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PubMed2002

Endothelial nitric oxide synthase pathophysiology after nonocclusive common carotid artery thrombosis in rats.

Although vascular dysregulation has been documented in patients with extracranial vascular disease, transient ischemic attacks, and stroke, the pathomechanisms are poorly understood. To model thromboembolic stroke in rats, photochemically induced nonocclusive common carotid artery thrombosis (CCAT) was used to generate a platelet thrombus in the carotid artery of anesthetized rats. After CCAT, platelet aggregates break off the thrombus, travel to the distal cerebral vasculature, damage blood vessels, and cause small infarctions. The authors hypothesized that deficits in the endothelial nitric oxide synthase (eNOS) pathway may be responsible for vascular dysfunction after embolic stroke. To examine the functional status of the eNOS system, they measured eNOS-dependent dilation after CCAT by applying acetylcholine through a cranial window over the middle cerebral artery. The authors also measured eNOS mRNA and protein in the middle cerebral artery to determine whether functional changes were caused by alterations in expression. eNOS-dependent dilation was reduced at 6 hours, elevated at 24 hours, and returned to baseline 72 hours after CCAT. Endothelial nitric oxide synthase mRNA increased at 2 hours and was followed by a rise in protein 24 hours after CCAT. Changes in the eNOS system may account for some of the observed vascular deficits in patients with cerebrovascular disease.

Acetylcholine↗
PubMed1995

Nonocclusive common carotid artery thrombosis in the rat results in reversible sensorimotor and cognitive behavioral deficits.

BACKGROUND AND PURPOSE: Microemboli released during transient ischemic attack, stroke, and cardiac surgery are thought to cause a variety of functional deficits in humans. The purpose of this study was to characterize the type and extent of neurobehavioral deficits present after photochemically induced common carotid artery thrombosis (CCAT), a thromboembolic model of stroke in the rat that results in a platelet emboli shower. METHODS: Thirty-two male Wistar rats were assigned to four groups. Groups 1 (n = 8) and 3 (n = 8) were long-term (6-week survival) and short-term (2-week survival) experimental groups subjected to right CCAT with the use of the photochemical technique. Groups 2 (n = 8) and 4 (n = 8) served as sham-operated controls for each experimental group. A battery of behavioral tests was applied daily beginning 24 hours after thrombosis; this consisted of elicited forelimb placing, postural reflex, beam balance, beam walking, and open field activity. Cognitive testing with a water maze task was performed on post-CCAT days 30 to 33 for groups 1 and 2 and on post-CCAT day 2 for groups 3 and 4. Ten-micrometer coronal brain sections were stained with hematoxylin and eosin, and infarct location and frequency were determined. RESULTS: Significant sensorimotor deficits were observed, which recovered within 2 weeks after CCAT. The data that follow are derived by combining the two experimental groups and comparing these with the two sham groups. The following tests showed significant effects after CCAT: contralateral elicited forelimb placing, ipsilateral elicited forelimb placing, beam balance, and beam walking score. Cognitive dysfunction was seen acutely (group 3 animals) at 2 days after CCAT; Morris water maze length and latency to target were significantly greater in the experimental group. No deficits were seen in postural reflex, open field activity, or delayed cognitive testing. Histopathological assessment revealed small infarcts in 11 of 16 thrombosed rats. However, a strong relationship between neurobehavioral deficits and infarct location was not consistently demonstrated. CONCLUSIONS: CCAT produces consistent sensorimotor and cognitive behavioral deficits that recover within 2 weeks of injury. Behavioral outcome was not necessarily associated with overt histopathological damage, suggesting that reversible injury mechanisms, both vascular and neuronal, may be partly responsible for the temporary loss of function. These data strengthen the role of CCAT as a clinically relevant model of thromboembolic stroke.

Animals↗
PubMed1994

Internal carotid artery thrombosis after cervical corpectomy.

SUMMARY OF BACKGROUND DATA: A 74-year-old man suffered an extensive right hemispheric infarct 72 hours after undergoing anterior corpectomies of the C4 and C5 vertebrae for cervical myelopathy resulting from ossification of the posterior longitudinal ligament. RESULTS: Angiography revealed proximal right internal carotid artery thrombosis with atherosclerosis and a normal left internal carotid artery. The thrombosis may have been due to stasis during lengthy retraction of an atherosclerotic carotid artery. CONCLUSIONS: Preoperative screening of internal carotid artery blood flow with Doppler ultrasonography is recommended before contemplating extensive anterior cervical surgery in middle-aged and elderly patients at significant risk for atherosclerotic disease.

Aged↗
PubMed1993

Prevention of experimental carotid artery thrombosis by applaggin.

Applaggin, an inhibitor of platelet aggregation via binding to the glycoprotein IIb/IIIa receptor, was examined in an anesthetized canine model of arterial thrombosis formation secondary to arterial wall injury. Both carotid arteries were isolated and instrumented with flow probes, intravascular anodal electrodes and adjustable constrictors. The right carotid artery was injured initially and served as the control response to vessel wall injury in each animal, whereas the left carotid was injured after applaggin administration (1.0 mg/kg, i.v.). Arterial occlusion in the control vessel occurred in each of seven animals. Time for occlusive thrombus development was 125.6 +/- 15.2 min. One of the seven left carotid arteries occluded after applaggin. Thrombus weight was greater in control vessels (44.2 +/- 7.0 mg) vs. thrombus weight after applaggin (11.2 +/- 2.4 mg). Cyclic flow variations occurred in all control arteries before development of an occlusive thrombus. In contrast, cyclic flow variations were observed only in two of seven vessels injured after applaggin. One of the latter vessels developed an occlusive thrombus. Platelet counts, heart rate and blood pressure were unaltered over the course of the experimental protocol. Ex vivo platelet aggregation to arachidonic acid was examined before and after applaggin administration. Platelet-rich plasma from animals having initial normal baseline aggregation no longer aggregated 30 min after administration of applaggin. Aggregation returned to normal within 3 hr. Applaggin binds to stimulated and unstimulated platelets and two classes of binding sites were identified. The results demonstrate that applaggin possesses an antithrombotic effect in the experimental model of canine carotid artery thrombosis.

Adenosine Diphosphate↗
PubMed1991

Hemodynamic consequences of common carotid artery thrombosis and thrombogenically activated blood in rats.

We documented the hemodynamic consequences of nonocclusive common carotid artery thrombosis (CCAT) and tested the hypothesis that vasoactive substances capable of altering local CBF (LCBF) are released into the systemic circulation following cerebrovascular injury. Ten minutes after photochemically induced CCAT, an autoradiographic determination of LCBF was conducted with [14C]iodoantipyrine. In blood transfusion studies using donor and recipient rats, a 1-ml sample of thrombogenically activated blood (TAB) collected downstream from the forming thrombus was reinjected into a recipient rat 15 or 60 min before CBF study. A heterogeneous pattern of abnormal LCBF was documented in the ipsilateral hemisphere of CCAT rats and recipient rats receiving TAB 15 min before CBF study. Acute hemodynamic abnormalities included ischemic (less than 35% of control) and hyperemic (greater than 125% of control) foci and more global reductions (50-80% of control) in cortical and subcortical LCBF. Border zone hyperemia exceeding 2.0 ml/g/min was associated with focal sites of severe LCBF reductions. Although recipient rats that received TAB 15 min before CBF study displayed similar hemodynamic abnormalities, LCBF values in 60-min recipient rats were not significantly different from control despite ischemic foci. Humoral factors generated during CCAT appear to be responsible for the acute LCBF consequences of cerebrovascular thrombosis. Vasoactive substances released from a thrombotic site, capable of regionally affecting vascular reactivity in a time-dependent fashion, might be expected to participate in the pathogenesis of transient ischemic attacks and acute stroke.

Animals↗
PubMed1996

Coexistence of cerebral venous sinus and internal carotid artery thrombosis associated with exogenous sex hormones. A case report.

A forty-six year-old premenopausal woman developed headache, nausea and vomiting, left hemiparesis and seizure two days after parenteral use of progesterone and estradiol. Diabetes mellitus (DM) was found during admission. Computed tomography showed a hemorrhagic infarct in the right frontal lobe and increased density in the superior sagittal sinus (SSS). Left carotid angiography found occlusion of the left internal carotid artery (ICA). Right carotid angiograms failed to show the SSS and inferior sagittal sinus, suggestive of venous sinus thrombosis. Coexistence of the cerebral artery and the venous sinus occlusion has been described infrequently. In this case, the authors postulate that the use of estradiol and progesterone and the underlying DM increased vascular thrombogenicity, which provided a common denominator for thrombosis of both the ICA and the venous sinus.

Carotid Artery Thrombosis↗
PubMed1992

Antithrombotic effects of the prostacyclin analogue naxaprostene after oral and intraduodenal application in rabbit carotid artery thrombosis.

The antithrombotic efficacy of the prostacyclin analogue naxaprostene has been tested in rabbits with copper coil-induced carotid artery thrombosis. With oral pretreatment, 10 mg/kg naxaprostene prevented thrombotic arterial occlusion; with intraduodenal pretreatment the efficacy of naxaprostene was enhanced and 1 mg/kg was sufficient to exert an antithrombotic effect. The final average carotid blood flow at 180 min compared to the flow immediately before thrombus induction was 85 +/- 25% and 47 +/- 18% in animals treated with 10 mg/kg p.o. resp. 1 mg/kg i.d. naxaprostene. Parallel to the antithrombotic effect, naxaprostene inhibited ADP- and collagen-induced fall in circulating platelets. In anesthetized rabbits there was no dissociation between antithrombotic and hypotensive effects of naxaprostene.

Adenosine Diphosphate↗
PubMed1996

Monoclonal antibody against tissue factor shortens tissue plasminogen activator lysis time and prevents reocclusion in a rabbit model of carotid artery thrombosis.

BACKGROUND: Tissue factor (TF)-dependent activation of the coagulation is important in the pathophysiology of intravascular thrombus formation. We tested the effects of a monoclonal antibody against TF (AP-1) on lysis time induced by tissue-type plasminogen activator (TPA) and on reocclusion rate in a rabbit model of carotid artery thrombosis. METHODS AND RESULTS: Intravascular thrombosis was obtained by placing an external constrictor around carotid arteries with endothelial injury. Carotid blood flow velocity ws measured continuously with a Doppler flow probe. Thirty minutes after thrombus formation, the rabbits received either AP-1 (0.15 mg/kg IV, n=8) or placebo (n=8). All rabbits also received TPA (80 microg/kg bolus plus 8 microg x kg(-1) x min(-1) infusion for up to 90 minutes or until reperfusion was achieved) and heparin (200 U/kg IV as a bolus). At reperfusion, TPA was discontinued, and the rabbits were followed for an additional 90 minutes. AP-1 shortened lysis time from 44+/-8 minutes (mean+/-SEM) in control rabbits to 26+/-7 minutes in AP-1 rabbits (P<.01). Reocclusion occurred in all control rabbits in 10+/-3 minutes, whereas it occurred in only two of eight AP-1 treated rabbits in 72 and 55 minutes (P<.01). No changes in prothrombin time and ex vivo platelet aggregation in response to various agonists were observed after AP-1 administration, indicating the absence of systemic effects by this antibody. CONCLUSIONS: TF exposure and activation of the extrinsic coagulation pathway play an important role in prolonging lysis time and mediating reocclusion after thrombolysis in this model. AP-1, a monoclonal antibody against TF, might be suitable as adjunctive therapy to TPA.

Animals↗