P375Hemolysed blood elicits substantial constriction of isolated basilar artery, which is restored by calcium channel blocker and increased CO2

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Previous studies reported that acute cerebrovascular hemorrhage (stroke, trauma) is followed by increased vascular resistance and thus reduced blood flow in the affected area. However, the underlying vasoconstrictor mechanisms have not yet been clarified. We hypothesized that extraluminal hemolysed blood (HB) has substantial effects on the tone and vasomotor responses of isolated cerebral arteries.


Basilar artery (BA) from male rats was isolated and placed in apressure-myograph chamber into Krebs-solution. The diameters of vessels were measured by videomicroscopy in the presence of 80 mmHg of intraluminal pressure. During incubation a substantial active vasomotor tone (AD) developed. After administration of autologous HB the vasomotor function of vessels was studied in responses to acetylcholine, sodium-nitroprusside, nifedipine and CO2, which were obtained in control condition, in the presence of HB, and after washout of HB. At the end of the experiments passive diameter of vessels (PD) was determined in Ca2+-free Krebs solution.


The active diameters of BA were 277,5 ± 11,5 μm, whereas their PDs were 392 ± 8,1 μm. HB reduced the basal diameters of BA (to 163,8 ± 11,1 μm; 59,13 ± 4% ofAD). After washing out of HB, the active diameters of BA reached the control level:284 ± 9 μm. In control, acetylcholine, sodium nitroprusside, nifedipine and CO2 elicited substantial dilations in cerebral arteries (20 ± 2%, 26 ± 2%, 32 ± 3%and 26 ± 2%). In contrast, HB decreased the dilation to acetylcholine, sodium nitroprusside, but not to nifedipine and CO2 (7 ± 1%, 12 ± 2%, 28 ± 3% and30 ± 2%). After washout of HB NO-dependent dilations were significantly reduced compared to control (ACh: 6 ± 1%, SNP:14 ± 2%).


In conclusion, the findings of the present study show that extraluminal hemolysed blood elicits substantial constrictions and inhibits NO-dependent dilations, but does not affect Ca-channel blocker and CO2-induced dilations. Further elucidation of the underlying mechanisms of hemolysed blood-induced vasomotor dysfunction could contribute to a better understanding and treatment of intracranial hemorrhage.


(Support: Hungarian Scientific Research Fund (OTKA K71591, K67984), AHA Founders Aff. 0855910D,MHT2010/2011)

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