intermittent positive pressure ventilation. Within 1 h of introducing continuous positive pressure ventilation the alveolar-to-arterial oxygen gradient was reduced in most patients, with an increase in functional residual capacity and a decrease in total pulmonary blood shunt. Physiological dead space was also reduced, a feature not observed in other studies, and the significance of this finding is discussed. The use of continuous positive pressure ventilation in broncho-pulmonary infection was shown to be effective even at small pressures, and can be recommended especially for patients requiring long-term ventilation.

Experimental neurogenic pulmonary edema in cats.

Hemorrhagic pulmonary edema was produced consistently in 19 of 20 anesthetized, paralyzed, ventilated cats when intracranial pressure (ICP) was raised for 30 minutes by intraventricular infusion of mock CSF to 150 mm Hg in 14, or 200 mm Hg in six. However, under identical conditions, except that ICP was raised to only 100 mm Hg, three of seven animals did not develop hemorrhagic edema of the lungs and the remaining four had spotty hemorrhage. Thirteen control animals with normal ICP had normal lungs. Gravimetric lung water analysis by Pearce's method confirmed gross and microscopic appearance of hemorrhagic pulmonary edema. Extravascular lung water (p less than 0.05) and lung blood (p less than 0.05) were significantly greater than control values when ICP was raised to or exceeded 150 mm Hg. Despite hemorrhagic edema, pulmonary gas exchange (O2, CO2) remained unaffected. This animal model allows quantitative measurement of neurogenically-mediated hemorrhagic edema of the lungs before gas exchange is impaired. The model may facilitate clarification of the pathogenesis of neurogenic pulmonary edema and, consequently, refine evaluation of therapy.

Physiologic and morphologic observations of the effects of intravenous elastase on the lung.

Intravenous administration of porcine pancreatic elastase to hamsters produced significant loss of elastic recoil at low volumes. Histology and mean linear intercept of the lungs fixed at a pressure of 20 cm H2O and studied for 3 weeks after administration of elastase were normal. Larger doses of elastase caused immediate fatal, hemorrhagic pulmonary edema. These results confirmed previous morphologic observations of the effects of intravenously administered elastase, but demonstrated that the loss of elastic recoil at low lung volumes is not invariably associated with histologic changes or morphologically with loss of elastin fibers. These observations suggest that submicroscopic lesions may be present and may antedate the earliest morphologic evidence of emphysema and aging in the lung.

Effects of Positive End-expiratory Pressure on Gas Exchange in Dogs with Normal and Edematous Lungs

The effects of positive end-expiratory pressure (PEEP) at 5, 10, 15, and 20 cm H2O on the distribution of ventilation-perfusion (VA/Q) ratios was determined in four normal dogs and in ten with oleic acid-induced acute hemorrhagic pulmonary edema. Tidal volume and frequency were held constant at all times with mechanical ventilation during intravenous pentobarbital and gallamine anesthesia. Normal dogs had little or no shunt, and no areas of low (less than 0.1) or high VA/Q (greater than 10.0) at zero end-expiratory pressure (intermittent positive-pressure breathing). In these animals increasing PEEP caused progressive depression of cardiac output, associated with an increase in ventilation to both high VA/Q and unperfused regions. PEEP greater than or equal to 10 cm H2O resulted in a reduction in Pao2 and an increase in PaCO2. In dogs with pulmonary edema, PEEP's of 5 and 10 cm H2O resulted in dramatic reductions in shunt, virtual obliteration of low VA/Q regions, and market improvement in Pao2. However, at 15 and 20 cm H2O PEEP's high VA/Q and dead space ventilation with CO2 retention again developed in all but the most severely affected (shunt greater than 40%) dogs.

Haemorrhagic pulmonary oedema: post-pulmonary embolectomy.

A case of haemorrhagic pulmonary oedema after successful pulmonary embolectomy is presented. The relevant literature is reviewed. Thirteen cases are analysed as well as the four survivors. The aetiology appears to be ischaemic damage of the capillary bed. This had previously been called incomplete infarction by Castleman. The incidence is low after acute pulmonary embolectomies but appears to be much higher after chronic endarterectomies, especially with severe pulmonary hypertension. Therapy is outlined.

Pulmonary insufficiency induced by oleic acid in the sheep: A model for investigation of extracorporeal oxygenation

Most previous studies of the efficiency of bypass techniques for respiratory support have been conducted in hypoxic but otherwise normal animals. However, mechanisms of improved oxygenation by partial venoarterial bypass in the presence of acute respiratory insufficiency can be better studied with an appropriate pathophysiologic model; for this purpose, acute hemorrhagic pulmonary edema was induced in sheep by injection of oleic acid into the right atrium. The model presented a 3 hour period of elevated pulmonary shunting with stable hemodynamics. This preparation is being employed to the study of the mechanisms of extracorporeal oxygenation.

Bacterial growth in vivo. An important determinant of the pulmonary clearance of Diplococcus pneumoniae in rats.

Lung clearance of Diplococcus pneumoniae was markedly reduced in rats with acute hemorrhagic pulmonary edema produced by instillation of hydrochloric acid. Bacterial clearance was enhanced in both control and acid-instilled animals by pretreatment with a bacteriostatic antibiotic, tetracycline, 30 mg/kg. From these data the contributions of bacterial multiplication and bacterial elimination to net lung bacterial clearance were estimated. In control animals the constant for exponential bacterial elimination was -1.4283 (fractional clearance = 76% per h), and the doubling time for the pneumococcus was 170 min. In acid-instilled rats the elimination constant was -0.5336 (fractional clearance = 41% per h), and the doubling time of the pneumococcus was 47 min, approximating the doubling time of 42 min observed with pneumococci grown in broth. These results indicate that, in the case of pneumococci, both bacterial elimination and bacterial growth contribute to lung bacterial clearance in normal animals as well as animals with damaged lungs. In the present study changes in both parameters were required to explain the observed results in acid-instilled animals. The pulmonary pathogenicity of some bacterial species may be determined by their capacity for growth in the lung, since infection of the lung occurs when bacterial multiplication exceeds the rate of elimination of viable organisms.

Effect of increased intracranial pressure on pulmonary vascular resistance.

ARTICLESEffect of increased intracranial pressure on pulmonary vascular resistanceT. C. Lloyd JrT. C. Lloyd JrPublished Online:01 Sep 1973https://doi.org/10.1152/jappl.1973.35.3.332MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByNeurogenic Pulmonary EdemaNeurologic Clinics, Vol. 11, No. 2Vasopressor responses and hypoxemia with acutely increased intracranial pressureLife Sciences, Vol. 38, No. 19Mechanisms of neurogenic pulmonary edema.Circulation Research, Vol. 57, No. 1Effects of brain hypoxia on pulmonary hemodynamicsJournal of Surgical Research, Vol. 35, No. 1Centrogenic pulmonary hemorrhagic edema induced by cerebral compression in rats. Mechanism of volume and pressure loading in the pulmonary circulation.Circulation Research, Vol. 47, No. 3 More from this issue > Volume 35Issue 3September 1973Pages 332-335 Copyright & PermissionsCopyright © 1973 the American Physiological Societyhttps://doi.org/10.1152/jappl.1973.35.3.332PubMed4732325History Published online 1 September 1973 Published in print 1 September 1973 Metrics

Acute promyelocytic leukemia with disseminated intravascular coagulation.

Three patients with acute promyelocytic leukemia, all of whom had rapidly fatal downhill courses associated with marked bleeding tendencies, are described. Two of the three patients had hypofibrinogenemia. At autopsy, all patients had extensive hemorrhage involving internal organs, including the heart, liver, spleen, kidneys and brain. Massive hemorrhagic pulmonary edema was found in two patients. Striking leukemic involvement of the bone marrow was found, but only minimal to mild involvement of the spleen, liver, and lymph glands was evident. In addition, in all three cases autopsy disclosed evidence of disseminated intravascular clotting in small blood vessels. The significance of this finding in relation to the hypofibrinogenemia and bleeding phenomena encountered is discussed. This finding provides further support in favor of consumption (defibrination) as the cause of the bleeding diathesis in this disease.

Alterations in Pulmonary Microanatomy after Fat Embolism: In Vivo Observations via Thoracic Window of the Oleic Acid-embolized Canine Lung

This study was designed to view directly via a thoracic window implanted in living dogs the alterations in lung microanatomy induced by oleic acid in the pulmonary circulation. Time-lapse cinemicrography was employed to record the dynamic evolution of events. Observations in ten dogs indicate that contact of oleic acid with vascular endothelium produces a toxic vasculitis and consequent “leaky vessel syndrome.” The resultant hemorrhagic pulmonary edema forms the basis for many of the arterial blood gas, hemodynamic and pathoanatomical derangements noted in this animal model of pulmonary fat embolism.

Nitrogen Dioxide—The New "Yellow Peril"

Oxides of nitrogen are a by-product of combustion in a number of industrial processes and may be formed in agricultural procedures, such as the ensilage of corn. A major emitter is the automobile internal combustion engine, and oxides of nitrogen from this source are major components of smog. Colorless nitric oxide reacts with oxygen in the air to form yellow-brown nitrogen dioxide, a gas which in appropriate concentrations reduces visibility, reacts with hydrocarbons in photochemical smog to form ozone, and is toxic to plants and animals in its own right. The biological effects on the lungs from inhalation of nitrogen dioxide have been thoroughly studied in experimental animals. 1,2 Similar lesions occur in humans subjected to accidental exposures to the gas; these include acute hemorrhagic pneumonia, pulmonary edema, and bronchiolitis fibrosa obliterans. In this issue (p 1341), Tse and Bockman describe acute and chronic pulmonary disorders in firefighters after exposure

Nitrogen dioxide--the new "yellow peril".

Oxides of nitrogen are a by-product of combustion in a number of industrial processes and may be formed in agricultural procedures, such as the ensilage of corn. A major emitter is the automobile internal combustion engine, and oxides of nitrogen from this source are major components of smog. Colorless nitric oxide reacts with oxygen in the air to form yellow-brown nitrogen dioxide, a gas which in appropriate concentrations reduces visibility, reacts with hydrocarbons in photochemical smog to form ozone, and is toxic to plants and animals in its own right. The biological effects on the lungs from inhalation of nitrogen dioxide have been thoroughly studied in experimental animals. 1,2 Similar lesions occur in humans subjected to accidental exposures to the gas; these include acute hemorrhagic pneumonia, pulmonary edema, and bronchiolitis fibrosa obliterans. In this issue (p 1341), Tse and Bockman describe acute and chronic pulmonary disorders in firefighters after exposure

Continuous positive-pressure breathing in acute hemorrhagic pulmonary edema

Continuous positive-pressure breathing in acute hemorrhagic pulmonary edema

Relation of pulmonary arterial pressure to pressure in the pulmonary venous system.

ArticleRelation of pulmonary arterial pressure to pressure in the pulmonary venous system.T C Lloyd Jr, and A J SchneiderT C Lloyd JrSearch for more papers by this author, and A J SchneiderSearch for more papers by this authorPublished Online:01 Oct 1969https://doi.org/10.1152/jappl.1969.27.4.489MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe efficacy of using pulmonary vein wedge pressure for the estimation of pulmonary artery pressure in children with congenital heart disease27 January 2003 | Catheterization and Cardiovascular Interventions, Vol. 58, No. 2The Pathophysiology of Pulmonary Vascular Disease Associated with Congenital Cardiac LesionsPulmonary lymphatic flow alterations during intracranial hypertension in sheepAnnals of Neurology, Vol. 15, No. 2Experimental neurogenic pulmonary edemaJournal of Neurosurgery, Vol. 54, No. 5An analysis of the pulsatile hemodynamic responses of the pulmonary circulation to acute and chronic pulmonary venous hypertension in the awake dog.Circulation Research, Vol. 47, No. 6Centrogenic pulmonary hemorrhagic edema induced by cerebral compression in rats. Mechanism of volume and pressure loading in the pulmonary circulation.Circulation Research, Vol. 47, No. 3Supravalvular mitral stenosis associated with tetralogy of FallotThe American Journal of Cardiology, Vol. 37, No. 1Variations in pulmonary gas exchange due to changes in pulmonary artery pressure and flowJournal of Surgical Research, Vol. 18, No. 4Comparison of pulmonary artery and pulmonary venous wedge pressure in congenital heart disease.Heart, Vol. 35, No. 4Pulmonary Hypertension in Disorders of the Left Heart Observations in a Catheterization Material8 July 2009 | Scandinavian Journal of Clinical and Laboratory Investigation, Vol. 31, No. 4Hemodynamic effects of isoproterenol on the pulmonary and systemic circulations in dogsPfl�gers Archiv European Journal of Physiology, Vol. 322, No. 4Anomalous Systemic Arterial Supply to the Lung Causing Pulmonary-Artery HypertensionNew England Journal of Medicine, Vol. 283, No. 20 More from this issue > Volume 27Issue 4October 1969Pages 489-97 https://doi.org/10.1152/jappl.1969.27.4.489PubMed4390411History Published online 1 October 1969 Published in print 1 October 1969 Metrics