Aims: 

Acute cerebrovascular hemorrhage (stroke, trauma) is followed by increased vascular resistance and thus reduced blood flow in the affected area. 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.

Methods: 

The middle cerebral artery (MCA) and basilar artery (BA) from male rats were isolated and placed in a pressure-myograph chamber into Krebs-solution. The diameters of vessels were measured by videomicroscopy in the presence of 80 mmHg intraluminal pressure. During incubation a substantial active tone (AD) developed. After administration of autologous HB the vasomotor function of vessels was studied in responses to acetylcholine, sodium-nitroprusside and nifedipine, which were obtained in control condition, in the presence of HB and after washout of HB.

Results: 

The active diameters of MCA and BA were 170±4.5mm and 264±6.5mm, respectively; whereas their PDs were 269±10mm and 392±8.1 mm, respectively. HB reduced the basal diameter of both MCA and BA (MCA: to 143±4 mm, 84.1±4% of AD; and BA: 163.8±11.1mm, 62.05±4% of AD). After washing out of HB, the active diameters of MCA and BA returned to 187±7 mm and 284±9 mm, respectively. In control, acetylcholine, sodium nitroprusside and nifedipine elicited substantial dilations in cerebral arteries (BA: 20±2%, 26±2% and 33±3%). In contrast, HB decreased the dilation to acetylcholine, sodium nitroprusside, but not to nifedipine (BA: 7±1%, 12±2%, 28±3%). After washout of HB NO-dependent dilations were still reduced (BA: 6±1%, 14±2%, 30±2%, respectively). Similar responses were obtained in MCA.

Conclusion: 

Our findings show that extraluminal hemolysed blood elicited substantial constrictions and inhibited NO-dependent dilations, but did not affect Ca-channel blocker-induced dilations. Elucidating the underlying mechanisms of hemolysed blood-induced vasomotor dysfunction could contribute to the better treatment of intracranial hemorrhage.

Support: 

AHA-FA 0855910D, OTKA K71591 and K67984