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Background. Today, acute pancreatitis is a common form of acute abdomen in the clinic, the incidence of which has been increasing in recent years. The aim of the work was to study the dynamics of ultrastructural changes of the hemocapillaries of the alveolar wall of the lungs in the late stages of experimental acute pancreatitis. Material and methods. The experiments were carried out on 54 white Wistar male rats weighing 180–220 g. The animals were divided into three groups: first — intact, second — control, third — experimental with a model of acute pancreatitis, which was reproduced by intraperitoneal administration of a 20% solution of L-arginine at a total dose of 5 g/kg at one-hour interval. The control group of animals was intraperitoneally injected with an equivalent dose of isotonic sodium chloride solution. All research were performed under sodium thiopental anesthesia at the rate of 60 mg/kg body weight. Lung tissue for electron microscopic examination was collected from the lower lobe of the left lung at 3–5 and 7 days. Pieces of lung tissue measuring 1×1×1 mm were fixed in a 2.5% glutaraldehyde solution, followed by additional fixation in a 1% osmium tetroxide solution. After dehydration, the material was poured into Epon-Araldite. Sections with a thickness of 20–50 nm obtained on “Tesla BS-490” ultramicrotome were studied in a PEM-125K electron microscope. Results. The ultrastructural analysis showed that already 3 days after the study, dystrophic-destructive changes, as well as adhesion and aggregation of leukocytes, were detected in the endothelial cells. As the study period increased (5–7 days), the intensity of changes in the hemocapillaries of the alveolar wall increased significantly. In the lumen erythrocyte sludge, thromboleukocyte adhesion and aggregation are determined in hemocapillaries. Conclusion. Acute experimental pancreatitis is accompanied by marked changes in the ultrastructural structure of hemocapillaries of the alveolar wall. The nature and severity of structural changes in the hemocapillaries of the alveolar wall depends on the duration of the course of arginine-induced acute pancreatitis.

Background. Today, acute pancreatitis is one of the most common and severe visceral disorders in patients worldwide. The aim of the work was to study the dynamics of ultrastructural changes of type II alveolocytes in the long-term periods of development of experimental acute pancreatitis. Material and methods. The experiments were carried out on 54 white Wistar male rats weighing 180–220 g. The animals were divided into three groups: first — intact, second — control, third — experimental with a model of acute pancreatitis, which was reproduced by intraperitoneal administration of a 20% solution of L-arginine at a total dose of 5 g/kg at one-hour interval. The control group of animals was intraperitoneally injected with an equivalent dose of isotonic sodium chloride solution. All research were performed under sodium thiopental anesthesia at the rate of 60 mg/kg body weight. Lung tissue for electron microscopic examination was collected from the lower lobe of the left lung at 3–5 and 7 days. Pieces of lung tissue measuring 1×1×1 mm were fixed in a 2.5% glutaraldehyde solution, followed by additional fixation in a 1% osmium tetroxide solution. After dehydration, the material was poured into Epon-Araldite. Sections with a thickness of 20–50 nm obtained on “Tesla BS-490” ultramicrotome were studied in a PEM-125K electron microscope. Results. It was found that three days after the start of the study, along with dystrophic-destructive changes, type II alveolocytes in a state of increased functional activity were observed. Continuation of the experiment (5 days) leads to the progression of ultrastructural changes in type II alveolocytes are determined, which are most pronounced on the 7 day of the study. Conclusion. Acute experimental pancreatitis is accompanied by marked changes in the ultrastructural structure of type II alveolocytes. The nature and severity of structural changes of type II alveolocytes depends on the duration of the course of arginine-induced acute pancreatitis.

Background. Nowadays, acute pancreatitis continues to remain an actual problem both in surgery and in intensive care medicine. The aim of the work was to study the dynamics of ultrastructural changes of alveolar macrophages in the long-term development of experimental acute pancreatitis. Material and methods. The experiments were carried out on 62 white Wistar male rats weighing 180–220 g. The animals were divided into three groups: first — intact, second — control, third — experimental with a model of acute pancreatitis, which was reproduced by intraperitoneal administration of a 20% solution of L-arginine in a total dose of 5 g/kg at one-hour interval. The control group of animals was intraperitoneally injected with an equivalent dose of isotonic sodium chloride solution. All research were performed under sodium thiopental anesthesia at the rate of 60 mg/kg body weight. Lung tissue for electron microscopic examination was collected from the lower lobe of the left lung at 3–5 and 7 days. Pieces of lung tissue measuring 1×1×1 mm were fixed in a 2.5% glutaraldehyde solution, followed by additional fixation in a 1% osmium tetroxide solution. After dehydration, the material was poured into Epon-Araldite. Sections with a thickness of 20–50 nm obtained on “Tesla BS-490” ultramicrotome were studied in a PEM-125K electron microscope. Results. It was found that three days after the start of the study, significant heterogeneity of alveolar macrophages was observed in the alveolar lumen. Next to active phagocytic macrophage elements with dystrophic-destructive changes are determined. Continuation of the experiment (5 days) leads to the progression of submicroscopic changes in alveolar macrophages, which are most pronounced on the7 day of the study. Conclusion. Acute experimental pancreatitis is accompanied by pronounced changes in the ultrastructural structure of alveolar macrophages. The features and severity of structural changes in alveolar macrophages depends on the duration of arginine-induced acute pancreatitis.

Background. Diabetes mellitus is a metabolic disease characterized by persistent hyperglycemia, the prevalence and incidence of which have dramatically increased worldwide. Our research aimed to study the dynamics of changes in the components of the respiratory part of the lungs in streptozotocin-induced diabetes. Materials and methods. The experiments were performed on 88 white male Wistar rats weighing 170-210 g. The animals were divided into three groups: 1 - intact (n=10); 2 - control (n=40); 3 - experimental (n=38) with a model of diabetes mellitus, which was reproduced by intraperitoneal injection of streptozotocin company "Sigma" (USA), diluted in 0.1 M citrate buffer with pH 4.5, at a rate of 60 mg/kg body weight. The control group of animals received an intraperitoneal injection with an equivalent dose of 0.1 M citrate buffer solution with a pH of 4.5. Pulmonary tissue collection for electron microscopic examination was performed under thiopental anesthesia 14, 28, 42, and 70 days after streptozotocin injection. Pieces of lung tissue were fixed in 2.5% glutaraldehyde solution, followed by fixation in 1% osmium tetroxide solution. After dehydration, the material was poured into epon-araldite. Sections obtained on an ultramicrotome "Tesla BS-490" were studied in an electron microscope «PEM-125K». All studies were performed under sodium thiopental anesthesia at the rate of 60 mg/kg of body weight. Results. Our research showed that 14 days after the modeling of streptozotocin-induced diabetes, mainly reactive changes were observed in the components of the respiratory part of the lungs. With an increase in the duration of the study (28-70 days), changes of a dystrophic-destructive nature were noted in alveolocytes of types I and II, and endotheliocytes of hemocapillaries. At the same time, cells with increased functional activity were determined in the components of the respiratory part of the lungs. Conclusion. Streptozotocin-induced diabetes leads to violations of the ultrastructural organization of components of the respiratory part of the lungs. The nature and severity of structural changes in type I, II alveolocytes, and endotheliocytes of hemocapillaries depend on the duration of diabetes.

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Copyright of Polish Surgery / Chirurgia Polska is the property of VM Medica-VM Group (Via Medica) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The renal biopsy is a principal diagnostic method to provide information on type, activity and the intensity of the disease. The aim of the article is to describe the handling, fixation and processing of the renal tissue in pathomorphological laboratories, as well as to provide any information about histopathological glomerular lesions observed in glomerulopathies. The assessment of the renal biopsies includes light microscopy, immunofluorescence microscopy and electron microscopy. In each case clinicians should provide information on the patient's clinical history and recent laboratory values. Immunomorphological evaluation of the renal biopsy specimen should be done in all cases. In view of the high cost of the electron microscopy it seems that the best solution is to preserve the renal tissue in epon and provide ultrastructural evaluation according to the clinical data and light microscopy and immunofluorescence findings. The diagnosis of glomerulopathies requires a close cooperation between clinicians and pathologists. Pathologists should have access to clinical data, and clinicians should understand the limitations of the pathomorphological techniques.

The functional and morphological changes in myocardium of diabetic patients is caused by diabetic macroangiopathy, diabetic microangiopathy, autonomic neuropathy and metabolic disorders. Mechanism of these changes in the course of diabetes is not fully known. To determine whether there are myocardial ultrastructure differences between patients with diabetic cardiomyopathy (normal coronary angiograms) and diabetic patients with coronary artery disease, electron microscopy examination were performed of 70 sections received from seven biopsied patients (1F, 6M), average age 53 years (range: 42-60) with diabetes type II WHO (group A) without clinical evidence of prior coronary artery disease and hypertension, and 100 sections from 10 patients (2F, 8M), average age 54 years (range: 42-65) with diabetes and coronary atherosclerosis. These patients had clinical evidence of heart failure and were submitted to bypass-graft operations (group B). Endomyocardial biopsy tissues were obtained from the right ventricle without complications either during or after the procedure. Obtained biopsy specimens were fixed in 3% glutaraldehyde stabilized with 1M cacodylate buffer at pH 7.4, postfixed in 1% OsO4 on cacodylate buffer. The materials were then dehydrated and embedded in epon. The Irvin-Fischer test for statistical analysis was used. A p value < 0.05 was considered significant. The presence of focal mild loss of myofibrils (+) was statistically more frequent in the patients in A group (p < 0.05). It was found in 86% (6/7) of cases in A group, while in the B group was observed in 20% of (2/10) cases.(ABSTRACT TRUNCATED AT 250 WORDS)