On the effect of calcium antagonists on cerebral blood flow in rats. A comparison of nimodipine and flunarizine
Abstract To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group o...
Ausführliche Beschreibung
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Englisch |
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1997 |
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Springer Online Journal Archives 1860-2002 |
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in: Neurosurgical review - 1978, 20(1997) vom: Apr., Seite 259-268 |
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volume:20 ; year:1997 ; month:04 ; pages:259-268 ; extent:10 |
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520 | |a Abstract To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group of controls (n =10). Cerebral blood flow was estimated during arterial normo-, hyper-and hypotension. The lowest cerebral blood flow estimates calculated for nimodipine were 43.8 ± 7.8, 90.9 ± 13.3, and 33.6 ± 6.1 ml/min/100 g for normo-, hyper- and hypotension, respectively. Cerebral blood flow in the nimodipine placebo group was 84.1 ±10.3,139.9 ± 19.9, and 55.2 ± 10.5 ml/min/100 g. In the flunarizine group, the blood flow was 77.3 ± 15.2,144.7 ± 15.0, and 43.8 ± 5.9 ml/min/100 g. In the control group, cerebral blood flow was 90.0 ± 29.1, 143.0 ± 42.1, and 75.5 ± 29.8 ml/min/100 g. The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates. Thus impaired blood flow reduces the usefulness of nimodipine in the prevention of vasospasm. Flunarizine is a potential alternative treatment of vasospasm treatment as well as for cerebral blood flow improvement, as shown in our experimental study. | ||
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(DE-627)NLEJ206359039 DE-627 ger DE-627 rakwb eng On the effect of calcium antagonists on cerebral blood flow in rats. A comparison of nimodipine and flunarizine 1997 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group of controls (n =10). Cerebral blood flow was estimated during arterial normo-, hyper-and hypotension. The lowest cerebral blood flow estimates calculated for nimodipine were 43.8 ± 7.8, 90.9 ± 13.3, and 33.6 ± 6.1 ml/min/100 g for normo-, hyper- and hypotension, respectively. Cerebral blood flow in the nimodipine placebo group was 84.1 ±10.3,139.9 ± 19.9, and 55.2 ± 10.5 ml/min/100 g. In the flunarizine group, the blood flow was 77.3 ± 15.2,144.7 ± 15.0, and 43.8 ± 5.9 ml/min/100 g. In the control group, cerebral blood flow was 90.0 ± 29.1, 143.0 ± 42.1, and 75.5 ± 29.8 ml/min/100 g. The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates. Thus impaired blood flow reduces the usefulness of nimodipine in the prevention of vasospasm. Flunarizine is a potential alternative treatment of vasospasm treatment as well as for cerebral blood flow improvement, as shown in our experimental study. Springer Online Journal Archives 1860-2002 Zumkeller, Matthias oth Heissler, Hans Egmont oth Dietz, Hermann oth in Neurosurgical review 1978 20(1997) vom: Apr., Seite 259-268 (DE-627)NLEJ188987444 (DE-600)1474861-7 1437-2320 nnns volume:20 year:1997 month:04 pages:259-268 extent:10 http://dx.doi.org/10.1007/BF01105897 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 20 1997 4 259-268 10 |
spelling |
(DE-627)NLEJ206359039 DE-627 ger DE-627 rakwb eng On the effect of calcium antagonists on cerebral blood flow in rats. A comparison of nimodipine and flunarizine 1997 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group of controls (n =10). Cerebral blood flow was estimated during arterial normo-, hyper-and hypotension. The lowest cerebral blood flow estimates calculated for nimodipine were 43.8 ± 7.8, 90.9 ± 13.3, and 33.6 ± 6.1 ml/min/100 g for normo-, hyper- and hypotension, respectively. Cerebral blood flow in the nimodipine placebo group was 84.1 ±10.3,139.9 ± 19.9, and 55.2 ± 10.5 ml/min/100 g. In the flunarizine group, the blood flow was 77.3 ± 15.2,144.7 ± 15.0, and 43.8 ± 5.9 ml/min/100 g. In the control group, cerebral blood flow was 90.0 ± 29.1, 143.0 ± 42.1, and 75.5 ± 29.8 ml/min/100 g. The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates. Thus impaired blood flow reduces the usefulness of nimodipine in the prevention of vasospasm. Flunarizine is a potential alternative treatment of vasospasm treatment as well as for cerebral blood flow improvement, as shown in our experimental study. Springer Online Journal Archives 1860-2002 Zumkeller, Matthias oth Heissler, Hans Egmont oth Dietz, Hermann oth in Neurosurgical review 1978 20(1997) vom: Apr., Seite 259-268 (DE-627)NLEJ188987444 (DE-600)1474861-7 1437-2320 nnns volume:20 year:1997 month:04 pages:259-268 extent:10 http://dx.doi.org/10.1007/BF01105897 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 20 1997 4 259-268 10 |
allfields_unstemmed |
(DE-627)NLEJ206359039 DE-627 ger DE-627 rakwb eng On the effect of calcium antagonists on cerebral blood flow in rats. A comparison of nimodipine and flunarizine 1997 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group of controls (n =10). Cerebral blood flow was estimated during arterial normo-, hyper-and hypotension. The lowest cerebral blood flow estimates calculated for nimodipine were 43.8 ± 7.8, 90.9 ± 13.3, and 33.6 ± 6.1 ml/min/100 g for normo-, hyper- and hypotension, respectively. Cerebral blood flow in the nimodipine placebo group was 84.1 ±10.3,139.9 ± 19.9, and 55.2 ± 10.5 ml/min/100 g. In the flunarizine group, the blood flow was 77.3 ± 15.2,144.7 ± 15.0, and 43.8 ± 5.9 ml/min/100 g. In the control group, cerebral blood flow was 90.0 ± 29.1, 143.0 ± 42.1, and 75.5 ± 29.8 ml/min/100 g. The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates. Thus impaired blood flow reduces the usefulness of nimodipine in the prevention of vasospasm. Flunarizine is a potential alternative treatment of vasospasm treatment as well as for cerebral blood flow improvement, as shown in our experimental study. Springer Online Journal Archives 1860-2002 Zumkeller, Matthias oth Heissler, Hans Egmont oth Dietz, Hermann oth in Neurosurgical review 1978 20(1997) vom: Apr., Seite 259-268 (DE-627)NLEJ188987444 (DE-600)1474861-7 1437-2320 nnns volume:20 year:1997 month:04 pages:259-268 extent:10 http://dx.doi.org/10.1007/BF01105897 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 20 1997 4 259-268 10 |
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(DE-627)NLEJ206359039 DE-627 ger DE-627 rakwb eng On the effect of calcium antagonists on cerebral blood flow in rats. A comparison of nimodipine and flunarizine 1997 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group of controls (n =10). Cerebral blood flow was estimated during arterial normo-, hyper-and hypotension. The lowest cerebral blood flow estimates calculated for nimodipine were 43.8 ± 7.8, 90.9 ± 13.3, and 33.6 ± 6.1 ml/min/100 g for normo-, hyper- and hypotension, respectively. Cerebral blood flow in the nimodipine placebo group was 84.1 ±10.3,139.9 ± 19.9, and 55.2 ± 10.5 ml/min/100 g. In the flunarizine group, the blood flow was 77.3 ± 15.2,144.7 ± 15.0, and 43.8 ± 5.9 ml/min/100 g. In the control group, cerebral blood flow was 90.0 ± 29.1, 143.0 ± 42.1, and 75.5 ± 29.8 ml/min/100 g. The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates. Thus impaired blood flow reduces the usefulness of nimodipine in the prevention of vasospasm. Flunarizine is a potential alternative treatment of vasospasm treatment as well as for cerebral blood flow improvement, as shown in our experimental study. Springer Online Journal Archives 1860-2002 Zumkeller, Matthias oth Heissler, Hans Egmont oth Dietz, Hermann oth in Neurosurgical review 1978 20(1997) vom: Apr., Seite 259-268 (DE-627)NLEJ188987444 (DE-600)1474861-7 1437-2320 nnns volume:20 year:1997 month:04 pages:259-268 extent:10 http://dx.doi.org/10.1007/BF01105897 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 20 1997 4 259-268 10 |
allfieldsSound |
(DE-627)NLEJ206359039 DE-627 ger DE-627 rakwb eng On the effect of calcium antagonists on cerebral blood flow in rats. A comparison of nimodipine and flunarizine 1997 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group of controls (n =10). Cerebral blood flow was estimated during arterial normo-, hyper-and hypotension. The lowest cerebral blood flow estimates calculated for nimodipine were 43.8 ± 7.8, 90.9 ± 13.3, and 33.6 ± 6.1 ml/min/100 g for normo-, hyper- and hypotension, respectively. Cerebral blood flow in the nimodipine placebo group was 84.1 ±10.3,139.9 ± 19.9, and 55.2 ± 10.5 ml/min/100 g. In the flunarizine group, the blood flow was 77.3 ± 15.2,144.7 ± 15.0, and 43.8 ± 5.9 ml/min/100 g. In the control group, cerebral blood flow was 90.0 ± 29.1, 143.0 ± 42.1, and 75.5 ± 29.8 ml/min/100 g. The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates. Thus impaired blood flow reduces the usefulness of nimodipine in the prevention of vasospasm. Flunarizine is a potential alternative treatment of vasospasm treatment as well as for cerebral blood flow improvement, as shown in our experimental study. Springer Online Journal Archives 1860-2002 Zumkeller, Matthias oth Heissler, Hans Egmont oth Dietz, Hermann oth in Neurosurgical review 1978 20(1997) vom: Apr., Seite 259-268 (DE-627)NLEJ188987444 (DE-600)1474861-7 1437-2320 nnns volume:20 year:1997 month:04 pages:259-268 extent:10 http://dx.doi.org/10.1007/BF01105897 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 20 1997 4 259-268 10 |
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on the effect of calcium antagonists on cerebral blood flow in rats. a comparison of nimodipine and flunarizine |
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On the effect of calcium antagonists on cerebral blood flow in rats. A comparison of nimodipine and flunarizine |
abstract |
Abstract To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group of controls (n =10). Cerebral blood flow was estimated during arterial normo-, hyper-and hypotension. The lowest cerebral blood flow estimates calculated for nimodipine were 43.8 ± 7.8, 90.9 ± 13.3, and 33.6 ± 6.1 ml/min/100 g for normo-, hyper- and hypotension, respectively. Cerebral blood flow in the nimodipine placebo group was 84.1 ±10.3,139.9 ± 19.9, and 55.2 ± 10.5 ml/min/100 g. In the flunarizine group, the blood flow was 77.3 ± 15.2,144.7 ± 15.0, and 43.8 ± 5.9 ml/min/100 g. In the control group, cerebral blood flow was 90.0 ± 29.1, 143.0 ± 42.1, and 75.5 ± 29.8 ml/min/100 g. The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates. Thus impaired blood flow reduces the usefulness of nimodipine in the prevention of vasospasm. Flunarizine is a potential alternative treatment of vasospasm treatment as well as for cerebral blood flow improvement, as shown in our experimental study. |
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Abstract To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group of controls (n =10). Cerebral blood flow was estimated during arterial normo-, hyper-and hypotension. The lowest cerebral blood flow estimates calculated for nimodipine were 43.8 ± 7.8, 90.9 ± 13.3, and 33.6 ± 6.1 ml/min/100 g for normo-, hyper- and hypotension, respectively. Cerebral blood flow in the nimodipine placebo group was 84.1 ±10.3,139.9 ± 19.9, and 55.2 ± 10.5 ml/min/100 g. In the flunarizine group, the blood flow was 77.3 ± 15.2,144.7 ± 15.0, and 43.8 ± 5.9 ml/min/100 g. In the control group, cerebral blood flow was 90.0 ± 29.1, 143.0 ± 42.1, and 75.5 ± 29.8 ml/min/100 g. The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates. Thus impaired blood flow reduces the usefulness of nimodipine in the prevention of vasospasm. Flunarizine is a potential alternative treatment of vasospasm treatment as well as for cerebral blood flow improvement, as shown in our experimental study. |
abstract_unstemmed |
Abstract To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group of controls (n =10). Cerebral blood flow was estimated during arterial normo-, hyper-and hypotension. The lowest cerebral blood flow estimates calculated for nimodipine were 43.8 ± 7.8, 90.9 ± 13.3, and 33.6 ± 6.1 ml/min/100 g for normo-, hyper- and hypotension, respectively. Cerebral blood flow in the nimodipine placebo group was 84.1 ±10.3,139.9 ± 19.9, and 55.2 ± 10.5 ml/min/100 g. In the flunarizine group, the blood flow was 77.3 ± 15.2,144.7 ± 15.0, and 43.8 ± 5.9 ml/min/100 g. In the control group, cerebral blood flow was 90.0 ± 29.1, 143.0 ± 42.1, and 75.5 ± 29.8 ml/min/100 g. The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates. Thus impaired blood flow reduces the usefulness of nimodipine in the prevention of vasospasm. Flunarizine is a potential alternative treatment of vasospasm treatment as well as for cerebral blood flow improvement, as shown in our experimental study. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ206359039</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210706200708.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070528s1997 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ206359039</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">On the effect of calcium antagonists on cerebral blood flow in rats. A comparison of nimodipine and flunarizine</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1997</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">10</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group of controls (n =10). Cerebral blood flow was estimated during arterial normo-, hyper-and hypotension. The lowest cerebral blood flow estimates calculated for nimodipine were 43.8 ± 7.8, 90.9 ± 13.3, and 33.6 ± 6.1 ml/min/100 g for normo-, hyper- and hypotension, respectively. Cerebral blood flow in the nimodipine placebo group was 84.1 ±10.3,139.9 ± 19.9, and 55.2 ± 10.5 ml/min/100 g. In the flunarizine group, the blood flow was 77.3 ± 15.2,144.7 ± 15.0, and 43.8 ± 5.9 ml/min/100 g. In the control group, cerebral blood flow was 90.0 ± 29.1, 143.0 ± 42.1, and 75.5 ± 29.8 ml/min/100 g. The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates. Thus impaired blood flow reduces the usefulness of nimodipine in the prevention of vasospasm. Flunarizine is a potential alternative treatment of vasospasm treatment as well as for cerebral blood flow improvement, as shown in our experimental study.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zumkeller, Matthias</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Heissler, Hans Egmont</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dietz, Hermann</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Neurosurgical review</subfield><subfield code="d">1978</subfield><subfield code="g">20(1997) vom: Apr., Seite 259-268</subfield><subfield code="w">(DE-627)NLEJ188987444</subfield><subfield code="w">(DE-600)1474861-7</subfield><subfield code="x">1437-2320</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:20</subfield><subfield code="g">year:1997</subfield><subfield code="g">month:04</subfield><subfield code="g">pages:259-268</subfield><subfield code="g">extent:10</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF01105897</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">20</subfield><subfield code="j">1997</subfield><subfield code="c">4</subfield><subfield code="h">259-268</subfield><subfield code="g">10</subfield></datafield></record></collection>
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