[Intravascular aggregation ("sludge") Pathogenesis and relations with circulatory resuscitation].
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Small bowel transplantation has great potential for the treatment of short bowel syndrome, but the poorly understood rapid rejection of the bowel has hindered progress in this field. In this study, the rat model was used to evaluate the earliest detectable changes of bowel rejection. Eleven pairs of outbred rats underwent heterotopic transplantation of 10-15 cm segments of proximal jejunum on a pedicle of superior mesenteric artery and vein, anastomosed microsurgically to recipient aorta and inferior vena cava, respectively. The bowel extremities were exteriorized. Eight successfully transplanted rats were studied with serial punch biopsies, immediately post-transplantation and daily for 7 successive days. Biopsies were evaluated by light (LM) and transmission electron microscopy (TEM). Ultrastructural changes were evident before any gross or histologic changes. Endothelial damage, detected only by TEM, was common and resulted in exposure of the thrombus-promoting subendothelial components. Activated platelets as well as platelet aggregates adhered to these damaged areas. The lumen of some vessels was filled with tightly packed erythrocytes, at times showing intravascular hemolysis, suggestive of stasis. Extravascular features included edema and small numbers of immunocompetent cells. The epithelium showed a variable morphology depending on the degree of change in the underlying vessels and submucosa. The findings suggest that vascular damage and thrombosis as well as immunologic events are important in the early phase of the rejection process. Sustaining a viable segment of transplanted intestine may depend on suppressing both the microthrombotic aspect (with anticoagulants and/or antiplatelet agents) and the ensuing immunologic process with newer modalities such as cyclosporine.
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Circulation in ocular conjunctival vessels was studied in patients with viral hepatites B and B + C. Intravascular, vascular (mainly venular), and capillary changes were observed during the acute period of disease. The most common disorders were erythrocyte aggregation, venous congestion, and reduction of capillary network. Use of narcotics augments the disorders in blood delivery. Pathological changes in microcirculatory system did not normalize by the end of hospital stay.
BACKGROUND: Thrombocytopenia is commonly observed in severe leptospirosis. However, previous studies on coagulation alterations during leptospirosis resulted in inconsistent conclusions. Some findings showed that the prominent levels of thrombocytopenia observed in severe leptospirosis did not reflect the occurrence of disseminated intravascular coagulation (DIC) syndrome, while the others reached the conclusion that the hemorrhages observed in leptospirosis were due to DIC. The aim of this study is to elucidate whether DIC is an important feature of leptospirosis. METHODS: The leptospirosis model of guinea pig was established by intraperitoneal inoculation of Leptospira interrogans strain Lai. Hematoxylin and eosin (HE) staining, electron microscopy and immunohistochemistry staining were used to detect the pathologic changes. Platelet thrombus or fibrin thrombus was detected by HE, Martius Scarlet Blue (MSB) staining and electron microscopy. Hemostatic molecular markers such as 11-dehydrogenate thromboxane B2 (11-DH-TXB2), thrombomodulin (TM), thrombin-antithrombin III complex (TAT), D-Dimer and fibrin (ogen) degradation products (FDPs) in the plasma were examined by quantitative enzyme-linked immunosorbent assay (ELISA) to evaluate the hematological coagulative alterations in leptospirosis models. RESULTS: Pulmonary hemorrhage appeared in the model guinea pig 24 hours after leptospires intraperitoneal inoculation, progressing to a peak at 96 hours after the infection. Leptospires were detected 24 hours post-inoculation in the liver, 48 hours in the lung and 72 hours in the kidney by immunohistochemistry staining. Spiral form of the bacteria was initially observed in the liver, lung and kidney suggestive of intact leptospires, granular form of leptospires was seen as the severity increased. Platelet aggregation in hepatic sinusoid as well as phagocytosis of erythrocytes and platelets by Kupffer cells were both observed. Neither platelet thrombus nor fibrin thrombus was found in the liver, lung or kidney via morphological observation. Thrombocytopenia was observed in all infected guinea pigs of our experimental leptospirosis study. Analysis of hematologic molecular markers showed that 11-DH-TXB2 and TM in the plasma were elevated significantly. TAT that reflects the thrombin activation had a trend of decline after infection. Although D-dimer and FDPs increased statistically, the increasing may not bear clinical significance. CONCLUSION: Pathologic and hematological studies for experimental leptospirosis of guinea pig indicated that the thrombocytopenia found in guinea pigs did not correlate with the occurrence of DIC. The platelet aggregation and Kupffer cells phagocytosis might be the potential causes of thrombocytopenia in severe leptospirosis.
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Protein and lipid composition of erythrocyte membranes as well as loss of erythrocyte filtrability were studied in two experimental models: staphylococcal toxicosis and post-ischemic syndrome. Lipid spectrum of erythrocytes was studied in 16 experiments, protein composition--in 28 experiments and deformation of erythrocytes--in 46 experiments. Considerable destruction of erythrocyte membrane protein moiety and of lipid composition were found under extreme conditions involving distinct loss of phospholipid bilayer and decrease in content of main high molecular proteins. These impairments of erythrocyte membranes and a decrease in erythrocyte flow properties may be referred as principal reasons for development of microcirculation disturbance and of microvascular channel blockade. The alterations observed appear to be responsible for occurrence of components with various ability to aggregation in body fluid media as well as for development of disseminated intravascular coagulation in microcirculation.
Rheologic properties of blood cells and a state of oxidative-reductive processes and blood systems have been studied in 75 patients in acute period of ischemic stroke. The signs of oxidative stress development and simultaneous augmentation of blood cells aggregation were found. Shifts of redox-equilibrium in thiol-disulfide and ascorbate oxidative-reductive blood systems and cells aggregation dependence on their state were detected. An interrelation of oxidative processes and blood cells aggregation with clinical course severity and outcome was revealed. The authors discuss possible mechanisms for blood cells aggregation in oxidative stress. Including of antioxidants in the pathogenetic therapy and their earlier usage reduce essentially the intensity of oxidative stress and blood cells aggregation and promote neurological symptoms regress. The results obtained allow considering antioxidant treatment as a pathogenic modality for prevention and treatment of ischemic stroke. Clinico-laboratory correlations suggest a pathogenic role of oxidative stress in ischemic stroke as a factor augmenting aggregation processes and promoting intravascular thrombogenesis.
Proliferation of the vascular endothelium of the parathyroid glands of dogs exposed to ozone inhalation was studied. Direct observation of mitoses in the endothelial cells were made. Focal hemorrhages in the form of the presence of erythrocytes, clotting, and fibrin deposition in the extravascular spaces were seen. Ultrastructural analysis of transverse section of blood vessels showed intravascular platelet aggregation. Lymphoid cells were observed in the lumen of the blood vessels as well as in the perivascular areas as infiltrates. The possibility is discussed that present vascular reactions signify the morphologic equivalent of an immunologic response.
Large granule complexes are structures found in a small percentage of chicken erythrocyte nuclei when observed in ultra-thin sections in the electron microscope. They consist of an amorphous region associated with a number of large (approximately 30 min) granules. We have shown, by a novel use of phenylhydrazine to synchronize populations of chicken erythrocytes in vivo, that large granule complexes do not occur in the nuclei until the cells have reached one-third to one-half of their normal intravascular lifespan. The mature large granule complexes are formed by aggregation of pre-existing fibrillar, granular and amorphous material, and their presence is correlated with the presence of another ultrastructural feature of the nucleus, the so-called "filled cavities' in the chromatin. Digestion of ultra-thin sections of erythrocytes embedded in the hydrophilic resin glycol methacrylate (GMA) has shown that the major component of the amorphous region is a rather acidic protein that is not haemoglobin, the most abundant protein in the erythrocyte. The large granules also contain protein and, almost certainly, RNA. The problems encountered in reaching this conclusion have emphasized the lack of unambiguous cytochemical tests for use on ultra-thin sections. We have shown that the large granule complex differs in many respects from the nucleolus in the erythrocyte series, even though the two organelles have certain superficial similarities such as their overall dimensions and the presence of granular and fibrillar regions. The most likely function of the large granule complex is as a repository for material, including RNA, the processing of which has ceased in the inactivated erythrocyte nucleus.
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Studies on microcirculation in the elderly include observations in the small vessels of the bulbar conjunctiva and of the nailbed with respect to a classification of the findings according to a number of semeiologic criteria (diameter and shape alterations, terminal capillary network, intravascular red cell aggregation). In vascular diseases of the elderly there are typical alterations of the capillaroscopic findings in the bulbar conjunctiva and in the nailbed, particularly in cases of arteriosclerosis, arterial hypertension, diabetic microangiopathy, heart failure, ischemic myocardiopathies. During the treatment with some vasoactive drugs (nicotinic acid and its derivatives, buflomedil, CPD-choline) there are marked modifications of the small conjunctival vessels, with evident dilatations, appearance of collaterals, increased homogeneity of the blood flow, better evidence of the capillary network and reduction of intravascular red cell aggregation.