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PubMed1996

Comparative pathogenesis of human WA1 and Babesia microti isolates in a Syrian hamster model.

The pathogenesis of a newly recognized, molecularly and antigenically distinct human babesial isolate (WA1) and Babesia microti, the common cause of human babesiosis in the United States, were compared in a Syrian hamster model. A group of 33 adult female hamsters were inoculated intraperitoneally with either WA1-infected, B. microti-infected, or uninfected hamster erythrocytes. All WA1-infected animals became parasitemic by postinoculation (PI) day 3 or 4 and were severely lethargic and dyspneic by PI days 6 to 10. Death often occurred spontaneously by PI day 10, with parasitemia of 12 to 90%. Hamsters inoculated with B. microti became parasitemic by PI day 7 and developed peak parasitemia (42 to 60%) by PI day 14 that subsequently decreased to low or undetectable values. Although the B. microti-infected hamsters developed severe anemia, they generally remained asymptomatic. Postmortem examination of WA1-infected hamsters revealed intravascular aggregates of large mononuclear inflammatory cells that occasionally occluded small to medium veins, pulmonary leukoclastic phlebitis, thrombosis, and multifocal coagulative necrosis in the heart, spleen, lung, and liver. No vascular lesions or areas of coagulative necrosis were detected in any B. microti-infected or control hamsters. The results of this study suggest that marked leukocytosis followed by acute necrotizing phlebitis resulting in disseminated intravascular coagulation, thromboembolism, and infarction may be central to the pathogenesis of WA1 infections.

Anemia↗
PubMed1998

Intravascular coagulation activation in a murine model of thrombomodulin deficiency: effects of lesion size, age, and hypoxia on fibrin deposition.

We consecutively inactivated both alleles of the thrombomodulin (TM) gene in murine embryonic stem (ES) cells and generated TM-deficient (TM-/-) chimeric mice. Quantitation of an ES-cell marker and protein C cofactor activity indicates that up to 50% of pulmonary endothelial cells are ES-cell derived and therefore TM deficient. Infusions of 125I-fibrinogen into mice show a significant increase (fourfold, P <.005) in radiolabeled cross-linked fibrin in TM-/- chimeric mouse lung as compared with wild-type mice. However, only chimeric mice that exhibit at least a 30% reduction in protein C cofactor activity and are at least 15 months old display this phenotype. Immunocytochemical localization of TM in chimeras shows a mosaic pattern of expression in both large and small blood vessels. Colocalization of cross-linked fibrin and neo (used to replace TM) reveals that fibrin is deposited in TM-/- regions. However, the fibrin deposits were largely restricted to pulmonary vessels with a lumenal area greater than 100 micrometer2. The hypercoagulable phenotype can be induced in younger chimeric mice by exposure to hypoxia, which causes a fivefold increase in beta-fibrin levels in lung. Our findings show that TM chimerism results in spontaneous, intravascular fibrin deposition that is dependent on age and the magnitude of the TM deficiency.

Age Factors↗
PubMed1999

Cocaine-induced erythrocytosis and increase in von Willebrand factor: evidence for drug-related blood doping and prothrombotic effects.

BACKGROUND: Mechanisms that mediate cocaine-induced cardiovascular events following vasoconstriction are incompletely understood. OBJECTIVE: To examine the effects of cocaine in moderate doses on hematologic and hemostatic parameters that influence blood viscosity and thrombotic potential. METHODS: Changes in hemoglobin concentration, hematocrit, and red blood cell counts were measured in human subjects who met Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for long-term cocaine abuse, before and sequentially after moderate intranasal and intravenous doses of cocaine. Hemostatic parameters, including von Willebrand factor, fibrinolytic activity, fibrinogen, plasminogen activator inhibitor antigen, and tissue-type plasminogen activator antigen, were sequentially measured after intravenous cocaine or saline placebo with cardiac troponin subunits T and I. RESULTS: Hemoglobin level (P= .002), hematocrit (P =.01), and red blood cell counts (P = .04) significantly increased from 4% to 6% over baseline from 10 to 30 minutes after intranasal (n = 14) and intravenous (n = 7) cocaine administration in doses of 0.9 mg/kg and 0.4 mg/kg, respectively, with no change in white blood cell or platelet counts. There was a significant increase (P =.03) in von Willebrand factor from 30 to 240 minutes, peaking at 40% over baseline following intravenous cocaine administration in a dose of 0.4 mg/kg (n = 12), with no change after 0.2 mg/kg (n = 3) or placebo (n = 6). Other hemostatic factors, creatinine, blood urea nitrogen, and cardiac troponin subunits T and I showed no changes. CONCLUSIONS: Cocaine induced a transient erythrocytosis that may increase blood viscosity while maintaining tissue oxygenation during vasoconstriction. An increase in von Willebrand factor without a compensatory change in endogenous fibrinolysis may trigger platelet adhesion, aggregation, and intravascular thrombosis.

Adult↗
PubMed1978

Pilot epidemiological studies in thrombosis.

Some differences in the blood of farmers in Nurmijarvi, Finland, Canino, Italy, and Beltsville, Maryland in the United States apparently were associated with differences, among the areas, in the farmers' diets. Those associations suggested that diets that are high in saturated fats (Nurmijarvi) could predispose humans to develop intravascular disease. Such predisposition has been observed in experimental animals. Low levels of the parameters that are considered active in such predisposition apparently were associated with diets that were low in saturated fats (Canino) or with diets that were low in saturated and high in unsaturated fats (Beltsville). Within the limits of the experimental design, the data from the three population groups indicated that a more comprehensive study might establish a relation between diet and intravascular disease in humans.

Adult↗
PubMed2000

Pharmacological concentrations of arginine influence human whole blood viscosity independent of nitric oxide synthase activity in vitro.

l-Arginine, the natural precursor of NO, is infused in patients to restore endothelial function. Concentrations up to 7.5 mM l-arginine have been measured after parenteral administration. We investigated whether such high concentrations of amino acids influence blood viscosity in vitro. Incubation of whole blood from healthy volunteers with l-arginine, d-arginine, which has no effect on stereospecific NO synthases (NOS), the NOS substrate L-AME, the NOS inhibitor L-NNA, the amino acids l-lysine and l-glutamic acid, and finally NaCl dose-dependently decreased (up to 30% at 10(-2) M) low shear viscosity, which is primarily determined by erythrocyte aggregation. In contrast, the lipophilic NOS inhibitor L-NAME had no effect on low shear viscosity. All molecules failed to influence high shear viscosity, which is primarily determined by red cell deformability, and the erythrocyte shape remained unaltered. We conclude that high concentrations amino acids may decrease blood viscosity at low shear rate independent of NOS activity. This effect may contribute to the improved blood flow after intravascular administration of l-arginine.

Adult↗
PubMed1979

An evaluation of biomicroscopy of the conjunctival vessels.

Human clinical biomicroscopy is an aid to the assessment of the microcirculation in health and disease. It has only limited diagnostic value but in some important conditions gives helpful clues and in a few conditions pathognomonic information. Features which can be evaluated include intravascular red cell aggregation, small blood vessel patterns, diameter of vessels, stasis pools, microaneurysms, petechiae and vasomotion. Red cell aggregation correlates well with sedimentation rate. Some of these factors, or combinations of them, correlate well with arteriosclerosis, diabetes, and hypertension. The apparatus required is relatively simple, and the method is noninvasive.

Aneurysm↗
PubMed1990

Proteases in the schistosome life cycle: a paradigm for tumour metastasis.

Cancers and parasites have a number of properties in common, particularly those that relate to their respective capacities to evade host defence mechanisms. This review highlights the similarities between metastatic tumours and schistosomes in particular, and describes the role that proteases may have in the migration, growth, survival and transmission of the different stages of the schistosome life-cycle in the vertebrate host. An elastase-like serine protease of schistosome larvae has been particularly well characterized, and its substrate profile and other properties are indicative of a role in facilitating migration of the parasite through skin tissue early after infection. The primary structures of a cathepsin B-like enzyme, and a putative 'haemoglobinase' found in adult worms have also recently been derived, these enzymes being responsible for degradation of haemoglobin in erythrocytes upon which the adults feed. Adult schistosome worms reside and produce eggs intravascularly, and the processes that mediate the extravasation and subsequent migration of the egg through host tissue are dependent on both blood platelets and the immune response. Fibrino(geno)lytic enzymatic activity that is present in the egg could modulate the thrombogenic potential that eggs might have as a result of their capacity to cause platelet aggregation in vitro and in vivo. The roles of other proteases and peptidases that have been found in schistosome larvae, worms and eggs are less clear. Some of these enzymes may modulate immunological and haemostatic defence mechanisms and thus prolong survival of the parasite, and the consequences of the interactions between schistosomes and host protease inhibitors could also be immune modulatory.

Animals↗
PubMed2002

[Significance of changes in individual indicators on intravascular homeostasis in development of circulatory hypoxia in aging].

The study comprised 45 healthy subjects aged 60-74. It was designed to examine the state of skin and bulbar microcirculation using the method of television capillaroscopy. The functional state of endothelial microvessels was studied with the help of laser doppler flowmeter by means of functional tests with postocclusion hyperaemia and intradermal injection of epinephrine solution in the dose of 0.1 ml (1.10-6 mol/l). The platelets aggregation activity was studied using the method of turbidimetry. The blood viscosity and functional state of erythrocytes were determined with the help of rotary viscosimeter at the shift velocity of 10 to 200s-1 with estimating the erythrocytes deformability and aggregation indexes. Oxygen saturation of the subcutaneous fat fibers was studied by polarography. It has been found that the increase of adrenalin-induction aggregation of platelets, the decrease of erythrocyte deformation and the endothelium synthesis disturbance caused relaxing factors play role in the circulatory hypoxia development.

Adult↗
PubMed1980

Studies of intravascular components in cerebral vasospasm following subarachnoid hemorrhage.

Cerebral vasospasm with subsequent infarction gives important influence to the prognosis of patients with ruptured intracranial aneurysms. Many factors should be considered in the pathogenesis of cerebral infraction. Clinical and experimental studies of intravascular components with particular reference to platelet and coagulation factors were performed. Both studies revealed systemic platelet hyperactivity and a hypercoagulable state; in further experimental studies, crenated red blood cells were recognized in the course of cerebral vasospasm. These systemic changes of intravascular components are thought to accelerate cerebral ischemia through formation of microthrombosis, increased blood viscosity and reduced deformability of the red blood cells.

Animals↗
PubMed1977

[State of microcirculation following massive administration of homologous donor blood to dogs].

Homologous normovolemic donor blood exchange provoked a moderate slowing down of the blood flow in the microcirculation and intravascular aggregation of the red blood cells--moderate or severe. Acute phenomena of blood deposition in the mesenteric vessels with a simultaneous reduction of the perfusion level in the microvessels of the bulbar conjunctiva developed in 25% of cases. Acute microcirculatory disturbances were transitory in character.

Acute Disease↗
PubMed1999

Microcirculatory stasis induced by hemorheological disorders: further evidence.

OBJECTIVE: Reinvestigate the microcirculatory alterations immediately responsible for blood rheological disorders and blood stases, which are related to red blood cell (RBC) aggregation in capillaries. METHODS: Blood rheological disorders were produced by significantly intensified intravascular red blood cell aggregation in the intestinal mesentery of Wistar rats and in the cerebral cortex of Chinchilla rabbits, either systemically (by intravascular administration of high molecular-weight dextran) or locally (by increase of high-molecular compounds in blood plasma inside individual or groups of capillaries). RESULTS: Under conditions where the microvascular lumina were not decreased and the arteriolovenular pressure gradients got even higher, the significantly enhanced intravascular RBC aggregation resulted in the slowing down of blood flow in the microvessels to a full stop. CONCLUSION: A significant increase in microvascular RBC aggregation results in local hemorheological disorders, which is, in all probability, related to derangement of the blood-flow structuring in microvessels.

Animals↗
PubMed2005

The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease.

CONTEXT: The efficient sequestration of hemoglobin by the red blood cell membrane and the presence of multiple hemoglobin clearance mechanisms suggest a critical need to prevent the buildup of this molecule in the plasma. A growing list of clinical manifestations attributed to hemoglobin release in a variety of acquired and iatrogenic hemolytic disorders suggests that hemolysis and hemoglobinemia should be considered as a novel mechanism of human disease. EVIDENCE ACQUISITION: Pertinent scientific literature databases and references were searched through October 2004 using terms that encompassed various aspects of hemolysis, hemoglobin preparations, clinical symptoms associated with plasma hemoglobin, nitric oxide in hemolysis, anemia, pulmonary hypertension, paroxysmal nocturnal hemoglobinuria, and sickle-cell disease. EVIDENCE SYNTHESIS: Hemoglobin is released into the plasma from the erythrocyte during intravascular hemolysis in hereditary, acquired, and iatrogenic hemolytic conditions. When the capacity of protective hemoglobin-scavenging mechanisms has been saturated, levels of cell-free hemoglobin increase in the plasma, resulting in the consumption of nitric oxide and clinical sequelae. Nitric oxide plays a major role in vascular homeostasis and has been shown to be a critical regulator of basal and stress-mediated smooth muscle relaxation and vasomotor tone, endothelial adhesion molecule expression, and platelet activation and aggregation. Thus, clinical consequences of excessive cell-free plasma hemoglobin levels during intravascular hemolysis or the administration of hemoglobin preparations include dystonias involving the gastrointestinal, cardiovascular, pulmonary, and urogenital systems, as well as clotting disorders. Many of the clinical sequelae of intravascular hemolysis in a prototypic hemolytic disease, paroxysmal nocturnal hemoglobinuria, are readily explained by hemoglobin-mediated nitric oxide scavenging. CONCLUSION: A growing body of evidence supports the existence of a novel mechanism of human disease, namely, hemolysis-associated smooth muscle dystonia, vasculopathy, and endothelial dysfunction.

Disease↗
PubMed1994

Pharmacodynamic effects of iomeprol for injection in experimental animals.

Iomeprol for injection is a new nonionic triiodinated contrast medium for diagnostic radiology, which combines low osmolality with low viscosity. The effects of iomeprol for injection on the cardiovascular system, blood parameters, renal function and the central nervous system were studied after intravascular administration to several animal species of doses at least as high as the highest presumed clinical doses. The following observations were made with respect to the central circulatory system: moderate and short-lasting increases of left ventricular end-diastolic pressure and cardiac output, no significant effects on heart rate either in vitro or in vivo, some episodes of arrhythmia and ventricular fibrillations only at doses far higher than the highest presumed clinical ones, no significant increases in diastolic and systolic coronary flow. The following observations were made with respect to peripheral circulation: no significant changes on blood pressure, moderate and short-lasting increases in renal and pulmonary arterial flow, together with a decrease in peripheral vascular resistance, no crossing of the blood-brain barrier in healthy animals. Cardiovascular and haemodynamic changes were all significantly milder than those induced by ionic contrast media (CM) and were similar to effects caused by some other nonionic contrast media. When injected into the femoral artery of rats, iomeprol was shown to be less algogenic than iopamidol and iohexol. In comparison with the same reference CM, iomeprol affected to a lesser extent the filterability of red blood cells in vitro and showed a less marked effect on their deformability. When administered intravenously at very high dosages, iomeprol had no effect on the glomerular filtration rate, but increased both renal blood flow and diuresis. Proteinuria and enzymuria were also increased, albeit more transiently. The neurotolerance of iomeprol for injection after intravenous administration was higher than or at worst equal to that of iopamidol and iohexol. Iomeprol is therefore a promising new contrast agent particularly suitable for intravascular use in humans.

Animals↗
PubMedDate not supplied

Effects of combined parenchymal and vascular injury on platelet aggregation in pial arterioles of living mice: evidence for release of aggregate-inhibiting materials.

Platelet aggregation was produced in pial arterioles by exposing them to appropriately filtered light from a mercury lamp, following intravascular injection of sodium fluorescein. The dye acted as a target for the radiant energy and initiated a sequence of events resulting in the platelet aggregation. The aggregates adhered to the vessel in which they first appeared. When a microneedle punctured the brain adjacent to a subsequently irradiated arteriole, platelet aggregation was inhibited, even though the arteriole was not touched by the microneedle. Inhibition was manifested by prolongation of the exposure time required for the light-dye stimulus to initiate an adherent aggregate and by lengthening the time required for the aggregate to grow and totally block erythrocyte flow in the affected vessel. It is suggested that a material(s) diffuses from the zone of brain puncture, to and through the arteriolar wall, with a resultant inhibition of aggregation. It is noted that the inhibiting effect is reduced as the distance between puncture and wall increases.

Animals↗
PubMed1979

[Pathogenesis of acute osteomyelitis].

Pathogenesis of acute osteomyelitis is analyzed from the standpoint of disorders in the bone microcirculation. It is stated that in acute osteomyelitis there occur some disorders in microcirculation due to extravascular compression and intravascular occlusion of the bone vessels. The analysis of pathogenesis of acute osteomyelitis from the standpoint of disorders in the microcirculation of the osseous tissue is believed to be expedient for the correct understanding of pathological processes occurring in the bone, and for purposeful pathogenetic therapy.

Acute Disease↗
PubMedDate not supplied

[Pulmonary hemodynamics and hemostasis in rabbits exposed to high altitude].

Pulmonary hemodynamics, homeostasis and red blood parameters were studied in 77 rabbits in the mountains of the Tien Shan (3200 m above sea-level). Exposure of animals in alpine environment gave rise to pulmonary hypertension, polycythemia, alterations of homeostasis by the pattern of hyper- and hypocoagulation syndrome. On certain stages of adaptation products of paracoagulation were observed in blood as well as intravascular aggregation of formed elements, increased sensitivity of blood plates to platelet activation, increased fibrinolysis. Given existing hypothesis about involvement of changes in homeostasis and red blood in the pathogenesis of altitude pulmonary hypertension, the coefficients of paired linear correlation between indices of pulmonary hemodynamics and blood have been calculated. These coefficients are valid only for low values of the ratio.

Adaptation, Physiological↗