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At least 937 records · Page 52Linked to original sources
PubMed1989

Human recombinant lipocortin 1 has acute local anti-inflammatory properties in the rat paw edema test.

Human recombinant lipocortin 1 has been tested for anti-inflammatory activity in a conventional model of acute inflammation. Microgram amounts of the protein, locally administered, inhibited edema of the rat paw when induced by subplantar injections of carrageenin: the ED50 was 10-20 micrograms per paw, and inhibition (maximum of 60-70%) was not dependent upon an intact adrenal cortex. Doses of lipocortin that produced approximately 50% inhibition in the carrageenin test were inactive against edema elicited by bradykinin, serotonin, platelet-activating factor-acether, or dextran, whereas edema caused by Naja mocambique venom phospholipase A2 was strongly inhibited by lipocortin. The protein inhibited edema when rats were pretreated with agents that depleted mast-cell amines, kininogen, or polymorphonuclear leukocytes prior to initiation of the carrageenin edema but had no inhibitory action when rats were pretreated with the dual cyclooxygenase/lipoxygenase inhibitor BW 755C. These results demonstrate that human recombinant lipocortin has potent local anti-inflammatory activity, probably through selectively interfering with eicosanoid generation. Lipocortin is relatively ineffective against edema caused by mast-cell degranulation or kinins, except when degranulation is caused by phospholipase A2.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed2001

Infrared micropulsed laser treatment for diabetic macular edema--subthreshold versus threshold lesions.

PURPOSE: To assess the effectiveness of subthreshold (invisible after placement) and threshold (barely visible after placement) 810nm laser photocoagulation in the treatment of clinically significant diabetic macular edema. METHODS: A grid of subthreshold laser spots was used to treat patients with diabetic edema. Retrospectively, the results of treatment of 20 eyes of 20 patients were compared to the results of treatment of 120 eyes of 120 patients using a grid of threshold laser lesions. RESULTS: At six months, 60% of subthreshold treated eyes and 75% of threshold treated eyes showed anatomic resolution of macular edema. Improvement or stabilization of visual acuity was achieved in 85% of threshold or subthreshold treated eyes. CONCLUSION: Gentle grid treatment of regions of diabetic macular edema was effective in ameliorating the edema and limiting visual loss. Subthreshold laser was less effective in promoting resolution of edema compared to threshold lesions, though the difference was not significant in this instance.

Chi-Square Distribution↗
PubMed2003

Anti-inflammatory effect of the hydralcoholic extract of Zingiber officinale rhizomes on rat paw and skin edema.

Plant extracts have been used for centuries as a popular mode of treatment for several health disorders. Over the last ten years, the study of those extracts has attracted attention in different fields of the biological sciences. Ginger, the rhizome of Zingiber officinale Roscoe (Zingiberaceae), is a commom constituent of diet worldwide and it has been reported that its extracts present some pharmacological activities. Here we investigate the effects of the crude hydralcoholic extract of ginger rhizomes on the classical models of rat paw and skin edema. The carrageenan-, compound 48/80- or serotonin-induced rat paw edema were inhibited significantly by the intraperitoneal administration of alcoholic ginger extract. Ginger extract was also effective in inhibiting 48/80-induced rat skin edema at doses of 0.6 and 1.8 mg/site. Rat skin edema induced by substance P or bradikinin was not affected by treatment with Z. officinalle extract. The intraperitoneal administration of ginger extract (186 mg/kg(-1) body wt.) 1 h prior to serotonin injections, reduced significantly the serotonin-induced rat skin edema. Our results demonstrated that crude extract of Zingiber officinale was able to reduce rat paw and skin edema induced by carrageenan, 48/80 compound and serotonin. The antiedematogenic activity seems to be related, at least partially, to an antagonism of the serotonin receptor.

Animals↗
PubMed1983

Edema-producing activity of group A streptococcal polysaccharide and its possible role in the pathogenesis of cell wall-induced polyarthritis.

Edematous responses were induced in the limbs of Sprague-Dawley rats by intravenous, intraperitoneal, or intra-articular injections of group-specific polysaccharide (PS) isolated from the cell walls of group A streptococci. After intravenous injection of the edema-producing PS, vascular permeability increase (measured by 125I-human serum albumin) was detected in the limbs, but not in the heart, lungs, spleen, liver, thymus, kidney, skin, skeletal muscle, submandibular lymph nodes, mesenteric lymph nodes, or ascending colon. This indicates a selective effect on vascular endothelium of the joints. Evidence to suggest that the edema-producing activity of the PS might play an important role in the pathogenesis of cell wall-induced polyarthritis included the following: (a) the presence of edema-producing activity in arthropathogenic cell wall preparations; (b) cell wall preparations without edema-producing activity were significantly less active in inducing arthritis than were those which contained edema-producing activity; and (c) the addition of edema-producing PS to cell wall preparations increased both the incidence and the severity of arthritis.

Animals↗
PubMed2001

Serum progesterone levels correlate with decreased cerebral edema after traumatic brain injury in male rats.

Previous animal research suggests that progesterone may have powerful neuroprotective effects in traumatic brain injury (TBI). This experiment tested the hypothesis that progesterone levels correlate with decreased cerebral edema in male rats with bilateral medial frontal cortex injuries. Three groups of male Sprague-Dawley rats were used: injured given progesterone (4 mg/kg), injured given vehicle (oil), and uninjured controls given vehicle. Progesterone or vehicle was administered intraperitoneally at 1, 6, and 24 h postinjury. At 48 h postinjury, the rats were killed, brains extracted, and assayed for edema. Percent difference in water content of the area surrounding the lesion was compared to posterior cortex. A strong inverse relationship was found between serum progesterone levels and percent cerebral edema; the higher the progesterone levels, the lower the percent edema. Both progesterone and oil-treated animals had some edema compared to sham-operated controls. The brains of the injured animals given control solution were higher in water content than either the uninjured group or injured progesterone-treated rats 48 h postinjury. These findings confirm that progesterone significantly decreases cerebral edema after TBI in adult male subjects.

Animals↗
PubMed2005

Correlation between development of pulmonary edema and response of pulmonary metastases of metastatic melanoma and kidney cancer to high-dose continuous-infusion interleukin-2.

The administration of high-dose continuous intravenous infusion interleukin-2 (IL-2) is able to induce the presence of lymphokine-activated killer (LAK) cells. LAK are able to nonspecifically lyse tumor cells. They are also able to lyse endothelial cells, which accounts for, at least in part, the capillary leak syndrome seen as one of the toxicities with this therapy. A pulmonary manifestation of capillary leak syndrome is the presence of pulmonary edema. We postulated that capillary leak may also be a mechanism by which LAK could conceivably reach pulmonary metastases or could be a reflection of damage of endothelial cells in vasculature supplying metastases and that capillary leak syndrome may actually correlate with the response of pulmonary metastases. We examined our database of patients with lung metastases treated with high-dose continuous infusion IL-2 (18 MIU/m(2)/day for 3 days) regimens. Eighteen patients had the following characteristics: melanoma (11), renal cancer (7), median age of 67 years (range, 28-79 years), and males (15). All patients were treated by oncology nurses on either the stem cell transplant unit or oncology ward. Pulmonary edema was defined as the presence of pleural fluid on a chest X-ray, computed tomography (CT) scan, and/or as noted on a physical examination by at least 2 observers. No patients required endotracheal intubation, mechanical ventilation, or an intensive care unit transfer. The median number of cycles received was 6 (range, 1-13). All 8 responding patients (6 patients with melanoma, 2 patients with kidney cancer) manifested pulmonary edema during interleukin-2 therapy. Four patients with pulmonary edema were nonresponders. The presence of pulmonary edema correlated with the response to therapy (p = 0.01). The median duration of response of pulmonary nodules was 5 months (range, 1-16 months). There is a correlation between the development of pulmonary edema and the response of pulmonary metastases in patients with melanoma and kidney cancer treated with high-dose continuous infusion interleukin-2.

Adult↗
PubMed2000

Application of 2,3,5-triphenyltetrazolium chloride staining to evaluate injury volume after controlled cortical impact brain injury: role of brain edema in evolution of injury volume.

A reliable method for measuring injury volume after traumatic brain injury (TBI) is of great importance when studying pharmacological protective agents in the field of head trauma research. Utilization of 2,3,5-triphenyltetrazolium chloride (TTC) has gained extensive acceptance in stroke research and has recently been applied to injury volume measurement in the lateral fluid percussion model. The present study was undertaken to apply this method to the controlled cortical impact (CCI) model and to study the role of brain edema. Male Sprague-Dawley rats were subjected to CCI brain injury at a velocity of 3 m/sec and 1 mm (mild), 2 mm (moderate), and 3 mm (severe injury) deformation, while rats in the control group were subjected to the same surgical procedure but received no injury. Absolute and corrected injury volumes with TTC staining and brain edema measurements with the wet-dry method were evaluated at 1, 2, 3, 4, and 7 days after TBI. The most prominent injury volume in the moderate injury group (2 mm deformation) was seen at postinjury day 1 and 2 (day 1, absolute: 49.1+/-5.6, corrected: 40.5+/-7.9; day 2, absolute: 46+/-6.9, corrected: 40.2+/-10.5), whereas the smallest injury volume was found at postinjury day 7 (absolute: 24.9+/-7, corrected: 27.4+/-7.4). The time course of brain edema studies demonstrates that brain edema formation peaks at postinjury day 1. A statistically significant reduction of injury volume was observed after postinjury day 4. We also observed that due to the presence of brain edema absolute injury volume is more than corrected injury volume in the first 3 days after injury as opposed to injury volume at postinjury day 7. These results suggest that the measurement of injury volume with TTC staining should be corrected for brain edema in the CCI brain injury model.

Animals↗
PubMed1990

Influence of high voltage pulsed direct current on edema formation following impact injury.

Edema results in pain and may lead to reduced functional mobility. High voltage pulsed direct current (HVPC) has recently been advocated for edema control. The purpose of our study was to determine the effect of HVPC on edema formation in frogs. Hind limbs of 20 anesthetized frogs were injured by dropping a 450-g weight onto the plantar aspects of the feet. One hind limb of each frog was randomly selected to receive continuous 120-Hz HVPC at voltages 10% lower than those needed to evoke muscle contraction. Four 30-minute treatments were administered at 1.5-hour intervals beginning 10 minutes after trauma. Limb volumes were measured by water displacement. An analysis of variance for repeated measures and a Newman-Keuls post hoc test were used to determine the significance of treatment effects. The HVPC significantly (p less than .01) reduced edema formation. We hypothesize that HVPC may also be effective in controlling edema formation after impact injuries in humans. [Bettany JA, Fish DR, Mendel FC: Influence of high voltage pulsed direct current on edema formation following impact injury.

Animals↗
PubMed1992

The electrical effect of two commonly used clinical stimulators on traumatic edema in rats.

The purposes of this study were to determine the effect of electrical stimulation on traumatic rat hind-paw edema and to establish whether there would be a difference in edema reduction when two types of stimulators were used. The animals were divided into a control group (n = 15) and two experimental groups, one group receiving monophasic pulsed current (MPC group, n = 15) and the other group receiving symmetrical biphasic pulsed current (SBPC group, n = 14). The right hind-paw volume of all groups was measured prior to traumatization and at 24, 48, 72, and 96 hours posttrauma. Following the 24-, 48-, and 72-hour measurements, 1 hour of electrical stimulation was administered to the experimental groups. The control group received sham treatment. Results revealed significant edema reduction in all groups over the 96-hour period, with each group's greatest change in paw volume occurring 48 hours posttrauma. At the final paw volume measurement, there was no significant difference between the MPC and control groups or between the MPC and SBPC groups. The SBPC group, however, showed less reduction in edema than did the control group. One hour of electrical stimulation per day over 3 consecutive days failed to demonstrate significant edema reduction in either the MPC group or the SBPC group as compared with the control group. The results of this study demonstrated that the electrical stimulation characteristics and procedures currently used in the clinic do not significantly reduce extant edema caused by trauma in rat hind limbs.

Analysis of Variance↗
PubMed1998

Treatment of leg edema and wounds in a patient with severe musculoskeletal injuries.

This case report describes the application of a technique for the treatment of leg edema and wounds resulting from a severe distal tibiofibular fracture. Following injury and numerous fracture- and wound-related surgeries in the first year postinjury, this patient developed leg edema, required daily treatment of 2 leg wounds, and was unable to wear a shoe due to foot swelling. He was referred to the physical therapy clinic 1 year postinjury for ankle rehabilitation and to diminish the leg edema. Therapy consisting of manual lymph drainage, compressive bandaging, exercise, and skin care was provided for 7 weeks. A compression stocking was issued near the end of treatment, which the patient continued to wear daily thereafter. At the time of discharge from therapy, the leg edema had decreased 74% and the wound area of both wounds had decreased 89%. Improvements continued following discharge. By 10 weeks after the start of treatment, edema had decreased 80.9%, one wound had healed, and the second wound was 93% improved. The patient was able to wear a shoe and resume recreational activities. This case report provides insight into a treatment that may shorten rehabilitation and control the cost of caring for injuries complicated by prolonged edema.

Bandages↗
PubMed2004

Aquaporin-4 facilitates reabsorption of excess fluid in vasogenic brain edema.

Aquaporin-4 (AQP4) is the major water channel in the brain, expressed predominantly in astroglial cell membranes. Initial studies in AQP4-deficient mice showed reduced cellular brain edema following water intoxication and ischemic stroke. We hypothesized that AQP4 deletion would have the opposite effect (increased brain swelling) in vasogenic (noncellular) edema because of impaired removal of excess brain water through glial limitans and ependymal barriers. In support of this hypothesis, we found higher intracranial pressure (ICP, 52+/-6 vs. 26+/-3 cm H2O) and brain water content (81.2+/-0.1 vs. 80.4+/-0.1%) in AQP4-deficient mice after continuous intraparenchymal fluid infusion. In a freeze-injury model of vasogenic brain edema, AQP4-deficient mice had remarkably worse clinical outcome, higher ICP (22+/-4 vs. 9+/-1 cm H2O), and greater brain water content (80.9+/-0.1 vs. 79.4+/-0.1%). In a brain tumor edema model involving stereotactic implantation of melanoma cells, tumor growth was comparable in wild-type and AQP4-deficient mice. However, AQP4-deficient mice had higher ICP (39+/-4 vs. 19+/-5 cm H2O at seven days postimplantation) and corresponding accelerated neurological deterioration. Thus, AQP4-mediated transcellular water movement is crucial for fluid clearance in vasogenic brain edema, suggesting AQP4 activation and/or up-regulation as a novel therapeutic option in vasogenic brain edema.

Animals↗
PubMed2005

Opposing effects of isoflurane and sevoflurane on neurogenic pulmonary edema development in an animal model.

BACKGROUND: The current study was undertaken to investigate the effects of pretreatment with isoflurane and sevoflurane on the development of neurogenic pulmonary edema in an animal model. METHODS: Rats were exposed to room air (control), 1.5% isoflurane, or 2.5% sevoflurane for 4 h. They were then anesthetized with intraperitoneal injections of pentobarbital sodium, and fibrinogen and thrombin were injected into the cisterna magna to induce neurogenic pulmonary edema. RESULTS: Consecutive injections of fibrinogen and thrombin caused increases in blood pressure, with the peak values obtained in the isoflurane and sevoflurane groups being lower than the control values. The incidence of significant neurogenic pulmonary edema was 58%, 100%, and 8% in the control, isoflurane, and sevoflurane groups, respectively. The lung water ratio, an index of severity of edema, was 4.86 +/- 0.78, 6.15 +/- 0.64, and 4.40 +/- 0.32 in the control, isoflurane, and sevoflurane groups, respectively. Furthermore, immunohistochemical staining for vascular endothelial growth factor demonstrated an increase of expression in the rat lungs exposed to isoflurane. Treatment with an anti-vascular endothelial growth factor antibody during exposure to isoflurane completely inhibited the effect of isoflurane to promote neurogenic pulmonary edema in this model. CONCLUSION: Exposure to 1.5% isoflurane enhances the development of neurogenic pulmonary edema development in this animal model, most likely via release of vascular endothelial growth factor from bronchial epithelial cells, an effect not observed with sevoflurane.

Animals↗
PubMed1981

Hemodynamics of LeVeen shunt pulmonary edema.

In order to characterize the circulatory changes which may lead to pulmonary edema following the surgical placement of a LeVeen peritoneovenous shunt, intraoperative hemodynamic studies were performed on five consecutive patients without clinical evidence of cardiac disease undergoing shunt insertion. Within 30 minutes after opening the peritoneovenous shunt, there was a marked increase in pulmonary capillary wedge pressure, cardiac output, and stroke work index, and a sharp decline in both pulmonary and systemic vascular resistances. In three patients, pulmonary edema did not occur; in one patient, pulmonary edema occurred transiently but responded to furosemide administration. In these four patients, systemic vascular resistance continued to drop over the ensuing hours and the elevated pulmonary capillary wedge pressure also decreased appropriately with furosemide. The fifth patient developed persistent pulmonary edema. In this subject, systemic vascular resistance continued to rise and the elevated pulmonary capillary wedge pressure did not respond to intravenous furosemide. This study suggests that uncomplicated LeVeen peritoneovenous shunt insertion may result in a drop in systemic vascular resistance which lowers left ventricular afterload, and, thus, may protect most patients from pulmonary edema. In contrast, a continued rise in systemic vascular resistance and afterload may contribute to pulmonary edema refractory to diuretic therapy and should probably be treated with a parenteral afterload-reducing agent.

Ascites↗
PubMed1991

Phosphatic metabolism and corneal edema.

From three groups of patients with corneal edema, the degree of edema was clinically quantified prior to penetrating keratoplasty. Corneas from patients with failed grafts (n = 16) had the greatest edema (mean score 3.8 +/- 0.6 SE), corneas with Fuchs' endothelial dystrophy (n = 12) had the least edema (1.4 +/- 0.4), and corneas with aphakic and pseudophakic bullous keratopathy (n = 40) had intermediate edema (2.7 +/- 0.5). Phosphorus-31 nuclear magnetic resonance spectroscopy was used to quantitate five high-energy phosphates and nine low-energy phosphates and calculate 12 metabolic indices from the specimens of these three edematous groups. Corneas with aphakic and pseudophakic bullous keratopathy had lower alpha-glycerophosphate (alpha-GP) and glycerol 3-phosphorylethanolamine and glycerol 3-phosphorylcholine (GPE & GPC), and higher phosphocreatine (PCr), adenosine diphosphate (ADP), monoesters/diesters, PCr/Pi (phosphocreatine/inorganic orthophosphate), and PCr/ATP (phosphocreatine/adenosine triphosphate) than corneas with Fuchs' endothelial dystrophy (p less than 0.05). Corneas from failed grafts had lower alpha-GP, ethanolamine phosphate (EP), ethanolamine phosphate and choline phosphate (EP&CP), monoesters/Pi, ATP/Pi, and energy modulus, no detectable GPE and GPC, and higher Pi, phosphorylglycans (PG), PCr, ADP, diesters, PCr/Pi, and PCr/ATP than those with Fuchs' endothelial dystrophy (p less than 0.05). Corneas from failed grafts had lower ATP, monoesters/Pi, ATP/Pi, PCr/Pi, and energy modulus and higher Pi, PG, ADP, diesters, and PCr/ATP than corneas with aphakic and pseudophakic bullous keratopathy (p less than 0.05). In summary, there was increasing decline in the high-energy metabolites and energy status with increasing edema.

Adenosine Triphosphate↗
PubMedDate not supplied

First annual Herbert S. Shubin Memorial Lecture. Acute circulatory failure (shock) associated with cardiogenic pulmonary edema.

Our findings confirm that acute pulmonary edema, when caused by left ventricular failure, represents a form of acute perfusion failure (shock) with metabolic acidemia, lactacidemia, and a reduction in forward blood flow. It is associated with a marked increase in peripheral resistance and an increase in venous capacitance. Most importantly, acute pulmonary edema is associated with a reduction in the intravascular blood volume. Acute pulmonary edema is not fundamentally different from other types of shock in which the shock state is initiated by one primary defect, and during the course of its progression, other primary mechanisms are called into action. In the instance of acute cardiogenic edema, the primary defect is cardiac pump failure and the secondary defects include hypovolemia and distributive defects associated with arterial vasoconstriction and expanded venous capacitance. Furosemide reverses acute pulmonary edema by increasing rather than decreasing intravascular blood volume with consequent improvement in the distributive and hypovolemic defects. Under extreme conditions, the volume defect in acute pulmonary edema may be so great that the patient presents with primary hypovolemia. The utilization of volume repletion is warranted under these circumstances.

Acute Disease↗
PubMed1983

Clinical correlates of the spectrum of lung microvascular injury in human noncardiac edema.

We measured the clearance from blood to pulmonary edema fluid of a small molecular weight hydrophilic radiotracer, Indium-111-DTPA (In-DTPA) and a larger molecular weight radiotracer, Iodine-125-HSA (I-HSA), in patients with pulmonary edema on either a cardiac or noncardiac (permeability) basis. In previous investigations, we had noted an apparent relationship between the magnitude of clearance of I-HSA across the alveolocapillary membrane and the severity of noncardiac pulmonary edema. In this study, we were able to distinguish at least 2 distinct groups of patients with noncardiac pulmonary edema. Patients with the greatest damage to the alveolo-capillary exchanging membrane, defined by the flux of I-HSA from blood to edema fluid, were significantly differentiated from those with a lesser microvascular injury on the basis of higher mean heart rate (HR), temperature, cardiac index (CI), pulmonary artery pressures, right ventricular stroke work index (RVSWI), and a lower mean total white blood cell count (WBC), among others. Therefore, noncardiac pulmonary edema is characterized by a spectrum of permeability injury to the pulmonary microvasculature which seems to parallel other measurable indices of the severity of the systemic response to the illness.

Cell Membrane Permeability↗
PubMed2000

Effect of neutropenia and granulocyte colony stimulating factor-induced neutrophilia on blood-brain barrier permeability and brain edema after traumatic brain injury in rats.

OBJECTIVE: Granulocyte colony stimulating factor (GCSF) has been used to increase systemic absolute neutrophil count (ANC) in patients with severe traumatic brain injury to reduce nosocomial infection risk. However, the effect of increasing systemic ANC on the pathogenesis of experimental traumatic brain injury has not been studied. Thus, we evaluated the effect of systemic ANC on blood-brain barrier (BBB) damage and brain edema after traumatic brain injury in rats. DESIGN: Experimental study. SETTING: Research laboratory at the University of Pittsburgh, PA. SUBJECTS: Forty-three adult male Sprague-Dawley rats. INTERVENTIONS: Protocol I: rats were randomized to receive either vinblastine sulfate to reduce ANC, GCSF to increase ANC, or saline before controlled cortical impact (CCI) of moderate overall severity. Evans blue was used to assess BBB damage at 4-24 hrs after CCI. Protocol II: rats received GCSF or saline before CCI. Brain edema was estimated at 24 hrs using wet - dry) / wet weight method. Protocol III: rats received GCSF or saline before CCI. Brain neutrophil accumulation was estimated at 24 hrs using a myeloperoxidase assay. MEASUREMENTS AND MAIN RESULTS: Physiologic variables were controlled before CCI was maintained at normal in all animals before traumatic brain injury. No rats were anemic, hypoglycemic, or hypotensive before CCI. Protocol I: compared with control, systemic ANC decreased in vinblastine-treated rats and increased in GCSF-treated rats. BBB damage correlated with systemic ANC. Protocol II: mean systemic ANC before traumatic brain injury increased 15-fold in rats given GCSF vs. control; however no difference in brain edema was observed at 24 hrs after injury between groups. Protocol III: median systemic ANC at the time of CCI was increased ten-fold in rats given GCSF vs. control. No difference in brain myeloperoxidase activity 24 hrs after CCI was observed in rats treated with GCSF vs. control. CONCLUSIONS: Systemic ANC influences BBB damage after traumatic brain injury produced by CCI. Because BBB damage and brain edema are discordant, mechanisms other than BBB damage likely predominate in the pathogenesis of brain edema after contusion. The implications of increased BBB permeability with the administration of GCSF in our model remains to be determined. Increasing systemic ANC before CCI with GCSF administration does not increase posttraumatic brain neutrophil accumulation or brain edema after CCI in rats. The finding that neutrophil infiltration is not enhanced by systemic neutrophilia suggests that the ability of GCSF-stimulated neutrophils to migrate into injured tissue may be impaired. Further studies are needed to evaluate the effects of GCSF administration on secondary injury and functional outcome in experimental models of traumatic brain injury.

Animals↗
PubMed1989

Intralobular distribution of oleic acid-induced pulmonary edema in the pig. Evaluation by high-resolution CT.

The objective of this study was to elucidate the features of experimentally induced pulmonary edema at the lobular level, using high-resolution CT (HRCT) with pathological correlation. We selected the pig as the experimental animal because the pig has well-defined pulmonary lobules. Twelve Yorkshire pigs were included in this study. Five animals were used for studying normal anatomy of the pig lung. Pulmonary edema was induced by oleic acid infusion in 7 pigs. All computed tomographic (CT) scans were performed on a GE 9800 scanner, using 1.5 mm slice-thickness, 16 cm field of view with 512 X 512 matrix and bone reconstruction algorithm. The animals were killed after CT scans and the lungs were removed, inflated, fixed and dried, and subsequently sliced in sections which corresponded to the CT sections. Using CT images, specimen radiography, and histology, we studied the intralobular distribution of pulmonary edema in selected lobules of each animal. Oleic acid infusion caused multifocal hemorrhagic pulmonary edema within the pulmonary lobule. The distribution was uneven and areas surrounding the lobular bronchi were less involved. HRCT permits evaluation of morphological changes of oleic acid-induced pulmonary edema at the lobular level. The intralobular distribution of the lesions may provide additional information about the mechanism of permeability pulmonary edema.

Animals↗