Activation of the coagulation system in the subarachnoid space after subarachnoid haemorrhage: serial measurement of fibrinopeptide A and bradykinin of cerebrospinal fluid and plasma in patients with subarachnoid haemorrhage.

Fibrinopeptide A (FPA) levels as an indicator of thrombin activity in the cerebrospinal fluid (CSF) and plasma of 25 patients with subarachnoid haemorrhage (SAH) were measured serially by radioimmunoassay (RIA). FPA levels in CSF were extremely high on days 0-1 (1253 +/- 269 ng/ml, mean +/- standard error) but decreased rapidly (11.3 +/- 3.9 ng/ml on days 2-4, 10.7 +/- 5.9 ng/ml on days 5-7, and 6.3 +/- 1.5 ng/ml on days 8-14). In the controls the FPA concentration in CSF was 1.2 +/- 0.9 ng/ml (mean +/- standard deviation). Plasma FPA levels in patients with SAH showed no statistically significant changes with time. The bradykinin (BK) concentration in CSF and plasma in 27 patients with SAH was measured serially by RIA. The concentrations in CSF were 122.7 +/- 22.7 pg/ml (mean +/- standard error) on day 0, 38.6 +/- 6.1 pg/ml on day 1, 22.7 +/- 6.3 pg/ml on day 2, and 17.1 +/- 3.0 pg/ml or less thereafter. Plasma BK levels in patients with SAH were higher than those in the control group, but there was no statistically significant change over time. From the measurement of FPA it was apparent that the coagulation system in the subarachnoid space is strongly activated in the early stage of SAH. The formation of BK in CSF after SAH is thought to be due to the contact activation of Hageman factor (intrinsic factor) in the subarachnoid space. Trabeculae as collagen bundles in the subarachnoid space were considered to have a possible role in activating the Hageman factor of the coagulation system in SAH.

[A study of continuous cerebrospinal fluid drainage in patients with subarachnoid hemorrhage].

The influences of continuous cerebrospinal fluid (CSF) drainage on vasospasm and hydrocephalus were analyzed retrospectively in 150 patients with subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysms (32 cases of grade 1, 85 cases of grade 2, and 33 cases of grade 3 by the Hunt and Hess classification). One hundred and seven of these cases received CSF drainage (cisternal, ventricular, lumbar, or a combination of these). The volume of CSF drainage within the first week after onset was 975 +/- 513 ml (mean +/- SD). The total volume of CSF drainage was 2063 +/- 1635 ml (mean +/- SD). The duration of CSF drainage was 10.6 +/- 6.8 days (mean +/- SD). Ten of 46 cases given no drainage within the first week after onset, nine of 55 cases with a drainage volume of less than 1000 ml within the first week, and 24 of 49 cases with a drainage volume of more than 1000 ml within the first week showed vasospasm. There was a statistically significant dose-response (drainage volume-vasospasm) relationship (p less than 0.005, Mantel extension method). Four of 43 cases with no drainage, 26 of 67 cases with a total drainage volume of less than 2000 ml, and 24 of 40 cases with a total drainage volume of more than 2000 ml developed hydrocephalus. There was a statistically significant dose-response (drainage volume-hydrocephalus) relationship (p less than 0.005, Mantel extension method). Vasospasm and hydrocephalus were statistically associated (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

[Serial measurement of bradykinin of the cerebrospinal fluid in patients with subarachnoid hemorrhage].

The bradykinin (BK) concentration of the cerebrospinal fluid (CSF) in 21 patients with subarachnoid hemorrhage (SAH) was measured serially by radioimmunoassay (RIA). The values were 134.9 +/- 93.9 pg/ml (mean +/- standard deviation) on the day of onset, 38.3 +/- 31.8 pg/ml on the first day after onset, 23.4 +/- 22.8 pg/ml on the second day, 16.6 +/- 9.9 pg/ml on the third day, 15.5 +/- 6.0 pg/ml on the fourth day, and 14.8 +/- 5.9 pg/ml on the fifth day. In the controls the BK concentration in the CSF was 8.0 +/- 3.3 pg/ml (n = 10). On the other hand, none of 5 patients with intraventricular hematoma due to intracerebral hemorrhage had a high level of BK in the bloody CSF at the initial stage (15.2-26.0 pg/ml). This shows that BK is not produced only by the mixture of CSF and blood. BK is produced by the activation of Hageman factor that is considered to be activated by trabecula of collagen bundles in the subarachnoid space in the case of SAH.