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Neurosurgery. 2002 Dec;51(6):1468-74; discussion 1474-6.
Chronological changes of the contractile mechanism in prolonged vasospasm after subarachnoid hemorrhage: from protein kinase C to protein tyrosine kinase.
Koide M, Nishizawa S, Ohta S, Yokoyama T, Namba H.
Department of Neurosurgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.
OBJECTIVE: Protein kinase C (PKC) plays a role in vasospasm after subarachnoid hemorrhage with a "two-hemorrhage" canine model until Day 7. However, clinical vasospasm continues during the course of 2 weeks. This study sought to clarify whether the contractile property of cerebral arteries might change in prolonged vasospasm. METHODS: In this model, angiography was not performed until Day 14. The maximal contracting response induced by high K(+) was measured by using basilar arteries on Days 1, 7, and 14 in an isometric tension study. After stretching arteries equivalent to angiographic diameter, papaverine-sensitive (myogenic) and papaverine-insensitive (nonmyogenic) tones of the developed tension were also measured. On nonmyogenic tone, the effect of genistein, a specific inhibitor of protein tyrosine kinase (PTK), was examined. The PKC and PTK activities in basilar arteries were measured from Day 1 to Day 14. RESULTS: Angiographic vasospasm on Day 14 was equivalent to that on Day 7. However, the maximum contractile response on Day 14 was significantly decreased compared with Day 7. Myogenic tone was significantly decreased, and the effect of genistein on nonmyogenic tone was significantly increased on Day 14 compared with Day 7. The activity of PKC on Day 14 declined to the Day 1 level, whereas that of PTK was enhanced from Day 7 and persisted until Day 14. CONCLUSION: These results indicate that stiffness of the arterial wall increased and that the contractile property of the artery shifted from active myogenic tone to nonmyogenic tone, from PKC to PTK, with prolonged vasospasm.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12445353&dopt=Abstract hemorrhage
Neurosurgery. 2002 Dec;51(6):1499-505; discussion 1506.
Perfusion-weighted magnetic resonance imaging in adult moyamoya syndrome: characteristic patterns and change after surgical intervention: case report.
Wityk RJ, Hillis A, Beauchamp N, Barker PB, Rigamonti D.
Departments of Neurology and Medicine, The Johns Hopkins Hospital and Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA. rwityhmi.edu
OBJECTIVE AND IMPORTANCE: Moyamoya disease is a progressive arteriopathy of the intracerebral vessels resulting in stroke, intracerebral hemorrhage, and alteration of cerebral perfusion. Perfusion-weighted magnetic resonance imaging (PWI) tracks the passage of a bolus of gadolinium contrast material through brain tissue and is reflective of cerebral blood flow. We describe the characteristics of PWI in patients with moyamoya syndrome and present in detail the PWI findings of a patient studied before and after surgical intervention. CLINICAL PRESENTATION: A 24-year-old woman presented with recurrent ischemic strokes during a period of 1 year. Angiography disclosed findings consistent with bilateral moyamoya disease. PWI showed a striking contrast in perfusion between the anterior and posterior circulations, with relative hyperperfusion in the posterior fossa and marked hypoperfusion in the hemispheric deep white matter. Similar findings are reported in five other patients with moyamoya disease. Differences in time-to-peak measurements between the pons and the cerebral hemispheres ranged between 2 and 10 seconds, with the greatest difference seen in the two patients with recurrent stroke. INTERVENTION: The patient underwent a left encephalomyosynangiosis. One year later, she showed significant improvement in neurological function, and a repeat PWI study showed marked improvement in perfusion of the left hemisphere. Magnetic resonance imaging confirmed the growth of small vessels into the brain from the surgical site. CONCLUSION: PWI demonstrates characteristic patterns of cerebral perfusion in patients with moyamoya disease and documents improved perfusion after successful surgical intervention. Quantitative analysis of the difference of time-to-peak measurements between the anterior and posterior circulation may be a marker of the severity of the disease.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12445358&dopt=Abstract hemorrhage
Eur J Pharmacol. 2002 Nov 29;455(2-3):127-33.
Effect of a platelet-activating factor antagonist, E5880, on cerebrovasospasm following subarachnoid hemorrhage in a canine double-hemorrhage model.
Abe Y, Kasuya H, Suzuki S, Yamanishi Y, Hori T.
Developmental Pharmacology Research Section, Drug Safety and Disposition Research Laboratories, Eisai Company, Limited, Tsukuba City, Ibaraki, 300-2635, Japan. y2-abhc.eisai.co.jp
We investigated the effects of a platelet-activating factor (PAF) antagonist, E5880 (1-ethyl-2-[N-(2-methoxy)benzoyl-N-[(2)-2-methoxy-3-(4-octadecycarbamoylox)piperidinocarbonyloxy-propyloxy]carbonyl]aminomethyl-pyridiniumchloride), on subarachnoid hemorrhage-induced prolongation of cerebral circulation time and decrease in the basilar artery diameter in a canine double-hemorrhage model. Animals were assigned to three groups, control (saline), E5880 1.2 mg/kg and E5880 2.4 mg/kg. For measurement of cerebral circulation time, regions of interest were chosen at the basilar artery and the straight sinus in order to obtain time-density curves. Cerebral circulation time was defined as the difference between the arterial and venous peaks. Cerebral circulation time and basilar artery diameter were assessed by intra-arterial digital subtraction angiography (IA-DSA) on Days 0, 2 and 7. The prolongation of cerebral circulation time following subarachnoid hemorrhage was significantly inhibited by intravenous administration of 2.4 mg/kg of E5880. Basilar artery constriction was also reduced by E5880. Thus, E5880 had preventive effects on the prolongation of cerebral circulation time and the vasoconstriction of basilar artery in this model. These results suggest that E5880 may have a preventive effect on neurological symptoms aggravated by cerebrovascular lesions following subarachnoid hemorrhage. 2002 Elsevier Science B.V.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12445578&dopt=Abstract hemorrhage
Blood. 2003 Apr 15;101(8):3002-7. Epub 2002 Nov 21.
Distinct dose-dependent effects of plasmin and TPA on coagulation and hemorrhage.
Stewart D, Kong M, Novokhatny V, Jesmok G, Marder VJ.
Vascular Medicine Program, Los Angeles Orthopaedic Hospital, The David Geffen School of Medicine at UCLA, University of California Los Angeles, CA 90007, USA.
All thrombolytic agents in current clinical usage are plasminogen activators. Although effective, plasminogen activators uniformly increase the risk of bleeding complications, especially intracranial hemorrhage, and no laboratory test is applicable to avoid such bleeding. We report results of a randomized, blinded, dose-ranging comparison of tissue-type plasminogen activator (TPA) with a direct-acting thrombolytic agent, plasmin, in an animal model of fibrinolytic hemorrhage. This study focuses on the role of plasma coagulation factors in hemostatic competence. Plasmin at 4-fold, 6-fold, and 8-fold the thrombolytic dose (1 mg/kg) induced a dose-dependent effect on coagulation, depleting antiplasmin activity completely, then degrading fibrinogen and factor VIII. However, even with complete consumption of antiplasmin and decreases in fibrinogen and factor VIII to 20% of initial activity, excessive bleeding did not occur. Bleeding occurred only at 8-fold the thrombolytic dose, on complete depletion of fibrinogen and factor VIII, manifest as prolonged primary bleeding, but with minimal effect on stable hemostatic sites. Although TPA had minimal effect on coagulation, hemostasis was disrupted in a dose-dependent manner, even at 25% of the thrombolytic dose (1 mg/kg), manifest as rebleeding from hemostatically stable ear puncture sites. Plasmin degrades plasma fibrinogen and factor VIII in a dose-dependent manner, but it does not disrupt hemostasis until clotting factors are completely depleted, at an 8-fold higher dose than is needed for thrombolysis. Plasmin has a 6-fold margin of safety, in contrast with TPA, which causes hemorrhage at thrombolytic dosages.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12446443&dopt=Abstract hemorrhage
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The most common benign lesion of thyroid, multinodular goiter, may mimic papillary carcinoma if it contains papillary areas. Although it is usually not very difficult to distinguish between these benign and malignant lesions, some cases may be problematic in differential diagnosis. In these cases, we decided to use cytokeratin 19 (CK19), which is shown to be effective in discriminating papillary carcinoma from follicular carcinoma of thyroid, and we also evaluated the immunoreactivity of CK19 in follicular adenomas. Twenty-five cases of multinodular goiter showing papillary formations, 25 cases of papillary thyroid carcinoma, and 15 cases of follicular adenoma were selected from archives of our institution. Immunohistochemical staining for CK19 was performed on deparaffinized sections. Diffuse and intense CK19 positivity was found in the cells of all papillary carcinomas. In the multinodular goiter group, 20 of 25 cases showed no staining while the remaining 5 were focally reactive with CK19. Three of the five were thought to be false positive owing to hemorrhage. Weak and focal CK19 staining was seen in some follicular adenomas. Our observations suggest that the staining features of CK19 may be helpful in differential diagnosis between papillary carcinoma and multinodular goiter showing papillary areas. Focal and pale staining for CK19 may be seen in multinodular goiter with papillary formations, and this feature should be considered in evaluation.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12446919&dopt=Abstract hemorrhage
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