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Biomedical subjects

S Meterissian

Publications and source records attributed to S Meterissian.

16 recordsLinked to original sources

Merkel cell carcinoma: important aspects of diagnosis and management.

Merkel cell carcinoma (MCC) is a highly aggressive primary neuroendocrine tumor. It is suggested in the literature that postoperative radiotherapy may decrease local recurrence and improve overall survival. The purpose of this retrospective review was to determine our experience and review the literature on this aggressive malignancy. Charts of ten patients with MCC seen between 1985 and 1997 were reviewed to obtain clinicopathological data. Eight patients were male with a mean age of 72 years (range 49-90). The head and neck was the most common site, affecting 50 per cent of patients. All patients had primary excisions with documented negative margins. Pathological size ranged from 10 to 40 mm. Initial pathological diagnosis was lymphoma in three cases requiring immunohistochemistry for cytokeratin and neuron-specific enolase for definitive diagnosis. Lymphatic invasion was noted in three patients but only one of these patients had clinical lymph node involvement. The mean follow-up was 54 months (range 6-114) with an 80 per cent one-year survival and 30 per cent 2-year survival. Postoperative radiotherapy was administered to five patients. Of these three died with evidence of both local and distant recurrence. This small retrospective review highlights important points in the management of MCC including pathological diagnosis and benefits of adjuvant radiation therapy.

Aged↗

Sentinel lymph-node biopsy for melanoma of the trunk and extremities: the McGill experience.

OBJECTIVE: To determine the effectiveness of sentinel lymph-node (SLN) biopsy for melanoma of the trunk and extremities. DESIGN: Case series review. SETTING: Royal Victoria Hospital, a Canadian university hospital. PATIENTS: Thirty-six patients (18 women and 18 men) seen between October 1996 and December 1998 with melanoma 1 mm or more in thickness with clinically negative lymph-node basins. Follow-up was 396 days. INTERVENTIONS: SLN biopsy. Technetium-99m filtered sulfur colloid (0.5 mCi) was injected intradermally around the melanoma or the excision scar 10 to 15 minutes before the surgical skin preparation. The identification of the SLN(s) was done with a hand-held gamma probe. Local anesthesia was used mostly for inguinal SLN biopsy whereas general anesthesia was usually required for axillary SLN biopsy. Preoperative lymphoscintigraphy was used only for trunk melanomas. OUTCOME MEASURES: Morbidity, successful identification of the sentinel node and locoregional recurrence. RESULTS: The mean age of patients at diagnosis was 53.4 years (range from 22-76 yr). The melanomas were distributed between the lower extremities (20 patients), upper extremities (8 patients) and trunk (8 patients). The mean Breslow thickness was 2.35 mm (range from 1-8 mm). Lymphoscintigraphy accurately localized the lymph-node drainage basin for trunk melanomas. In 1 patient the SLN could not be identified because the radiocolloid failed to migrate (failure rate 2.8%). The average number of SLNs removed was 1.97. Eight patients (22%) had sentinel nodes positive for malignant disease. The postoperative complication rate was 8.5%. Seven of 8 patients with positive SLNs underwent a complete node dissection (1 patient refused). Of the completion dissections only 2 patients had positive non-SLNs. All patients with positive nodes received interferon alpha-2b as adjuvant treatment. At follow-up, 34 patients are alive with no evidence of disease, 1 patient with a positive SLN is alive with distant metastatic disease and 1 patient with a negative SLN is dead of disseminated disease. CONCLUSION: SLN biopsy is a feasible technique with an acceptable failure rate and is thus a useful tool in the surgical management of melanoma.

Adult↗

omega-3 fatty acids decrease endothelial adhesion of human colorectal carcinoma cells.

BACKGROUND: Diets rich in omega-3 fatty acids have been shown to decrease both the initiation and promotion of colon carcinogenesis although their effect on hepatic metastasis formation is less well understood. Since adhesion of human colorectal carcinoma (HCRC) cells to hepatic endothelial cells is an important step in the metastatic cascade, the effect of membrane omega-3 fatty acid alterations on endothelial cell adhesion was studied. MATERIALS AND METHODS: CX-1 cells, a moderately differentiated HCRC cell line known to produce hepatic metastases in an athymic mouse intrasplenic injection model, were used. Cells were grown in omega-3 fatty acid-enriched medium and membrane-free fatty acid modifications confirmed with gas chromatography. Both human umbilical vein and hepatic sinusoidal endothelial cells were used in the binding assays. Adhesion assays were performed in a standard fashion using (51)Cr-labeled cells to tumor necrosis factor (TNF)-stimulated endothelial cell monolayers. Immunohistochemical analysis was performed for sialyl-Lewis(x), the receptor involved in endothelial adhesion on the surface of control and fatty acid-modified cells. RESULTS: Gas chromatographic analysis confirmed membrane fatty acid modification of CX-1 cells by growth in docosahexanoic acid (omega-3) (4.761 nmol/10(6) cells vs 0.057 nmol/10(6) cells for controls). Binding of CX-1 to both human umbilical vein and hepatic sinusoidal endothelial cells decreased from 38.4 +/- 0.44 to 11.58 +/- 0.87% (P < 0.01). Immunocytochemical analysis showed a decrease in sialyl-Lewis(x) expression with omega-3 treatment. CONCLUSIONS: These data indicate that omega-3 fatty acids may also be protective against the formation of hepatic metastases. The mechanism for this may be decreased endothelial cell adhesion which in turn may be due to decreased expression of the endothelial receptor sialyl-Lewis(x).

Animals↗

Value of DNA ploidy and S-phase fraction as prognostic factors in stage III cutaneous melanoma.

OBJECTIVE: To determine the prognostic value of flow cytometric analysis (S-phase fraction and DNA index) performed on lymph-node metastases of patients with stage III melanoma. DESIGN: A retrospective chart review with flow cytometric analysis of paraffin-embedded tissues. SETTING: A university teaching hospital. PATIENTS: Among 332 patients with cutaneous melanoma, 33 with stage III were identified. Distant metastases developed in 16 patients; 17 had no further recurrence. Charts were reviewed to obtain clinicopathologic parameters such as sex, age, location of the primary tumour, histologic features, presence or absence of ulceration, and Clark's and Breslow's levels. INTERVENTION: DNA ploidy and S-phase fraction were determined on the paraffin-embedded nodes. MAIN OUTCOME MEASURES: The groups with or without recurrence were compared in terms of disease-free survival (DFS) and overall survival (OS). These survival parameters were correlated with DNA ploidy and S-phase fraction. RESULTS: By univariate analysis, clinicopathologic factors did not predict OS. A higher Clark's level of invasion and more than 3 positive lymph nodes were associated with shorter DFS (p < 0.05). Tumour thickness and S-phase fraction did not correlate with either DFS or OS. Patients with diploid lymph-node metastases had an 87% 12-month survival compared with 41% for those with aneuploid tumours. CONCLUSIONS: DNA ploidy may be used as a prognostic index in patients with lymph-node metastases. This could be particularly useful in the context of sentinel lymph-node mapping by which more patients are being identified with single microscopic lymph-node involvement.

Analysis of Variance↗

Rapid induction of cytokine and E-selectin expression in the liver in response to metastatic tumor cells.

The cytokine-inducible endothelial cell adhesion receptor E-selectin has been implicated in cancer metastasis. Previously, we reported that experimental liver metastasis of Lewis lung carcinoma subline H-59 cells could be abrogated in animals treated with an anti-E-selectin antibody. To gain further insight into the functional relevance of E-selectin expression to liver colonization, we investigated here the time course of cytokine and hepatic E-selectin expression after the intrasplenic/portal inoculation of H-59 cells by using a combination of reverse transcription-PCR, Northern blot analysis, immunohistochemistry, and in situ hybridization. In parallel, we analyzed cytokine induction in response to the injection of Lewis lung carcinoma subline M-27 and murine melanoma B16-F1 cells, which do not spontaneously metastasize to the liver. In livers derived from normal or saline-injected mice, only minimal basal levels of TNF-alpha and IL-1 mRNA were detectable by RT-PCR. Rapid cytokine mRNA induction was noted within 30-60 min of H-59 injection, reaching maximal levels at 4-6 h. This was followed by the appearance of E-selectin mRNA, which was detectable at 2 h after injection and reached maximal levels at 6-8 h, declining to basal levels by 24 h. In situ hybridization analysis and immunohistochemistry localized E-selectin mRNA and protein, respectively, to the sinusoidal endothelium. M-27 cells failed to induce cytokine or E-selectin expression, whereas B-16 cells elicited a delayed and more short-lived response. The results demonstrate that upon entry into the hepatic circulation, tumor cells can rapidly trigger a molecular cascade leading to the induction of E-selectin expression on the sinusoidal endothelium and suggest that E-selectin induction may contribute to the liver-colonizing potential of tumor cells.

Animals↗

Biologically active Fas antigen and its cognate ligand are expressed on plasma membrane-derived extracellular vesicles.

Exfoliation of plasma membrane components is a directed process that consumes energy and requires active cell metabolism. Proteins involved in regulating the survival and proliferation of eukaryotic cells are released on exfoliated vesicles. We examine here whether the Fas receptor and its cognate ligand (FasL) are present on vesicles shed from high metastatic potential CX-1 cells and low metastatic potential MIP-101 cells and from HuT 78 cells, respectively. Rates of exfoliation at 2 hours and cumulative levels of extracellular vesicles in serum-free medium conditioned by CX-1 cells are increased by 1.8-fold and 1.6-fold, respectively, relative to that in medium conditioned by MIP-101 cells. Although vesicles shed from both cancer cell lines contain Fas antigen, the amount of Fas per vesicle and the percentage of vesicles containing Fas are increased for vesicles isolated from MIP-101 cells, relative to those from CX-1 cells, as determined by immunogold particle labeling and electron microscopy and by immunofluorescence microscopy and flow cytometry. Results of metabolic labeling with 35S-methionine indicate that Fas biosynthesis is reduced by up to 3.3-fold for CX-1 cells, relative to that of MIP-101 cells, consistent with the finding of decreased Fas on vesicles shed from the plasma membrane of CX-1 cells. Although mRNA for soluble Fas receptor is detectable in both cell lines, depletion of shed vesicles from serum-free medium by ultracentrifugation removes all detectable biological activity. FasL is detected on vesicles exfoliated from HuT 78 cells by immunoelectron microscopy and Western blot analysis. FasL-bearing vesicles induce apoptosis of Fas-expressing cancer cells at the same level as observed by treatment with monoclonal anti-Fas antibody. Furthermore, Fas-bearing extracellular vesicles from MIP-101 but not from CX-1 cells protect the CX-1 cell line from FasL-induced and anti-Fas-mediated apoptosis, indicating that Fas present on shed vesicles is biologically active. We conclude that the Fas antigen and its cognate ligand are exfoliated from the cell surface in a bioactive configuration. Exfoliation may provide a mechanism for long-range signal-directed apoptosis while maintaining Fas/FasL on a membrane surface.

Adenocarcinoma↗

Liver endothelial E-selectin mediates carcinoma cell adhesion and promotes liver metastasis.

E-selectin is a cytokine-inducible endothelial cell adhesion receptor which is involved in the process of leukocyte rolling, the first in a cascade of interactions leading to leukocyte transmigration. Several studies have implicated this receptor in carcinoma cell adhesion to the endothelium, an interaction thought to be required for tumor extravasation during metastasis. To study the role of this receptor in the process of metastasis, we utilized a murine carcinoma line H-59 which is highly metastatic to the liver in vivo. When adhesion of H-59 cells to primary cultures of murine hepatic endothelial cells was measured, it was found that the tumor cells had a low basal level of adhesion to the sinusoidal endothelial cells, which could be significantly and specifically augmented by pre-activation of the endothelial cells with rTNF alpha. This incremental increase in adhesion to the activated endothelium could be completely and specifically abolished by a neutralizing monoclonal antibody to murine E-selectin (MAb 9A9). Similar results were obtained with 2 highly metastatic human colorectal carcinoma lines, HM 7 and CX-1, but not with a second murine subline, M-27, which is poorly metastatic to the liver. To assess the role of E-selectin in metastasis to the liver in vivo, the effect of MAb 9A9 on experimental liver metastasis was evaluated using the syngeneic H-59 model. We show here that this antibody caused a marked, specific and Fc-independent inhibition of experimental liver metastasis, reducing the median number of metastases by 97% relative to the control groups. Our results provide evidence that endothelial E-selectin is a mediator of carcinoma metastasis to the liver.

Animals↗

Clinically occult breast carcinoma: diagnostic approaches and role of axillary node dissection.

BACKGROUND: Nonpalpable breast lesions are being detected with increasing frequency with the advent of improved mammographic techniques. Although only 20-30% of these lesions are malignant, definitive diagnosis has usually required a needle-localization excisional biopsy, which is costly and increases the psychological stress on the patient. The purpose of this retrospective study was to determine the sensitivity of ultrasound-guided fine-needle aspiration (FNA) biopsy of nonpalpable breast masses and the incidence of axillary nodal metastases in these subclinical lesions. METHODS: Seventy-one patients treated for clinically occult malignant breast tumors between 1985 and 1992 were identified. Charts were reviewed to determine the accuracy of breast ultrasonography in detecting occult mass lesions and whether ultrasound guidance improved the accuracy of FNA biopsy. In addition, the incidence of axillary lymph node involvement was noted. RESULTS: Of the 71 malignant tumors, 35 were in situ and 36 were invasive. The median diameter was 0.5 cm for noninvasive lesions and 0.8 cm for invasive tumors. A mass was seen on mammography in 32 (45%) patients, microcalcifications were seen in 36 (51%), and both a mass and microcalcifications were seen in three (4%). Of the 30 patients who underwent an axillary node dissection, 4 (13%) had disease-positive nodes. Ultrasound-guided FNA was performed in 15 patients with a mass lesion, with a sensitivity of 93%. CONCLUSIONS: These results indicate that ultrasound-guided FNA cytologic analysis is an accurate diagnostic technique even in small (< 1 cm), mammographically detected breast masses. In addition, the incidence of axillary nodal metastases indicates that an axillary lymph node dissection should be performed in invasive lesions, even those < 1 cm in diameter.

Axilla↗

Desialylation of metastatic human colorectal carcinoma cells facilitates binding to Kupffer cells.

Cell surface hypersialylation of human colorectal carcinoma (HCRC) cells correlates with increased metastatic potential after intrasplenic injection, while desialylation with various agents has been shown to inhibit hepatic metastases. In this study we examined the effects of desialylation of HCRC cell lines with a novel intracellular inhibitor of the CMP-sialic acid transport protein (KI-8110). HCRC cells, which are poorly differentiated and poorly metastatic in nude mice (Clone A and MIP-101) were compared to well-differentiated, highly metastatic cells (CX-1 and CCL-235). KI-8110 treatment has previously been shown to reduce sialic acid levels in each of these cell lines and to reduce hepatic metastases in CX-1 and CCL-235 cell lines. This study attempts to identify a mechanism by which desialylation inhibits hepatic metastases. After KI-8110 treatment, in vitro adhesion assays were performed with each cell line to examine binding to Kupffer cells and the extracellular matrix protein fibronectin. Binding of Clone A, CX-1, and CCL-235 to Kupffer cells was significantly increased after KI-8110 treatment. Desialylation had no significant effect on binding of HCRC cell lines to fibronectin. While the metastatic cascade involves many complex interactions, the cytotoxic effects of Kupffer cells in the hepatic sinusoid are known to be an important mechanism of host defense against tumor cells. Cell surface sialic acids may well mask Kupffer cell binding to HCRC cells, preventing their cytotoxic effects and enhancing the metastatic potential of circulating tumor cells.

Animals↗

Patterns of residual disease after preoperative chemoradiation in ultrasound T3 rectal carcinoma.

BACKGROUND: Rectal carcinoma tends to recur locally, with invasion of adjacent organs and significant pelvic pain. Both radiation therapy alone and combined chemoradiation have been used in an attempt to decrease the local recurrence rate and thereby improve survival. Although preoperative chemoradiation can clinically downstage rectal tumors, the pathologic extent of the residual disease has not been studied. METHODS: Thirty-seven patients with T3 rectal cancer diagnosed by transrectal ultrasonography (uT3) received 45 Gy with continuous infusion 5-fluorouracil (300 mg/m2/day). Proctoscopy with mucosal/submucosal biopsy was performed in patients (16 of 37) posttreatment and before definitive surgery. RESULTS: Microscopic evaluation of the 37 resected specimens showed a 30% (11 patients) pathologic complete remission rate. The pattern of residual disease in the remaining 26 patients showed that nine (25%) had microscopic residual tumor without evidence of mucosal involvement. Of the 14 patients with a negative proctoscopic evaluation and biopsy only, five (36%) had no residual tumor on final pathology. CONCLUSIONS: After chemoradiation, the pathologic presentation of rectal cancer may be altered, making endoscopic procedures and mucosal/submucosal biopsies unreliable in detection of residual disease. Despite the relatively good pathologic complete remission rate noted in this study, all patients undergoing chemoradiation for uT3 rectal carcinomas need definitive surgical resection to confirm a complete clinical remission.

Adenocarcinoma↗

Human and murine Kupffer cell function may be altered by both intrahepatic and intrasplenic tumor deposits.

The liver is the most common site of hematogenous metastases from colorectal carcinoma. Kupffer cells (KC), which line the hepatic sinusoids, may form the first line of defense against circulating tumor cells. The purpose of this study was to determine the effect of hepatic metastases and intra-abdominal tumor growth on KC binding of human colorectal carcinoma (HCRC) cells. MIP-101, a poorly metastatic cell line, and CX-1, a highly metastatic cell line, were injected intrasplenically into nude mice and KC were isolated by collagenase perfusion at varying intervals after injection. Conditioned media were collected from MIP-101, CCL 188 and CX-1 to determine their in vitro effect on KC function. KC from MIP-101 injected mice (14% liver metastases, 100% splenic tumors) bound a significantly greater number of MIP-101 and clone A cells than CX-1 cells in vitro. KC isolated from mice 5 weeks after CX-1 injection (100% liver metastases) also showed increased binding of MIP-101 and clone A cells compared to CX-1 cells. Similar results were obtained when tumor cell binding to normal human liver KC was compared to binding to KC from human livers from patients with hepatic metastasis from colorectal cancer. In contrast KC obtained from mice 3 weeks after CX-1 injection (44% liver metastases) showed significantly decreased binding of MIP-101 and clone A cells. The conditioned medium from CX-1 cells significantly decreased the in vitro binding of both MIP-101 and CX-1 by KC. These results indicate that the ability of KC to bind HCRC cells (which precedes phagocytosis and tumor cell killing) is a dynamic function and affected by concomitant tumor growth. HCRC cells may alter KC function via the production of specific tumor-derived soluble factors. In order to devise new and more effective therapeutic options in the treatment of liver metastases the nature of this tumor cell-KC interaction must be better understood.

Animals↗

Carcinoembryonic antigen: enhancement of liver colonisation through retention of human colorectal carcinoma cells.

Carcinoembryonic antigen (CEA) is an oncofetal antigen whose function in the progression of colorectal carcinoma remains unclear although recent studies suggest it participates in homotypic cellular adhesion. We have previously shown that 40 micrograms of CEA injected intravenously into athymic nude mice enhances experimental metastasis in liver and lung by two human colorectal carcinoma cell lines that are injected intrasplenically 30 min later. The metastatic potential of another three moderately to highly metastatic colorectal carcinoma cell lines and of one weakly metastatic line has now been analysed in this model. CEA pretreatment only enhanced colony formation by cell lines that were weakly metastatic in untreated nude mice; it did not affect experimental metastasis by highly metastatic lines. CEA pretreatment enhanced the retention of 125I Idudr-labelled weakly metastatic tumour cells within the liver and lungs 4 h after intrasplenic injection but not the retention of highly metastatic tumour cells or inert latex beads. A significant correlation existed between the formation of experimental metastases and the early retention of tumour cells within the liver after intrasplenic injection. Aggregation did not appear to be important for retention in liver because CEA did not aggregate colorectal carcinoma cells in vitro. Also CEA did not alter natural host effector cell function in a cytolysis assay in vitro. We suggest that CEA facilitates liver colonisation by three of eight human colorectal carcinomas in athymic nude mice by increasing the hepatic retention of tumour cells. The potential mechanisms by which CEA may increase the retention of tumour cells in the liver are discussed.

Animals↗

Fas/APO-1 expression and function on malignant cells of hematologic and nonhematologic origin.

Fas/APO-1 is a cell-surface protein capable of inducing apoptosis in a variety of cell types upon specific antibody engagement. Antibodies against Fas/APO-1 have been used successfully for the treatment of several lymphoid malignancies in mice. Before apoptosis triggered by anti-Fas can be fully exploited as a clinical therapy, Fas/APO-1 distribution, function, and regulation must be further studied. In this study, we analyzed freshly isolated B-cell and T-cell lymphomas as well as nonhematological tumor cell lines for Fas/APO-1 expression and sensitivity to the growth-inhibitory effects of anti-Fas. Constitutive Fas/APO-1 was expressed at very low levels on only one of eight B-cell lymphomas analyzed. Expression was markedly up-regulated, however, by culture with high-molecular-weight B-cell growth factor (HMW-BCGF). Fas/APO-1 was constitutively expressed on one of two T-cell lymphomas examined at levels comparable to those of activated normal lymphocytes. However, neither the B-cell nor T-cell lymphomas positive for Fas/APO-1 expression were growth inhibited by anti-Fas. Furthermore, in the case of one HMW-BCGF-activated B-cell lymphoma, a significant growth enhancement was observed upon anti-Fas treatment. Nonhematologic tumor cell lines showed a similar spectrum of biologic responses to anti-Fas, being growth inhibited, growth stimulated or unaffected by antibody treatment. In summary, these studies suggest that engagement of Fas/APO-1 may trigger a diverse spectrum of biologic effects not unlike other members of the nerve growth factor receptor/tumor necrosis factor receptor superfamily.

Antigens, Neoplasm↗

Assessment of cardiac function in patients who were morbidly obese.

Cardiac function of 30 patients who were morbidly obese was studied before bariatric surgery. Twelve patients were studied 13 +/- 4 months after surgery. These patients had a mean age of 37.1 +/- 2.9 years and a body mass index of 50.0 +/- 1.4 kg/m2. Cardiac function was measured by echocardiography, radionuclide angiography scanning, and right heart catheterization. To determine the degree of cardiac dysfunction, the patients were studied with exercise and intravenous fluid challenges. Ultrasonography produced evidence of myocardial thickening with an increased interventricular septum in eight patients (32%) and increased left ventricular mass in 17 patients (53%). The radionuclide scan suggested that morbid obesity was associated with a significantly (p less than 0.05) increased end-diastolic volume and decreased left ventricular ejection fraction as compared with patients who were of normal weight. With exercise the patient who was of normal weight had an increase in the end-diastolic volume, stroke volume, and heart rate, but the patient who was morbidly obese only increased heart rate to produce the necessary increase in cardiac output. Right heart catheterization indicated that the relationship of the pulmonary wedge pressure and the left ventricular stroke work index was abnormal in 14 of 29 patients (48.3%) and depressed in six of 29 patients (20.7%) with exercise. One liter of fluid caused an abnormal relationship of the pulmonary wedge pressure and the left ventricular stroke work index in 12 of 30 patients (40%) and a depressed response in 10 of 30 patients (33.3%). Cardiac studies were repeated in 12 patients after a 54.8 +/- 1.9 kg weight loss. Echocardiography indicated a decrease in dilatation (27.3% to 9.1%) and a significant (p less than 0.05) decrease in hypertrophy (45.5% to 0%). After the weight loss, radionuclide and right heart catheterization studies indicated improved cardiac function with reduced filling pressures and increased left ventricular work during fluid and exercise challenges. These results support the presence of obesity-related cardiomyopathy with ventricular dysfunction, which appears to be caused by a noncompliant ventricle. Significant weight loss achieved with gastroplasty results in increased ventricular compliance and improved cardiac function.

Adult↗

Morphometry of the distribution of hydrostatic pulmonary oedema in dogs.

Light microscopic morphometry was utilized to examine the distribution of fluid in the interstitium around arteries, veins and within bronchovascular bundles in hydrostatic oedema, comparing it with previous control and permeability oedema experiments. Pulmonary artery wedge pressure was raised with fluid overload and an aortic balloon in five anaesthetized dogs to produce oedema (wet weight to dry weight ratios of 11.66 +/- 0.84). Lung lobes were fixed by freeze-substitution at 20 mmHg airway pressure. Photomicrographs of arteries, veins and bronchovascular bundles were taken, and areas were digitized to obtain the following: for arteries and veins, an oedema ratio=perivascular oedema cuff area/vessel area; for bronchovascular bundles, T=total bundle area, A1=interstitial area around airways, B=airway (respiratory bronchiole, bronchiole, or bronchus) area, A2=periarterial interstitium, V=artery area. From these, oedema ratios were calculated as A1/B and A2/V. We found that the oedema ratios were greater (P less than 0.01) for arteries (1.18, n=675) than veins (0.56, n=263), and were greater for the larger vessels; A1 rose significantly (P less than 0.01) only in bronchovascular bundles with bronchioles and bronchi, not in those with respiratory bronchioles; A2 increased from three- to 25-fold (P less than 0.01) in all bundles; A1/B only increased in bundles with bronchi while A2/V increased two- to six-fold in all bundles with oedema compared with controls. We conclude that these preferential patterns of distribution resemble those reported in permeability oedema, and may shed light on mechanisms of accumulation, and on the physiological effects of oedema on airways and vessels of the lung.

Animals↗