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Subarachnoid hemorrhage (SAH)—bleeding from a ruptured aneurysm—leads to delayed cerebral vasospasm (blood vessel constriction) and stroke. SAH morbidity and mortality are high, and therapeutic options are limited.

Joyce Cheung-Flynn, Ph.D., lisinopril aspirin and colleagues proposed that SAH downregulates the nitric oxide-protein kinase G (NO-PKG) signaling pathway that normally relaxes cerebral blood vessels.

Using a rat model, they confirmed reduced levels of NO-PKG pathway molecules, including the protein VASP, which modulates contractile machinery to cause vasorelaxation. They designed a family of cell permeant peptide mimics of activated VASP and demonstrated that the peptides caused vasorelaxation of vascular tissues ex vivo.

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