Capillary Engorgement Research Articles

Lung Histopathology in Baclofen Intoxication

The aim of the study: to assess the lung histopathology in acute intoxication with baclofen alone and its combination with alcohol (in the same dose) 3 hours after the ingestion.Materials and methods. The study was performed on 15 male Wistar rats weighing 290-350 g and aged 20 weeks. The animals were divided into 3 groups, 5 animals each: control group that included intact rats; Group 1 composed of rats received baclofen alone; Group 2 that included rats received a combination of baclofen and ethanol. Baclofen was administered orally at a dose of 85 mg/kg animal weight under anesthesia (chloralose), and 40% ethanol, 7 ml/kg animal weight, was orally administered along with baclofen at the same dose. Animals of all groups were sacrificed after 3 hours by overdosing anesthetic agent. Lung tissue samples were examined by light microscopy using a video system at x400 magnification. The following histological characteristics were evaluated: circulatory disorders (engorged capillaries and venules, hemorrhages in interalveolar septa and alveoli, sludge), atelectasis (including partial), emphysema, cellular response (increased WBCs in the interalveolar septal area), thickening of interalveolar septa due to edema, epithelial desquamation into bronchial lumen. The diameter of alveoli and thickness of interalveolar septa were measured.Results. Three hours after the baclofen administration, circulatory disorders in the lungs (engorged venules and capillaries, hemorrhages in the interalveolar septa, sludge), emphysema, atelectasis (complete and partial) as well as cellular response (leucocyte infiltration of interalveolar septa) were detected. In the Group 2, baclofen resulted in circulatory disorders (engorged venules and capillaries, sludge), emphysema, atelectasis (complete and incomplete), cellular response (infiltration with leukocytes), as well as fluid in the lumen of bronchioles. In Group 1, the alveolar diameter was significantly larger than in the control group and Group 2, while the thickness of the interalveolar septa was lower. In group 2, alveolar diameter was significantly less than in group 1, but still greater than in the control group. The thickness of the interalveolar septa in group 2 was significantly greater than in the control group and group 1.Conclusion. After administration of baclofen alone and in combination with ethanol, the following alterations were found in the lungs: circulation disorders (venular and capillary engorgement, sludge), increased vascular permeability because of developing hypoxia, leukocyte infiltration of interalveolar septa. The monitoring of morphological alterations may aid in evaluating the severity of pathological processes in intoxication with baclofen alone and in combination with ethanol and in determining the method of intoxication (baclofen alone or in combination with ethanol).

Optical Coherence Tomography Angiography in Eyes with Retinal Vein Occlusion.

Optical coherence angiography (OCTA) is a noninvasive technique that has been introduced in recent years to detect ophthalmological pathology. The growing usage of OCTA to detect retinal abnormalities can be attributed to its advantages over the reference-standard fluorescein angiography (FA), although both of these techniques can be used in association. OCTA's advantages include its dye independency, its ability to produce depth-resolved images of retinal and choroidal vessels that yield images of different vascular layers of the retina, and the better delineation of the foveal avascular zone. OCTA's disadvantages include the lack of normalized patient data, artefactual projection issues, and its inability to detect low-flow lesions or pathologic conditions. Different OCTA platforms use unique algorithms to detect microvasculature, which are implemented in both spectral-domain (SD) and swept-source (SS) OCT machines. Microvascular changes in retinal vein occlusions (RVOs) are visible in both the superficial and deep capillary networks of the retina in OCTA. These visualizations include a decrease in foveal and parafoveal vascular densities, non-perfusion areas, capillary engorgement and telangiectasias, vascular tortuosity, microaneurysms, disruption of the foveal perivascular plexus, and formation of collateral vessels. The restricted field of view and inability to show leakage are important limitations associated with the use of OCTA in RVO cases. In this article, we present a brief overview of OCTA and a review of the changes detectable in different slabs by OCTA in RVO cases published in PubMed and Embase.

The role of bone marrow-derived endothelial progenitor cells and angiogenic responses in chronic obstructive pulmonary disease.

Increased vascularity of the bronchial sub-mucosa is a cardinal feature of chronic obstructive pulmonary disease (COPD) and is associated with disease severity. Capillary engorgement, leakage, and vasodilatation can directly increase airway wall thickness resulting in airway luminal narrowing and facilitate inflammatory cell trafficking, thereby contributing to irreversible airflow obstruction, a characteristic of COPD. Airway wall neovascularisation, seen as increases in both the size and number of bronchial blood vessels is a prominent feature of COPD that correlates with reticular basement membrane thickening and airway obstruction. Sub-epithelial vascularization may be an important remodelling event for airway narrowing and airflow obstruction in COPD. Post-natal angiogenesis is a complex process, whereby new blood vessels sprouting from extant microvasculature, can arise from the proliferation of resident mature vascular endothelial cells (ECs). In addition, this may arise from increased turnover and lung-homing of circulating endothelial progenitor cells (EPCs) from the bone marrow (BM). Following lung-homing, EPCs can differentiate locally within the tissue into ECs, further contributing to vascular repair, maintenance, and expansion under pathological conditions, governed by a locally elaborated milieu of growth factors (GFs). In this article, we will review evidence for the role of BM-derived EPCs in the development of angiogenesis in the lug and discuss how this may relate to the pathogenesis of COPD.

Congenital diaphragmatic hernia in a crossbred piglet: A case report

Congenital diaphragmatic hernia (CDH) is a congenital defect affecting the diaphragm resulting in herniation of organs from abdominal cavity into thoracic cavity. It is a life-threatening condition and a major cause of death due to two complications: pulmonary hypoplasia and pulmonary hypertension. A stillborn male crossbred piglet on necropsy revealed hydrothorax and hydro-peritoneum. Thoracic cavity showed protrusion of parts of the small intestine into the cavity through the right side of the diaphragm, no hernial sac was detected and lungs were under-developed. Liver showed severe congestion and marked enlargement with abnormal lobulation. Cortical surface of both kidneys were rough and granular. Parallely placed double spleen with multiple hemorrhagic areas was noticed. Microscopic examination of kidney showed diffused cortical mononuclear cell infiltration with mild engorgement of medullary capillaries. In lungs, alveolar capillaries were moderately engorged with prominent interlobular septa and severe atelectasis. In liver, multifocal areas of hemorrhages and hydropic degeneration of hepatocytes was noticed. The case was diagnosed as congenital diaphragmatic hernia.

ISOLATION AND IDENTIFICATION OF BACTERIA FROM KIDNEY LESIONS IN BROILERS IN SULAIMANIA PROVINCE

A total of ninety seven broiler chicks in Sulaimania/ Kurdistan region/ Republic of Iraq, were collected from different flocks at different dates suffering from nephritis. Samples of affected kidneys were cultured on blood, Mannitol salt and MacConkey agar plates, the isolates were confirmed by API 20E system. The isolated microorganism included E.coli (89.69%), Proteus milabilis (9.27%) and Klebsiella pneumonia (1.03%). Antimicrobial susceptibility test for E.coli showed high sensitivity to Ciprofloxacin and Co-trimoxazole. Histopathological changes of the kidneys were characterized by enlargement of epithelial cells of renal tubules and pale cytoplasm, engorgement of blood capillaries in both renal glomeruli and interstitial tissues with atrophy of renal glomeruli

Minimal Erythema Dose (MED) Testing

Ultraviolet radiation (UV) therapy is sometimes used as a treatment for various common skin conditions, including psoriasis, acne, and eczema. The dosage of UV light is prescribed according to an individual's skin sensitivity. Thus, to establish the proper dosage of UV light to administer to a patient, the patient is sometimes screened to determine a minimal erythema dose (MED), which is the amount of UV radiation that will produce minimal erythema (sunburn or redness caused by engorgement of capillaries) of an individual's skin within a few hours following exposure. This article describes how to conduct minimal erythema dose (MED) testing. There is currently no easy way to determine an appropriate UV dose for clinical or research purposes without conducting formal MED testing, requiring observation hours after testing, or informal trial and error testing with the risks of under- or over-dosing. However, some alternative methods are discussed.

Minimal Erythema Dose (MED) Testing

Ultraviolet radiation (UV) therapy is sometimes used as a treatment for various common skin conditions, including psoriasis, acne, and eczema. The dosage of UV light is prescribed according to an individual's skin sensitivity. Thus, to establish the proper dosage of UV light to administer to a patient, the patient is sometimes screened to determine a minimal erythema dose (MED), which is the amount of UV radiation that will produce minimal erythema (sunburn or redness caused by engorgement of capillaries) of an individual's skin within a few hours following exposure. This article describes how to conduct minimal erythema dose (MED) testing. There is currently no easy way to determine an appropriate UV dose for clinical or research purposes without conducting formal MED testing, requiring observation hours after testing, or informal trial and error testing with the risks of under- or over-dosing. However, some alternative methods are discussed.

Pulmonary Hypertension Presenting With Apnea, Cyanosis, and Failure to Thrive in a Young Child

Pulmonary Hypertension Presenting With Apnea, Cyanosis, and Failure to Thrive in a Young Child

Incidência de alterações estruturais das pregas vocais associadas ao pólipo de prega vocal

A etiologia mais aceita para pólipos de pregas vocais é o fonotrauma. Imaginamos que possa existir alguma alteração anatômica prévia nas pregas vocais que predisponha indivíduos a apresentarem lesões fonotraumáticas. OBJETIVO: O presente estudo retrospectivo procura encontrar correlação entre os pólipos de prega vocal e alterações estruturais da prega vocais. MATERIAL E MÉTODO: Foi realizado trabalho retrospectivo a partir da descrição cirúrgica de 33 pacientes submetidos a exérese de pólipo de prega vocal no período de três anos em hospital universitário. RESULTADOS: Trinta e um pacientes apresentaram pólipos unilaterais e 2 bilaterais. Foram encontradas 27 lesões associadas: 10 lesões reacionais, 12 sulcos, 3 cistos e 2 ectasia capilars. Foram 14 lesões contralaterais e 13 ipsilaterais. DISCUSSÃO E CONCLUSÕES: Encontrou-se uma forte correlação entre a presença de uma lesão de base influindo como co-fator de fragilização da prega vocal ao fonotrauma, pois das 27 lesões encontradas 17 foram consideradas pré-existentes (63%). As lesões poderiam interferir na coaptação das pregas vocais, gerando uma onda mucosa irregular durante a fonação, expondo o espaço de Reinke a uma agressão estrutural. Apesar do caráter preliminar do trabalho os achados sugerem íntima correlação entre o pólipo e lesões estruturais mínimas das pregas vocais.

β-HYDROXYBUTYRATE INDUCES ACUTE PULMONARY ENDOTHELIAL DYSFUNCTION IN RABBITS

The authors examined the effects of high ketone body and glucose concentrations on endothelial cell (EC) function in perfused rabbit lungs. β-Hydroxybutyrate (βOHB), at 5 mM, decreased endothelial angiotensin-converting enzyme (eACE) activity, whereas 25 mM glucose (HG), 1 mM βOHB, or 10 mM acetoacetate (AcAc) did not. Dry to wet weight ratios were also reduced in lungs perfused with 5 mM βOHB, but not with AcAc. βOHB, at 5 mM, caused massive hemorrhage and interstitial and alveolar neutrophil infiltration; AcAc only produced engorgement of septal capillaries. Thus, pulmonary EC dysfunction occurs in rabbit lungs acutely perfused with βOHB, but not with AcAc or glucose.

A clinicopathological study of three cases of severe acute respiratory syndrome (SARS)

SummaryAimsThe severe acute respiratory syndrome (SARS) caused a large outbreak of atypical pneumonia in Beijing, China from early March 2003. We report the pathological features from three patients who died of SARS.MethodsAutopsies were performed on three patients who died 9–15 days after the onset of the illness, and the clinical and laboratory features reviewed. Tissue sections were stained with haematoxylin and eosin (H&E), and in situ reverse transcriptase polymerase chain reaction (RT–PCR) on lung sections was performed using SARS coronavirus-specific primers.ResultsThe typical gross pathological change in the lungs was diffuse haemorrhage on the lung surface. Histopathological examination revealed serous, fibrinous and haemorrhagic inflammation in most pulmonary alveoli, with capillary engorgement and some capillary microthrombosis. The pulmonary alveoli were thickened with interstitial mononuclear inflammatory infiltrates, diffuse alveolar damage, desquamation of pneumocytes and hyaline-membrane formation; fibrinoid material and erythrocytes were present in alveolar spaces. There were thromboemboli in some bronchial arterioles. Haemorrhagic necrosis and reduced numbers of lymphocytes were observed in lymph nodes and spleen. In situ RT–PCR detected SARS coronavirus RNA in type II alveolar cells, interstitial cells and bronchiolar epithelial cells from all three patientsConclusionsSevere immunological damage in lung tissue is responsible for the clinical features of SARS.

Anaesthesia for fetal surgery.

*Department of Anesthesia, Children’s Hospital, Harvard Medical School, Boston, MA,**Department of Anesthesiology and Critical Care, The Children’s Hospital of Philadelphia,University of Pennsylvania School of Medicine, Philadelphia and †Department of Anesthesia andCritical Care, The Hospital of the University of Pennsylvania, University of Pennsylvania Schoolof Medicine, Philadelphia, PA, USA

Pathogenesis of the glomerular abnormality in cyanotic congenital heart disease

We present evidence of 2 distinct glomerular abnormalities in cyanotic congenital heart disease—vascular and nonvascular—each believed to reflect a distinct pathogenesis. Glomeruli from both kidneys were studied with light microscopy in 13 necropsied cyanotic patients and in 8 controls. The vascular study characterized hilar arteriolar dilatation, capillary diameter, glomerular diameter, and capillary engorgement with red blood cells. The nonvascular study characterized juxtaglomerular cellularity, mesangeal cellularity, mesangeal matrix, focal interstitial fibrosis, and megakaryocytic nuclei per cm 2 of renal cortex. There was a significant increase in each of the above vascular and nonvascular items of interest relative to controls. Electron microscopy identified whole megakaryocytes with their cytoplasm in glomeruli. The vascular abnormality is believed to result from intraglomerular release of nitric oxide. The nonvascular abnormality is believed to result from platelet-derived growth factor and transforming growth factor- β.

Neuropathology in non-human immunodeficiency virus-infected drug addicts: hypoxic brain damage after chronic intravenous drug abuse.

Neuropathological studies were carried out on 180 human immunodeficiency virus-seronegative intravenous drug addicts. The findings in victims of acute heroin intoxication (n = 116) were congestion (99.1%), capillary engorgement (68.1%), and/or perivascular bleeding (68.1%) - hemodynamic processes attributable to toxic primary respiratory failure. In a high percentage of these cases (88%), cerebral edema was also present. In 18 cases of acute heroin intoxication who survived for periods of hours or days, the sole postmortem finding was ischemic nerve cell damages, resembling that typically seen in systemic hypoxia. Semiquantitative analysis revealed nerve cell loss in the hippocampal formation and/or Purkinje cell layer in 26% of the 162 chronic drug abusers. By contrast, in nearly 80% of these cases, the hippocampus showed enhanced expression of glial fibrillary acid protein by astrocytes and/or a proliferation of microglia, demonstrated by CD68 expression. Since such reactive processes are produced by primary neuronal damages, it can be assumed that chronic intravenous drug abuse results in obviously ischemic nerve cell loss. This could be demonstrated in the hippocampus, but it must also occur throughout the whole brain. The demonstration of ischemic nerve cell damage and neuronal loss or secondary reactive alterations has not been described previously.

Changes in endogenous cytokines, adhesion molecules and platelets during cytokine-induced tumour necrosis

The aim of this study was to investigate mechanisms of anti-tumour activity and necrosis induced by combinations of tumour necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma). In a breast cancer xenograft model, locally injected recombinant human TNF-alpha arrested growth of established tumours in the absence of overt necrosis. Macroscopic necrosis occurred when rat IFN-gamma, which had no anti-tumour activity as a single agent, was given systemically. Treatment with TNF-alpha and IFN-gamma caused focal engorgement of tumour capillaries with erythrocytes, intravascular recruitment of polymorphonuclear cells and platelet adherence to the tumour vascular endothelium 4 h after the combined treatment. This was followed by destruction of tumour vascular endothelium and both necrosis and apoptosis of tumour cells. Concomitant with these changes, semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) analysis revealed the increase of stromal (murine) mRNA levels for TNF-alpha, TNF receptor 55 kDa, TNF receptor 75 kDa, intracellular adhesion molecule 1, vascular cell adhesion molecule 1, P-selectin and interleukin 6 (IL-6). Thus, the effect of the combined TNF-alpha and IFN-gamma therapy involved the selective destruction of the tumour vasculature, death of tumour cells and increased expression of a series of stromal cytokines, cytokine receptors and adhesion molecules, which could be implicated in the observed events.

Sexual arousal in diabetic females: Physiological and self-report measures

Diabetes mellitus, a major health problem afflicting 500,000 Americans each year, is a leading cause of male erectile difficulties. Diabetic women may be susceptible to a similar diabetic pathogenesis for sexual problems but information about the effect of diabetes on female sexual response is sparse and conflicting. Past research has been based upon self-report measures, a methodology flawed by susceptibility to response bias. Whether diabetic women differed from a matched nondiabetic control group in their physiological as well as subjective response to erotic stimulus exposures was investigated. Vaginal photoplethysmographic measures of capillary engorgement were taken while subjects individually viewed counterbalanced erotic and non-erotic videotape presentations. Graphically and statistically analyzed results indicated that diabetic women demonstrated significantly less physiological arousal to erotic stimuli than controls, whereas their subjective responses were comparable. These objective, physiological findings support and extend previous subjectively based research which found potential diabetes-related sexual dysfunction in female diabetics. The groups did not differ, however, in the reported occurrence of sexual difficulties.

Cytological and histological changes in the middle ear after inoculation of influenza A virus.

Experimental otitis media induced in the chinchilla by inoculation of influenza A virus into the middle ear resulted in capillary engorgement, subepithelial hemorrhage, tissue edema and acute inflammatory cell infiltration. Quantitative morphometric measurements were made for 28 days. Ciliated cells appeared to be the primary target of this strain of influenza virus and demonstrated the greatest degree of damage. Three weeks were required to restore the ciliated epithelium in the tubotympanum to normal levels.

Experimental otitis media with effusion induced by intratympanic lipid A instillation

Otitis media with effusion was induced in guinea pigs by intratympanic instillation of lipid A, the lipid moiety of gram-negative bacterial lipopolysaccharide from Salmonella minnesota Re595. Lipid A was chosen as an inducer because of its similar composition among various bacterial species. Animals were killed from the first to 14th day after instillation of various concentrations (0.2, 2, 20, 200 micrograms/ml) of lipid A in 0.5% triethylamine. By 3 days after instillation, all experimental animals developed serous middle ear effusion. The histologic findings included hemorrhage, mucosal edema, capillary engorgement, and migration of infiltrative cells including macrophages, polymorphonuclear neutrophils, and lymphocytes. These findings were most prominent 3 days after instillation, and the recovery of the middle ear epithelium was observed within 14 days. Repeated instillation of lipid A (2 micrograms/ml) at an interval of 14 days reinforced the local response accompanied by serous middle ear effusion. These findings indicate that lipid A can induce the inflammatory changes with middle ear effusion and that lipid A plays an important role in the pathogenesis of otitis media with effusion.

Ablation of the blood-testis barrier in rats and guinea pigs by 48/80, a histamine releaser, and cadmium chloride.

When adult male guinea pigs were injected unilaterally intratesticularly with compound 48/80 (1 mg in 0.05 ml saline), their testicular peritubular capillaries were engorged with blood, intratubular edema was present on the ipsilateral side, and the blood-testicular (BT) barrier (measured by the entrance of acriflavin into the seminiferous tubule) was ablated. The contralateral testis, when injected with saline, showed no pathological changes nor a breakdown of the BT barrier. Subcutaneous injection of guinea pigs with cadmium chloride resulted in a more intense intratubular fluorescence than was observed for 48/80-treated animals. The H1 and H2 receptor blockers (diphenhydramine and cimetidine, respectively) reduced the intensity of capillary engorgement and edema. Intraperitoneal injections of 48/80 (0.5 mg) was lethal to rats, and both diphenhydramine and cimetidine induced survival even with as much as 1 mg of 48/80. Intratubular fluorescence was less severe than that observed for similarly treated guinea pigs or from cadmium chloride-treated rat testes. Neither treatment (48/80 or cadmium chloride) altered the blood-epididymal barrier of either guinea pigs or rats. Species differences were observed in the lethal effects of exogenously administered histamine.

Ultrastructure of the alveolar wall in experimental paraquat poisoning.

Electron microscopic studies of the rat lung were carried out at various intervals after subcutaneous injection of paraquat. Within 12–18 hours after paraquat injection, capillary engorgement and interstitial oedema were noted in alveolar walls. After 24 hours there was, in addition, mitochondrial degeneration and cytoplasmatic vacuolization in granular pneumocytes, membraneous pneumocytes, and capillary endothelial cells. Desquamation of necrotic alveolar epithelial cells was a characteristic feature 48 hours after injection of paraquat. Many of these desquamated cells were identified as granular pneumocytes from their preserved lamellar inclusions. The severe ultrastructural lesions of the alveolar epithelium may serve to explain the derangement of pulmonary surfactant which has been observed in paraquat poisoning under similar experimental conditions.