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At least 73 records · Page 4Linked to original sources
PubMed2003

Effect of mechanical ventilation on carotid artery thrombosis induced by photochemical injury in mice.

BACKGROUND: Increasing use of transgenic and gene targeting techniques for the investigation of hemostasis and vascular biology has generated interest in experimental models of carotid artery thrombosis in mice. OBJECTIVES: We tested the hypothesis that hypoventilation in anesthetized mice may cause hypercapnia, increased carotid artery blood flow, and altered thrombotic responses to photochemical injury of the carotid artery. METHODS: Arterial blood gases and carotid artery blood flow were measured in pentobarbital-anesthetized BALB/c or C57BL/6 J mice with and without mechanical ventilation. Photochemical injury of the carotid artery was induced using the rose bengal method. RESULTS: Compared with ventilated mice, unventilated mice had a 45% increase in carotid artery blood flow (0.74 +/- 0.04 vs. 0.41 +/- 0.03 mL min-1; P < 0.001) that was associated with an elevation of arterial PCO2 (58 +/- 4 vs. 33 +/- 4 mmHg; P < 0.05) and a decrease in arterial pH (7.18 +/- 0.05 vs. 7.32 +/- 0.03; P < 0.05). Time to first occlusion of the carotid artery after photochemical injury was shorter in ventilated than in unventilated mice (29 +/- 6 vs. 73 +/- 9 min; P < 0.001). Time to stable occlusion was also shorter in ventilated mice (49 +/- 8 vs. 81 +/- 6 min; P < 0.05). Elevated carotid artery blood flow, hypercarbic acidosis, and prolonged occlusion times also were observed in mice ventilated with supplemental carbon dioxide. CONCLUSIONS: General anesthesia without mechanical ventilation has the potential to confound studies of experimental thrombosis in vivo by producing hypoventilation, hypercapnia, acidosis, and altered carotid artery blood flow. Mechanical ventilation with maintenance of normal blood gases may enhance the physiological insight gained from experimental models of carotid artery thrombosis in mice.

Anesthesia↗
PubMed2003

Accelerated thrombolysis in a rabbit model of carotid artery thrombosis with liposome-encapsulated and microencapsulated streptokinase.

The present study compares the efficacy of two formulations of encapsulated streptokinase to streptokinase in a rabbit model of carotid artery thrombosis. Arterial thrombosis followed the injection of thrombin mixed with autologous whole blood into a carotid artery of New Zealand white rabbits. Thirty minutes after the confirmation of an occlusive thrombus, one of four streptokinase formulations was infused at a dosage of 6000 IU/kg into the jugular vein. Free streptokinase (FREE SK) was compared to identical dosages of streptokinase encapsulated in a liposome (LESK), streptokinase entrapped in a water-soluble polymer (MESK), and free streptokinase admixed with blank microparticles (FREE SK + BLANK). Carotid arterial blood flow was determined by pulsed Doppler flowmetry to confirm clot formation and reperfusion. Two hours after drug infusion, the rabbits were killed and the residual thrombus mass was determined. Compared to FREE SK (74.5 +/- 16.9 min; mean +/- SEM), LESK demonstrated significantly reduced reperfusion times (19.3 +/- 4.6 min) while MESK exhibited even greater improvement (7.3 +/- 1.6 min). FREE SK + BLANK showed no statistical improvement versus FREE SK. LESK and MESK also resulted in reduced residual clot mass and greater return of arterial blood flow. These studies suggest that encapsulation of streptokinase offers a potential method of improved fibrinolytic treatment for patients with clot-based disorders. MESK performed slightly better than LESK with improved production and storage characteristics.

Animals↗
PubMed1997

Carotid artery thrombosis and stroke after blunt pharyngeal injury.

A 2-year-old child fell on a toothbrush, sustaining a pharyngeal injury. Eighteen hours later, localizing symptoms of a cerebrovascular accident became evident. Magnetic resonance angiography showed occlusion of the internal carotid artery and a cerebral infarction. She was treated with anticoagulation and made a complete recovery. Pharyngeal injuries may be complicated by internal carotid artery thrombosis and embolus. Management includes prompt diagnosis, anticoagulation, and carotid artery exploration in selected cases.

Carotid Artery Thrombosis↗
PubMed2003

Functional thrombomodulin deficiency causes enhanced thrombus growth in a murine model of carotid artery thrombosis.

Thrombomodulin (TM) bound thrombin initiates the protein C anticoagulant pathway and defects in TM result in enhanced coagulation. Recent studies suggest a role for TM in arterial vascular disease. In order to corroborate this association we studied arterial thrombus formation in mice with a functional TM defect. We used mice homozygous for a (404)Glu-to-Pro mutation in the TM gene (TM(pro/pro)) and compared these with wildtype littermates in a model of FeCl(3) induced carotid artery thrombosis. Time-to-occlusion (TTO) was assessed by arterial blood flow measurement, using a Doppler flow probe. Complete occlusion occurred in 8/10 (80%) TM(pro/pro) mice and in 3/11 (27%) littermate controls. Mean time to occlusion (TTO) [+/- SE] was 767 +/- 196 s in the F2-TM(pro/pro) mice, versus 1507 +/- 159 s in controls (p = 0.007, Mann Whitney U test). Histology and immunostaining for tissue factor did not reveal any differences in thrombus morphology or thrombogenicity between the two groups. These data confirm and extend the finding that a functional deficiency in TM results in enhanced thrombus formation in a murine model of carotid artery thrombosis and support a role for TM defects in arterial thrombotic disease.

Animals↗
PubMed1975

Rhincerebral phycomycosis and internal carotid artery thrombosis.

This is a report of a case of internal carotid artery occlusion associated with rhinocerebral phycomycosis. In 18 autopsied similar cases that have been reported previously, hyphae were described in the walls of the internal carotid artery. Four survivors have been reported even though arteriograms demonstrated internal carotid artery occlusion, and a high index of suspicion for this complication should be maintained in all patients with rhinocerebral phycomycosis.

Adolescent↗
PubMed1990

[Carotid artery thrombosis and myocardial infarction in nephrotic syndrome].

The authors report the case of a 18 year old man with a chronic corticosteroid-refractory nephrotic syndrome complicated by carotid artery thrombosis and myocardial infarction. Thromboembolism is one of the most serious complications of the nephrotic syndrome. Serious clotting factor disturbances are observed: changes in platelet function (hyperaggregability) increased plasma zymogens and cofactors, increased plasma fibrinogen, abnormalities of the fibrinolytic system and acquired deficiencies of coagulation inhibitors. The respective role of each of these abnormalities have not been clearly established, but it is likely that increased platelet aggregation and antithrombin III deficiency are important factors in producing a hypercoagulable state in the nephrotic syndrome. Hyperlipidemia is also a characteristic feature of the nephrotic syndrome: these is a wide spectrum of lipoprotein patterns with increased low density lipoproteins (LDL) or very low density lipoproteins (VLDL) or both; contradictory results have been reported with respect to the high density lipoproteins (HDL): decreased, normal or even increased plasma levels have been observed. In addition, changes in the distribution and composition of LDL and VLDL subclasses have been detected. Most of these changes have an atherogenic potential but controversy still surrounds the question of the prevalence of ischaemic heart disease in the nephrotic syndrome; it is unlikely that nephrotic syndromes of short duration have any influence on the incidence of coronary events, but patients with chronic heavy protein urea and long-term exposure to abnormalities of haemostasis and lipid profiles appear to have a significant risk of developing cardiovascular disease and may require long-term anticoagulant therapy.

Adolescent↗
PubMed1992

[Incidence of internal carotid artery thrombosis and disseminated intravascular coagulopathy in the early stages of acute myeloid leukemia].

The case history of a 15 year old boy in whom thrombosis of the internal carotid artery was associated with severe disseminated intravascular thrombosis (DIC) is described. Both peripheral blood smear and bone marrow aspirate revealed acute myelogenous leukemia FAB M-2 type as the cause of the disease. Consumption coagulopathy is common sign of hemostasis disturbances in leukemia. It is frequently observed in acute promyelocytic leukemia, but rarely it may be seen in the other forms of hemoblastosis, too.

Adolescent↗
PubMed1989

Danazol and internal carotid artery thrombosis.

The case of a 47-year-old woman suffering from a CT-assessed ischemic right hemisphere stroke, which occurred after a 2-month treatment with danazol (a synthetic androgen), is reported. The patient's thrombocytosis in association with danazol treatment and its possible correlations with the thrombotic event are discussed.

Carotid Artery Thrombosis↗
PubMed1990

Rhinocerebral mucormycosis and internal carotid artery thrombosis in a previously healthy patient.

Mucormycosis is a very serious fungal infection caused by habitual saprophytes of the human organism, in many cases concomitant with various pathological conditions marked by immunodepression. The rhinocerebral variant habitually accompanies ketoacidotic diabetes. We report a case of rhinocerebral mucormycosis in a subject free from immunodepression and non-diabetic, in apparently normal health. Following treatment with amphotericin B combined with 5-fluorocytosine and surgery, remission of the disease was finally secured and about one year after the last operation there are no sign of resumption.

Brain Diseases↗