dinoprost and Intracranial-Aneurysm

Sodium nitroprusside (SNP) is commonly used for controlled systemic hypotension during aneurysm surgery after acute subarachnoid hemorrhage (SAH). Few experimental studies have assessed cerebrovascular responsiveness to SNP acutely after a representative SAH (i.e., following arterial rupture within the subarachnoid space). Instead, most studies have focused on delayed reactivity after slow injections of unpressurized blood throughout several days. In the authors' study, SAH was created by endovascular rupture in spontaneously breathing rats under urethane anesthesia without craniotomy. After 3 hours, proximal middle cerebral arteries (MCAs) were harvested and mounted as ring preparations in vitro. After preconstriction with 30 mM prostaglandin F2a, concentration-response curves were generated to express SNP's sequential relaxation of preconstricted tone. The effective concentration of SNP for 50% relaxation was significantly lower after SAH (p < 0.001) as compared with non-operated and sham-operated controls. There was also a significantly greater maximum percentage relaxation from preconstricted tone (p < 0.001) with SNP. The results of this study suggest that SNP is a potent and efficacious dilator of MCAs in the hours immediately after acute SAH.

Topics: Acute Disease; Anesthetics, Intravenous; Aneurysm, Ruptured; Animals; Antihypertensive Agents; Cerebral Arteries; Cerebrovascular Circulation; Dinoprost; Dose-Response Relationship, Drug; In Vitro Techniques; Intracranial Aneurysm; Intracranial Pressure; Male; Nitroprusside; Rats; Rats, Wistar; Subarachnoid Hemorrhage; Urethane; Vasoconstrictor Agents; Vasodilator Agents

CSF eicosanoid levels are raised following subarachnoid haemorrhage but not sufficiently to be vasoactive per se within the cerebral circulation. Rebleeding and intraventricular haemorrhage are two factors associated with a worse outcome after aneurysmal SAH. We have examined the effects of these two factors on the CSF levels of TXB2 (TXA2 metabolite), PG6-keto F1 alpha (prostacyclin metabolite), PGF2 alpha and PGE2 in 44 patients following subarachnoid haemorrhage. In 15 patients who had received no non-steroidal anti-inflammatory agent or dexamethasone, intraventricular haemorrhage increased the median levels of all four eicosanoids in ventricular CSF by 2.1-5.1-fold. In 4 patients who rebled, the CSF median levels of all four eicosanoids were raised up to 250-fold over the normal range. These concentrations are just sufficient to have cerebrovascular and neuromodulatory effects.

Topics: 6-Ketoprostaglandin F1 alpha; Aspirin; Brain Damage, Chronic; Cerebral Ventricles; Dexamethasone; Dinoprost; Dinoprostone; Drug Therapy, Combination; Eicosanoids; Humans; Infusions, Intravenous; Intracranial Aneurysm; Nimodipine; Prognosis; Recurrence; Reference Values; Subarachnoid Hemorrhage; Thromboxane B2