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Background: Rupture of spinal aneurysms is a rare cause of subarachnoid hemorrhage. These aneurysms are often associated with a variety of vascular malformations that increase blood flow in the spinal circulation or with disorders that compromise the vessel wall. However, spinal aneurysms may be isolated, not associated with any known predisposing condition. The objective of this study is to explore the possible mechanisms associated with the formation and rupture of isolated spinal aneurysms (ISAs)., Methods: We conducted a retrospective review of a series of consecutive patients admitted for a ruptured ISA. In all cases, spinal angiography confirmed the presence of a spinal aneurysm responsible for the bleeding. Particular attention was paid to medical history and symptoms before bleeding, for potential factors predisposing to their formation and rupture., Results: Between 2008 and 2020, ten cases of spinal aneurysms were seen at our institution including 4 cases of ISA. All patients with ISA were female, and in 3 cases the aneurysm involved the territory of the posterior spinal artery. In 3 of these 4 (75%) ISA cases, there was a strikingly similar history of retching and vomiting preceding the thunderclap headache. In 1 patient, the aneurysm was surgically resected; pathologic analysis revealed a fusiform dissecting aneurysm. All 4 patients had a favorable outcome., Conclusions: We suggest that the straining during prolonged retching and vomiting plays a role in the formation and rupture of some ISAs, possibly because of pressure spikes, increased transmural arterial pressure, and increased wall shear stress during straining., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Endothelial cells (EC) were isolated from brain, lung, and renal cortex using magnetic microbeads cross-linked to an antibody directed against the platelet-endothelial cell adhesion molecule-1 (PECAM-1). Levels of endothelial nitric oxide synthase (eNOS) and PECAM-1 were measured by Western blots and both were enriched in the positively selected EC fractions. The multidrug resistance P-glycoprotein (P-gp) was strongly enriched (59-fold) in the EC fraction from brain and was absent in the negative fraction, in which the glial fibrillary acidic protein (GFAP), an astrocyte marker, was present. Lower P-gp levels were detected in EC from renal cortex and lung. Reverse transcription-polymerase chain reaction analysis showed that the mdr1a gene was preferentially expressed in EC fraction from the brain. The mdr1b gene was found in EC from renal cortex whereas both mdr1 genes were detected in EC from lung. Our results indicate that EC can be isolated using microbeads and that the isoform of P-gp found in brain is mostly mdr1a, associated with EC., (Copyright 2001 Academic Press.)