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Transient Perivascular Inflammation of the Carotid Artery (TIPIC) syndrome; is a rare, under-diagnosed clinico-radiologic entity comprising of acute unilateral neck pain and tenderness over the affected carotid bifurcation. In patients with TIPIC syndrome or idiopathic carotidynia, diagnostic imaging demonstrates a characteristic transient perivascular soft tissue thickening at the level of the affected carotid bifurcation. This article presents a short review of literature and highlights the role of Ultrasound in the diagnosis and follow-up of patients with a presumptive diagnosis of TIPIC syndrome.

Background and purpose Hypertension is a multifactorial disease, manifested by vascular dysfunction, increased superoxide production, and perivascular inflammation. In this study, we have hypothesized that 1,2,3,4,6-penta-O-galloyl-β-d-glucose (PGG) would inhibit vascular inflammation and protect from vascular dysfunction in an experimental model of hypertension. Experimental approach PGG was administered to mice every 2 days at a dose of 10 mg·kg-1 i.p during 14 days of Ang II infusion. It was used at a final concentration of 20 μM for in vitro studies in cultured cells. Key results Ang II administration increased leukocyte and T-cell content in perivascular adipose tissue (pVAT), and administration of PGG significantly decreased total leukocyte and T-cell infiltration in pVAT. This effect was observed in relation to all T-cell subsets. PGG also decreased the content of T-cells bearing CD25, CCR5, and CD44 receptors and the expression of both monocyte chemoattractant protein 1 (CCL2) in aorta and RANTES (CCL5) in pVAT. PGG administration decreased the content of TNF+ and IFN-γ+ CD8 T-cells and IL-17A+ CD4+ and CD3+ CD4- CD8- cells. Importantly, these effects of PGG were associated with improved vascular function and decreased ROS production in the aortas of Ang II-infused animals independently of the BP increase. Mechanistically, PGG (20 μM) directly inhibited CD25 and CCR5 expression in cultured T-cells. It also decreased the content of IFN-γ+ CD8+ and CD3+ CD4- CD8- cells and IL-17A+ CD3+ CD4- CD8- cells. Conclusion and implication PGG may constitute an interesting immunomodulating strategy in the regulation of vascular dysfunction and hypertension. Linked articles This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc.

Perimesencephalic subarachnoid hemorrhage (PM-SAH) refers to intracranial hemorrhage located in the perimesencephalic cistern. The etiology remains mainly unclear, although venous leakage or rupture has been postulated. We report an interesting case of a 57-year-old healthy man who presented initially with PM-SAH with worsening of subcortical lesions on follow-up neuroimaging. Histopathological examination demonstrated cerebral amyloid angiopathy with perivascular inflammation.

Introduction: Hypertension is associated with enhanced oxidative stress and perivascular inflammation. Although, that aging and oxidative stress are major factors in the development of hypertension their effect on perivascular inflammation remains unclear. Methods: Using flow cytometry we studied leukocytes infiltrating perivascular adipose tissue (PVAT) in 1-, 3-, 6- and 12-month-old SHR (Spontaneously Hypertensive Rats) and normotensive WKY (Wistar-Kyoto) rats. Additionally, 1-month-old rats were treated with GKT137831 (60mg/kg) or ML171 (NOX1/4 and NOX1 inhibitor, respectively) for 4 weeks. Blood pressure (PB) was measured by the tail cuff. Results: Aging in SHRs was associated with elevation of BP (139±4 vs 180±4 vs 202±2 vs 208±2 mmHg; 1 vs 3 vs 6 vs 12-month-old, respectively) when this effect was not seen in WKY rats. While the total number of leukocytes infiltrating PVAT were comparable between 1-month-old WKY and SHR (p=0.8) aging escalated their numbers only in SHRs (2096±164 vs 1994±296 vs 2311±470 vs 3255±408 cell/mg; p int int int int Conclusions: Aging in spontaneous hypertension is associated with elevation of BP and aggravation of perivascular inflammation which are hastened after NOX1/4 inhibitor treatment.

Juvenile dermatomyositis is a complex illness characterized by vascular/perivascular inflammation, primarily in the skin and muscles. In this review, we discuss how proteomic and genomic technologies have expanded our understanding of the immune pathogenesis of this disease. We will also discuss further directions that the field may take to use existing and developing technologies to further our understanding of this often-perplexing disease.

Objective: Hypertension (HT) is associated with perivascular inflammation and increased vascular fibrosis. MicroRNAs (miR) are a novel gene expression regulation mechanism and play a pivotal role in a range of pathological processes. The role and mechanism of miR214 in vascular fibrosis is unknown. Methods: 3-month-old C57BL/6, miR214KO and wild-type littermates were treated with angiotensin II (AngII, 490ng/kg/min; n=6-10) or control buffer for 14 days. PVATs from C57BL/6 animals were analysed using TaqMan_Rodent_microRNA_Arrays. Histological studies, wire myography, lucigenin-enhanced luminometry and cytometrical analysis was conducted, followed by statistical analysis with ANOVA or t-test. Data are expressed as a mean±SEM. Results: Out of 381 miRs, 16 were significantly overexpressed in C57BL/6 AngII animals, with only miR214 showing 8-fold induction (p Conclusions: MiR-214 plays a major role in modulation of aortic fibrosis, vascular function, oxidative stress and perivascular inflammation.

ObjectiveTo investigate the spatiotemporal evolution of venous narrowing in newly developing MS lesions in a longitudinal MRI study including susceptibility-weighted images (SWIs).MethodsWe retrospectively investigated serial MR examinations of 18 patients with MS acquired on a 3T MRI system including SWI for acute contrast-enhancing lesions with at least 1 MRI examination before contrast enhancement. The mean diameter of veins at the time point of contrast enhancement was compared with the mean diameter of veins before and after contrast enhancement.ResultsA total of 40 acute contrast-enhancing lesions with a corresponding intralesional central vein were included in the study. The mean diameter of intralesional veins at the time of contrast enhancement (0.80 ± 0.12 mm) was smaller than that at before (1.16 ± 0.19 mm) and after contrast enhancement (1.07 ± 0.15 mm; p < 0.001 for all comparisons).ConclusionsOur findings contribute to the increasing database of plaque development and evolution. The smaller diameter of intralesional veins on SWI at the time of blood-brain barrier breakdown may reflect morphologic changes because of perivascular inflammation and/or decreased levels of deoxygenated hemoglobin.

Cerebral amyloid angiopathy–related inflammation (CAA-I) was first described in 2004 with 7 cases of perivascular inflammation in patients with CAA.1 So far

Epicardial adipose tissue (EAT), deposited around subepicardial coronary vessels, may contribute directly to perivascular inflammation and smooth muscle cell proliferation. This study assessed the relationship between EAT and in-stent restenosis.Four hundred and seven patients had received successful coronary intervention. EAT thickness was measured by echocardiography. Angiographic follow-up was obtained between 6 months and 2 years. Restenosis was defined as target lesion revascularization (TLR). EAT thickness of patients was compared by TLR controlling for additional well-known predictors of restenosis. The TLR-free survival analysis according to EAT thickness was estimated using the Kaplan-Meier method and the differences between groups were assessed by the log-rank test.Median EAT thickness was significantly increased in patients undergoing TLR compared with those without restenosis (3.7 vs. 3.0 mm, p = 0.001). EAT thickness was one of the independent factors associated with restenosis (Odds ratio = 1.19, 95% confidence interval = 1.01-1.33, p = 0.007). The TLR-free survival of patients with thick EAT was significantly worse than patients with thin EAT (log-rank p = 0.001).EAT thickness is related with restenosis and may provide additional information for future restenosis.

Pulmonary arterial hypertension (PAH) is a devastating progressive disease associated with a high mortality despite current vasodilator therapies. Perivascular inflammation and high levels of neutrophil elastase are thought to play a pivotal role in the adverse vascular remodeling of small pulmonary arteries that causes PAH. Despite this, the function of neutrophils and in particular, their interaction with the pulmonary arterial endothelium has not been studied in PAH. We hypothesized that neutrophil functions such as adhesion to a substratum or to endothelial cells and transmigration across a substratum or trans-endothelial migration (TEM) are abnormal in PAH on the basis of dysfunction of both cell types. Using a neutrophil like cell line dHL-60 and isolated human neutrophils from donors and PAH patients, we demonstrated no significant difference in adhesion to PAH vs. control PAECs when stimulated with TNF-α (100μg/mL). However, TEM of both IL-8 (100ng/ml) and fMLP (100nM) stimulated dHL-60 cells and donor neutrophils was enhanced in PAH vs. control PAECs (p

Background Lobular keloid appears to be a consequence of hypertrophic inflammation secondary to ear piercings performed under unsterile conditions. We wish to understand the pathogenesis of lobular keloids and report operative outcomes with a literature review. Methods A retrospective review identified 40 cases of lobular keloids between January, 2005 and December, 2010. Patient records were reviewed for preclinical factors such as presence of inflammation after ear piercing prior to keloid development, surgical management, and histopathologic correlation to recurrence. Results The operation had been performed by surgical core extirpation or simple excision, postoperative lobular compression, and scar ointments. Perivascular infiltration was noted in intra- and extra-keloid tissue in 70% of patients. The postoperative recurrence rate was 10%, and most of the patients satisfied with treatment outcomes. Conclusion Histological perivascular inflammation is a prominent feature of lobular keloids. Proper surgical treatment, adjuvant treatments, and persistent follow-up observation were sufficient in maintaining a relatively low rates of recurrence.

Aims: To study the histological features on muscle biopsy and correlate them with clinical features, other laboratory data in adult patients to make a diagnosis of dermatomyositis (DM), applying the European Neuromuscular center (ENMC) criteria. Materials and Methods: Adult patients who fulfilled clinical, laboratory, and muscle biopsy findings according to ENMC criteria for DM during the period 2010-2013 were included in the study. Cryostat sections of muscle biopsy were reviewed with emphasis on Perifascicular atrophy (PFA), perivascular/endomysial inflammation. Muscular dystrophies and metabolic myopathies were excluded by appropriate immunohistochemistry and special stains. Results: The diagnosis of adult DM was made in 45 patients out of 170 clinically suspected idiopathic inflammatory myopathies. These included 33 definite, 4 probable, 7 possible sine dermatitis, and 1 amyopathic DM. All patients with definite DM had typical rash and proximal muscle weakness and muscle biopsy showed PFA with or without inflammation. Thirteen patients had quadriparesis, neck muscle weakness, dysphagia/dysphonia at presentation. Patients with probable DM had rash and showed perivascular/endomysial inflammation with no PFA. Possible DM sine dermatitis showed PFA with perivascular/endomysial infiltrates. One patient of amyopathic DM had typical heliotrope rash and characteristic skin biopsy. Conclusions: Histological features are important for the diagnosis of DM. Relying on PFA for diagnosis of definite DM underestimates the true frequency of DM.

The current understanding of the pathology that underlies pulmonary vascular and right ventricular remodeling in pulmonary hypertension is discussed. Although recent studies underscored the importance of intima and media remodeling and, for the first time, the relevance of perivascular inflammation, much is needed to move the field forward. Reassessment of distribution and extension of the different vascular lesions requires state-of-the-art stereological tools, allied to three-dimensional casting and integration with data concerning cellular and molecular pathobiological processes. This integrated approach is ever more pressing in the right ventricle, because our understanding of key structural alterations of the failing right ventricle in pulmonary hypertension is lacking. This enterprise will enable better translation of pathogenetic processes to the human disease and provide key data to guide diagnostic and prognostic imaging approaches.

Hypertension in obesity occurs as a result of abnormal increases in sympathetic nerve density over arteries controlling blood pressure; the causative factors underlying these changes are unknown. H...

Experimental autoimmune encephalomyelitis (EAE) induction in TNF gene-targeted mice has resulted in conflicting reports in part due to the strong association of TNF with the MHC locus. To define the participation of TNF in EAE development, we back-crossed TNF-deficient mice (H-2b) into the SJL/J strain and directly compared them to H-2b congenic SJL or inbred SJL/J mice. Induction of EAE with myelin basic protein (MBP) revealed that H-2b congenic SJL mice are fully susceptible, indicating that the H-2b haplotype does not affect disease susceptibility. Using H-2b congenic SJL mice we show here that TNF deficiency modifies the normal course of EAE by considerably delaying the onset for approximately 5 days, suggesting that TNF is required for the normal initiation of MBP-induced EAE. However, TNF-deficient mice eventually developed severe EAE with perivascular inflammation and primary demyelination similar to wild-type controls, indicating that TNF is not essential during these processes. Taken together, these results indicate that although TNF is not required for the progression of MBP-induced EAE, it contributes positively by advancing the onset of disease.

Four infants developed progressive muscle weakness after a normal initial postnatal development. All patients had a moderate elevation of serum creatine kinase (CK) activity. Muscle biopsies revealed, in addition to myopathic features, endomysial and perivascular inflammation. Electron microscopy disclosed prominent myonuclear abnormalities. Corticosteroids in 3 patients were moderately beneficial. This appears to be a clinicopathologically distinct form of inflammatory myopathy of infants.

Migraine is more common than previously reported. Three large epidemiological studies showed that the prevalence of migraine in the general population is 12-14% for women and 5-7% for men. Animal experiments suggest that the headache in migraine might be due to alterations of a trigemino-vascular reflex resulting in vasodilatation, plasma extravasation and perivascular inflammation of dural arteries. In addition to sumatriptan a number of other 5-HT-1D receptor agonists are under investigation and will be available for the treatment of acute migraine attacks in the near future. For the prevention of migraine, valproic acid has been shown to be effective in cases that are refractory to traditional migraine prophylaxis. Neurophysiological data indicate that the central pain threshold may be altered in chronic tension-type headache. Die Migrane ist haufiger als bisher angenommen. Drei grose epidemiologische Studien zeigen, dass die Pravalenz der Migrane bei Frauen zwischen 12-14% und bei Mannern zwischen 5-7% betragt. Fur die Entstehung der Kopfschmerzen bei der Migrane wird ein pathologischer trigemino-vaskularer Reflex verantwortlich gemacht, der zur Vasodilatation, Plasmaextravasation und perivaskularer Entzundung im Bereich von Duraarterien fuhrt. Eine Vielzahl neuer Serotonin (5HT-lD)-Rezeptor-Agonisten werden neben Sumatriptan in den nachsten Jahren Eingang in die Therapie der akuten Migraneattacke finden. Als neues Medikament fur die Migraneprophylaxe hat sich im letzten Jahr die Valproinsaure etabliert. Neue neurophysiologische Untersuchungen zeigen, dass beim chronischen Spannungskopfschmerz eine veranderte zentrale Schmerzschwelle besteht.

Fifty-eight cases of septal granulomatous panniculitis were reviewed; 14 cases were diagnosed as erythema nodosum migrans (migratory panniculitis) and 36 as chronic erythema nodosum on the basis of clinical and histopathologic features. Erythema nodosum migrans was characterized by markedly thickened and fibrotic septae, marked capillary proliferation (like granulation tissue), and massive granulomatous reaction (with giant cells) along the borders of the widened septa. Hemorrhage was rare, and phlebitis was not seen. Chronic erythema nodosum showed mild septal change, little fibrosis, and lymphohistiocytic perivascular inflammation with only focal granulomatous formation. Phlebitis and hemorrhage were common. The condition termed erythema nodosum migrans has many of the same clinical features as chronic erythema nodosum, and we think this term is preferable to migratory panniculitis. We believe that there are sufficient clinical and histopathologic features to justify considering erythema nodosum migrans as a unique clinicopathologic entity.

Carotidynia is a rare diagnosis for unilateral neck pain without a clear physical substrate. As such, it may be encountered in surgery practice when analysing carotid artery status in symptomatic patients. Here, a case is presented which outlines the diagnostic process and subsequent treatment of carotidynia. As opposed to vascular causes of unilateral neck pain, carotidynia can be easily treated conservatively. Relief of complaints as well as regression of perivascular inflammation on magnetic resonance imaging can be effectively achieved with the use of non-steroidal anti-inflammatory drugs.

We have recently developed a non-adhesive liquid embolic agent, hydroxyethylmethacrylate methylmethacrylate copolymer (HEMA-MMA), and used it for arteriovenous malformations (AVMs) in the central nervous system. To evaluate the toxicity and usefulness of this agent, we made a clinicopathological study of AVMs that were embolized with it and then excised surgically. This study includes ten cases: nine with pial AVM and one with scalp AVM. In a pathological study, special attention was paid to vascular and perivascular inflammation, angionecrosis, recanalization of the embolized vessels, and foreign body reactions. Inflammation was absent or very mild regardless of the interval between embolization and excision. There was no angionecrosis. Recanalization could be expected to occur in the partially occluded vessel. Foreign body reactions such as infiltration of monocytes or giant cells, and proliferation of fibroblasts or capillaries were also not seen in any case. It was concluded that HEMA-MMA is an excellent embolic material that is easy to handle, less vasotoxic than other agents, and highly his-tocompatible.

Sustained improvement with prolonged topical tretinoin for photodamaged skin has been well documented for up to 22 months of continuous treatment. We now report long-term (4 years) histologic effects of topical tretinoin in photodamaged skin of 27 patients, the longest study to date. The observed decreases in dermal elastin content and perivascular inflammation and increase in epidermal mucin in facial biopsies obtained after up to 4 years of treatment may be partly responsible for the continued clinical improvement. Furthermore, the study shows that there are no untoward effects on keratinocytes or melanocytes during long-term use of topical tretinoin.

We previously demonstrated that cytomegalovirus (CMV) infection enhanced perivascular inflammation in rat aortic allografts. In this study, we investigated the relationship between the CMV infection load and the magnitude of perivasculitis (chronic rejection) in aortic transplants. Rats received orthotopic abdominal aortic grafts, different degrees of total body irradiation (TBI) for immunosuppression and CMV inoculation. The spleens of the rats receiving 5 Gy of TBI contained more infectious virus and viral antigens than those of rats receiving 3 Gy of TBI or no TBI. Although the number of inflammatory cells infiltrating the perivascular area was decreased after TBI, CMV infection resulted in increased perivasculitis in rats that received 5 Gy of TBI as compared to non-infected animals. This virus-induced effect was characterized predominantly by an increased T-cell infiltration, including CD4 and CD8 T-cells. It is concluded that an enhanced systemic CMV infection during severe immunosuppressive therapy can accelerate the development of chronic rejection, which seems to be mediated mainly by T-cells.

Background Lipopolysaccharide (LPS) contained in tobacco smoke and a variety of environmental and occupational dusts is a toxic agent causing lung inflammation characterized by migration of neutrophils and monocytes into alveoli. Although migration of inflammatory cells into alveoli of LPS-treated rats is well characterized, the dynamics of their accumulation in the perivascular space (PVS) leading to a perivascular inflammation (PVI) of pulmonary arteries is not well described. Methods Therefore, we investigated migration of neutrophils and monocytes into PVS in lungs of male Sprague-Dawley rats treated intratracheally with E. coli LPS and euthanized after 1, 6, 12, 24 and 36 hours. Control rats were treated with endotoxin-free saline. H&E stained slides were made and immunohistochemistry was performed using a monocyte marker and the chemokine Monocyte-Chemoattractant-Protein-1 (MCP-1). Computer-assisted microscopy was performed to count infiltrating cells. Results Surprisingly, the periarterial infiltration was not a constant finding in each animal although LPS-induced alveolitis was present. A clear tendency was observed that neutrophils were appearing in the PVS first within 6 hours after LPS application and were decreasing at later time points. In contrast, mononuclear cell infiltration was observed after 24 hours. In addition, MCP-1 expression was present in perivascular capillaries, arteries and the epithelium. Conclusion PVI might be a certain lung reaction pattern in the defense to infectious attacks.

The effect of argon laser irradiation on the microvessels of the subcutaneous areolar tissue of the rabbit ear, mounted in a transparent chamber by Clark's method, was studied. The capillaries and venules, in which dysfunctional changes were found in the microcirculation, were most sensitive to argon laser irradiation. Besides destruction of the vessel walls and perivascular inflammation, active reorganization of the microcirculatory system and a redistribution of the blood flow were observed under the influence of the laser beam.

We have previously shown that cationic proteins localize to the dermal-epidermal junction (DEJ) after i.v. injection in experimental animals. In the present studies, cationized rabbit IgG was used as antigen for induction of chronic serum sickness in C57BL/6J mice over a period of 4 weeks. The formation of immune deposits was examined by immunofluorescence microscopy at weekly intervals during chronic antigen administration and at 7 weeks from the initiation of studies. Chronic administration of the cationized antigen led to immune complex deposits at the DEJ, while administration of the same antigen in native form did not lead to these deposits. Junctional immune deposits increased with higher doses of cationized antigen and paralleled renal extraglomular deposition in intensity, persistence, and morphology. Mice given cationized antigen also demonstrated vascular immune complex deposits without complement, while mice given native antigen had complement deposits and developed perivascular inflammation. No inflammation or complement deposition was detected at the DEJ in either group. Charge properties of circulating antigens are important in determining tissue sites of immune complex deposition and inflammation. Circulating cationic antigens can lead to immune deposits at the DEJ.

Systemic knockout of adipose triglyceride lipase (ATGL), the pivotal enzyme of triglyceride lipolysis, results in a murine phenotype that is characterized by progredient cardiac steatosis and severe heart failure. Since cardiac and vascular dysfunction have been closely related in numerous studies we investigated endothelium-dependent and -independent vessel function of ATGL knockout mice. Aortic relaxation studies and Langendorff perfusion experiments of isolated hearts showed that ATGL knockout mice suffer from pronounced micro- and macrovascular endothelial dysfunction. Experiments with agonists directly targeting vascular smooth muscle cells revealed the functional integrity of the smooth muscle cell layer. Loss of vascular reactivity was restored ~ 50% upon treatment of ATGL knockout mice with the PPARα agonist Wy14,643, indicating that this phenomenon is partly a consequence of impaired cardiac contractility. Biochemical analysis revealed that aortic endothelial NO synthase expression and activity were significantly reduced in ATGL deficiency. Enzyme activity was fully restored in ATGL mice treated with the PPARα agonist. Biochemical analysis of perivascular adipose tissue demonstrated that ATGL knockout mice suffer from perivascular inflammatory oxidative stress which occurs independent of cardiac dysfunction and might contribute to vascular defects. Our results reveal a hitherto unrecognized link between disturbed lipid metabolism, obesity and cardiovascular disease., Graphical abstract, Highlights • AKO mice suffer from severe micro- and macrovascular endothelial dysfunction. • Aortic eNOS protein is downregulated in ATGL deficiency due to enhanced proteasomal degradation. • PVAT of AKO mice exhibits characteristics of chronic inflammatory oxidative stress. • At least two independent mechanisms are involved in the endothelial defect.

In a study of a series of mild and spinal varieties of multiple sclerosis the following histological changes have been found in the macroscopically normal white matter: 1. Marked astrocytic proliferation. 2. Some sclerosis of blood vessels. 3. Some perivascular inflammation. 4. Occasional unsuspected demyelination.

A 3% topical minoxidil solution was used to treat 31 normotensive persons (13 male, 18 female) with extensive alopecia areata. After 15 months, three patients (14%) had 75%-100% regrowth, 13 (59%) had some form of regrowth, and nine (41%) had no regrowth. In the initial three-month double-blind portion of the study, minoxidil was not shown to be more effective than placebo. Biopsy specimens from eight patients who underwent biopsy prior to treatment, after three months, and posttreatment showed no significant change in peribulbar or perivascular inflammation. Prominent, new anagen follicles were observed. The 3% topical minoxidil was generally well tolerated and skin irritation was minimal. Blood pressure monitoring revealed no significant changes in diastolic or systolic pressures. Minoxidil is a relatively safe treatment for extensive alopecia areata and may be effective in the treatment of some cases of recalcitrant disease.

Three patients had documented fundus changes conforming to those of the recently described multiple evanescent white dot (MEWD) syndrome. All three patients were unilaterally affected with variously sized, soft, single, and coalescent white lesions at the level of the RPE and the deep retina. Fluorescein angiography demonstrated early staining and hyperfluorescence of the white dots and delayed staining around the optic disc. Some degree of optic disc edema could be seen in all three eyes, two of which had corresponding field defects. In all three eyes, characteristic “stippling,” or granularity, of the affected macula developed rapidly and vitreal cells were observed. One eye had signs of previous perivascular inflammation. ERG studies performed on one patient indicated a reduction in the a-wave and depression of the ERP, findings that correlated with the clinical observations of RPE affectation. RETINA 8:132-135, 1988

Histopathological alterations in kidneys have been studied in squirrels with repeated intraperitoneal injections of cadmium acetate at a dose of 1.0 mg Cd/Kg of body weight. Cloudy swelling, necrosis, denudation and destruction of tubular epithelium, focal aggregates of inflammatory cells, perivascular inflammation by chronic inflammatory cells and perinephric haemorrhage with infiltration by phagocytes containing haemosidirin were noticed after different exposure intervals. Squirrels revealed significant increase in body weight and kidney weight (P

Background Serious health problems and socioeconomic consequences of the illicit use of opiates have been proved in both developed and developing societies Objectives We aimed to evaluate" The effects of opiate addiction through different administration routes on pulmonary inflammation and its severity." Materials and Methods Our experiments were performed on eighteen adult male Syrian golden hamsters which were allocated to one of the three groups (n = 6): control group which did not receive opiate; the first study group were administered oral opiate via stomach tube; and another study group were administered inhaled opiate. After four weeks, all hamsters were anesthetized with diethyl ether and their lung tissues were isolated for pathological assessment. Results Severe perivascular inflammation was detected in 33.3% of the samples with oral opiate dependence and 20% of the cases addicted to opiate through inhalation. Also, severe peribronchial inflammation was observed in only 20% of the samples addicted to inhaled opiate and was not found in the other groups. No significant differences were found in the severity of perivascular and peribronchial inflammation across the three groups. Although the mean of total inflammation scale in the subjects with oral opiate dependence (3.00 ± 1.79) was numerically higher than that in the inhaled dependence group (1.40 ± 2.60) and the controls (2.25 ± 1.26), this difference was not statistically significant. Conclusions Administration did not influence the appearance or severity of pulmonary inflammation in animal models addicted to opiate.