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   <subfield code="a">10.1007/BF01411736</subfield>
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   <subfield code="a">CO2 and indomethacin vasoreactivity in patients with head injury</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[B. Dahl, B. Bergholt, G. Cold, J. Astrup, B. Mosdal, K. Jensen, J. Kjærsgaard]</subfield>
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   <subfield code="a">Summary: The purpose of this study was to compare the effect of hyper-ventilation and indomethacin on cerebral circulation, metabolism and pressures in patients with acute severe head injury in order to see if indomethacin may act supplementary to hyperventilation. Fourteen severely head injured patients entered the study. Intracranial pressure (ICP), mean arterial blood pressure (MABP) and cerebral perfusion pressure (CPP) were monitored continuously. Within the first four days after the trauma the CO2 and indomethacin vasoreactivities were studied by measurements of cerebral blood flow (CBF) (Cerebrograph 10a, intravenous133Xe technique) and arterio-venous difference of oxygen (AVdO2). Ischaemia was evaluated from changes in CBF, saturation of oxygen in the jugular bulb (SvjO2), lactate and lactate/oxygen index (LOI). Data are presented as medians and ranges, results are significant unless otherwise indicated. Before intervention ICP was well controlled (14.8 (9-24) mmHg) and basic CBF level was 39.1 (21.6-75.0) ml/100 g/min). The arterio-venous oxygen differences were generally decreased (AVdO2 = 4.3 (1.8-8.1) ml/100 ml) indicating moderate luxury perfusion. Levels of CMRO2 were decreased (1.54 (0.7-3.2) ml/100 g/min) as well. Duringhyperventilation (ΔAPaCO2 = 0.88 (0.62-1.55) kPa) CBF decreased with 11.8 (−33.4−29.7) %/kPa and ICP decreased with 3.8 (0-10) mmHg. AVdO2 increased 34.0 (4.0-139.2) %/kPa, MABP was unchanged, CMRO2 and CPP increased (ΔCPP = 3.9 (−10−20) mmHg). AVD (lactate) and LOI were unchanged. No correlations between CBF responses to hypocapnia and outcomes were observed. An i.v. bolus dose ofindomethacin (30 mg) decreased CBF 14.7 (−16.7−57.4) % and ICP decreased 4.3 (−1−17) mmHg. AVdO2 increased 27.8 (−40.0−66.7)%, MABP (ΔMABP = 4.9 (−2−21) mmHg) and CPP (ΔCPP = 8.7 (3-29) mmHg) increased while CMRO2 was unchanged. No changes in AVd (lactate) and LOI indicating cerebral ischaemia were found. Compared to hyperventilation (changes per 1 kPa, at PaCO2 level = 4.05 kPa) the changes in MABP, CPP and CBF were significantly greater after indomethacin, while the changes in AVdO2, ICP, SvjO2, and LOI were of the same order of magnitude. Nocorrelation between relative reactivities to indomethacin and CO2, evaluated from changes in CBF and AVdO2, or between the decrease in ICP after the two procedures were found. Thus, some patients reacted to indomethacin but not to hyperventilation, and vice versa. These results suggest that indomethacin and hyperventilation might act independently, or in a complementary fashion in the treatment of patients with severe head injury.</subfield>
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   <subfield code="a">Springer-Verlag, 1996</subfield>
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   <subfield code="a">Head injury</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">indomethacin reactivity</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">hyperventilation</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">intracranial pressure</subfield>
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   <subfield code="a">cerebral blood flow</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">cerebral ischaemia</subfield>
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   <subfield code="a">Dahl</subfield>
   <subfield code="D">B.</subfield>
   <subfield code="u">Department of Neuroanaesthesia, Århus University Hospital, Århus, Denmark</subfield>
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   <subfield code="a">Bergholt</subfield>
   <subfield code="D">B.</subfield>
   <subfield code="u">Department of Neurosurgery, Århus University Hospital, Århus, Denmark</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Cold</subfield>
   <subfield code="D">G.</subfield>
   <subfield code="u">Department of Neuroanaesthesia, Århus University Hospital, Århus, Denmark</subfield>
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   <subfield code="a">Astrup</subfield>
   <subfield code="D">J.</subfield>
   <subfield code="u">Department of Neurosurgery, Århus University Hospital, Århus, Denmark</subfield>
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   <subfield code="a">Mosdal</subfield>
   <subfield code="D">B.</subfield>
   <subfield code="u">Department of Neurosurgery, Århus University Hospital, Århus, Denmark</subfield>
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   <subfield code="a">Jensen</subfield>
   <subfield code="D">K.</subfield>
   <subfield code="u">Department of Neuroanaesthesia, Århus University Hospital, Århus, Denmark</subfield>
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   <subfield code="D">J.</subfield>
   <subfield code="u">Department of Neurosurgery, Århus University Hospital, Århus, Denmark</subfield>
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   <subfield code="t">Acta Neurochirurgica</subfield>
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   <subfield code="g">138/3(1996-03-01), 265-273</subfield>
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