Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

These studies determined the spasmogen(s) responsible for vasospasm. Application of fresh erythrocyte hemolysate to cerebral smooth muscle increases intracellular calcium ([Ca2+]i) that is mediated by adenosine triphosphate (ATP). Pure hemoglobin does not increase [Ca2+]i. ATP concentrations declined rapidly in hemolysate from erythrocytes incubated in vitro. A combination of low and high molecular weight components of incubated hemolysates was needed to increase [Ca2+]i,. To determine whether small molecules like ATP cause vasospasm, we placed agarose containing autologous hemolysate, ATP or pure hemoglobin into the subarachnoid space of monkeys. There was significant vasospasm afer ATP, hemolysate or hemoglobin placement. Hemoglobin and ATP levels were measured in cerebrospinal fluid and clots from the subarachnoid space of humans and monkeys at different times after subarachnoid hemorrhage. Hemoglobin remained at high levels for days but ATP declined within 48 hours to levels that would not contract arteries. To determine when blood clot had to be present and for how long in order to cause vasospasm, monkeys had bilateral SAH and serial angiography. Subarachnoid clot was removed on day 1, 3, 5 or not removed in controls. Vasospasm required subarachnoid clot through day 3. Clot removal on day 1 or 3 reversed spasm 4 days later whereas clot removal on day 5 did not alter vasospasm on day 7 or 9. While ATP levels were high enough acutely to cause vasospasm, there was no ATP in clot on day 3, yet vasospasm requires this clot. Multiple substances of different molecular weights may cause vasospasm. The substances may be different at different times.

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Presentation Number SAzhang, j0339
Keywords: vasospasm, subarachnoid, hemorrhage, hemoglobin, erythrocyte