[Subarachnoid hemorrhage due to a ruptured intracranial vertebral artery aneurysm associated with cerebrovascular fibromuscular dysplasia: case report].

Fibromuscular dysplasia (FMD) is comprised of a group of nonatherosclerotic and noninflammatory arterial diseases. Cerebrovascular FMD occurs more frequently in women, and the mean age at which it is diagnosed is 50 years. The most common angiographic pattern of cerebrovascular FMD is the "string-of-beads" deformity at the extracranial internal carotid artery. We report the case of a 52-year-old woman who presented with a sudden severe headache and went into a deep coma. She had been complaining of headaches for 2 weeks, but no specific imaging findings were obtained. A computed tomography scan obtained on admission showed a diffuse subarachnoid hemorrhage (SAH) from the cerebellomedullary cistern to the basal cistern with evidence of clot in the fourth and third ventricles. We performed digital subtraction angiography and made the diagnosis of cerebrovascular FMD. Right carotid angiography and left vertebral angiography showed the classic "string-of-beads" pattern with multiple constrictions of the lumen. Left carotid angiography showed a long segment of tubular stenosis. Right vertebral angiography also revealed the "string-of-beads" pattern and a ruptured aneurysm at the intracranial segment, which presented as a diverticulum-like outpouching. The patient was treated with conservative measures but passed away on the 23rd day of hospitalization. An autopsy was not performed. To our knowledge, during the last three decades, there are only four previous reports which showed intracerebral ruptured aneurysms of the vertebral artery or its branch in adults with cerebrovascular FMD. We demonstrate and discuss the radiologic findings here.

Carotid Artery Stenting for Symptomatic Carotid Artery Dissection Developing from Stanford Type A Aortic Dissection: A Report of Two Cases.

Objective: Stanford type A acute aortic dissection (AAD) is associated with carotid artery dissections (CADs). We report two cases of carotid artery stenting (CAS) for symptomatic CAD after ascending aortic replacement (AAR) for AAD. Case Presentation: Case 1: A 51-year-old man with AAD was transferred to our institute. He had no notable paralysis symptoms on initial presentation. However, after AAR for AAD was performed, left paralysis developed within a few hours. Emergency angiography revealed right CAD and pseudo-occlusion. CAS was performed successfully using intravascular ultrasound (IVUS). He was transferred to a rehabilitation hospital with a modified Rankin Scale (mRS) score of 2.Case 2: A 55-year-old man underwent AAR for AAD, but asymptomatic left CAD remained. Two weeks after the operation, he presented with slight signs of aphasia. Aspirin was prescribed and follow-up was performed, but his symptoms did not improve. He underwent magnetic resonance imaging in our department, which revealed acute cerebral infarction on the left pars opercularis and an artery-to-artery embolism from CAD. CAS was performed via the retrograde approach with direct puncture of the normal left common carotid artery using IVUS. He was discharged with no complications and a mRS score of 1. Conclusion: IVUS can be useful for CAS to confirm the true lumen and extension of long CAD lesions developing from AAD.

Infusion of solutions of pre-irradiated components in rats.

INTRODUCTION: The objective of this study was to conduct a 14-day toxicology assessment for intravenous solutions prepared from irradiated resuscitation fluid components and sterile water. METHODS: Healthy Sprague Dawley rats (7-10/group) were instrumented and randomized to receive one of the following Field IntraVenous Resuscitation (FIVR) or commercial fluids; Normal Saline (NS), Lactated Ringer's, 5% Dextrose in NS. Daily clinical observation, chemistry and hematology on days 1,7,14, and urinalysis on day 14 were evaluated for equivalence using a two sample t-test (p<0.05). A board-certified pathologist evaluated organ histopathology on day 14. RESULTS: Equivalence was established for all observation parameters, lactate, sodium, liver enzymes, creatinine, WBC and differential, and urinalysis values. Lack of equivalence for hemoglobin (p=0.055), pH (p=0.0955), glucose (p=0.0889), Alanine-Aminotransferase (p=0.1938), albumin (p=0.1311), and weight (p=0.0555, p=0.1896), was deemed not clinically relevant due to means within physiologically normal ranges. Common microscopic findings randomly distributed among animals of all groups were endocarditis/myocarditis and pulmonary lesions. DISCUSSION: These findings are consistent with complications due to long-term catheter use and suggest no clinically relevant differences in end-organ toxicity between animals infused with FIVR versus commercial fluids.

Effect of N-arachidonoyl-l-serine on human cerebromicrovascular endothelium.

N-arachidonoyl-l-serine (ARA-S) is an endogenous lipid, chemically related to the endocannabinoid, N-arachidonoyl ethanolamine (i.e., anandamide) and with similar physiologic and pathophysiologic functions. Reports indicate that ARA-S possesses vasoactive and neuroprotective properties resembling those of cannabinoids. However, in contrast to cannabinoids, ARA-S binds weakly to its known classical receptors, CB1 and CB2, and is therefore considered to be a 'cannabinoid-like' substance. The originally described ARA-S induced-endothelial-dependent vasorelaxation was not abrogated by CB1, CB2 receptor antagonists or TRPV1 competitive inhibitor. The present report demonstrates that ARA-S enhances the fluorescence staining of both cannabinoid receptors (CB1 and CB2) in human brain endothelial cells (HBEC). This reaction is specific since it was reduced by respective selective receptor antagonist (SR141716A and SR141728A). ARA-S alone or in the presence of ET-1 was shown to alter the cytoskeleton (actin). Both ARA-S stimulated phosphorylation of various kinases (MAPK, Akt, JNK and c-JUN) and alteration of cytoskeleton are mediated via CB1, CB2 and TRPV1 receptors. The findings also showed the involvement of Rho/Rock and PI3/Akt/NO pathways in the ARA-S-induced phosphorylation of kinases and actin reorganization in HBEC. All of the above mentioned ARA-S-induced effects were reduced by the treatment with LY294002 (inhibitor of PI3/Akt kinase), except MAPK kinase. In addition, MAPK, JNK, c-JUN phosphorylation were inhibited by H1152 (inhibitor of Rho/ROCK kinase), except Akt kinase. Furthermore, PI3/Akt pathway was inhibited by pretreatment with l-NAME (inhibitor of NOS). The findings suggest that ARA-S is a modulator of Rho kinase and may play a critical role in the regulation of its activity and subsequent effects on the cytoskeleton and its role in supporting essential cell functions like vasodilation, proliferation and movement.