Abstract
To clarify the contribution of vasoconstrictor prostaglandins to the hypoperfusion state typically following total global cerebral ischemia, 14 mongrel dogs were subjected to 11 minutes of global cerebral ischemia. They were then randomly assigned to receive either no treatment or an intravenous bolus of the calcium channel blocker nimodipine, 10 μg/kg, 15 minuts after ischemia followed by a continuous infusion of nimodipine, 1.0 μg/kg/min. Thromboxane (Tx) A2 production, as measured by cerebral venous levels of TxB2 (the stable metabolite of TxA2) increased similarly in the two groups. In contrast to previous studies, mean postischemic cerebral blood flow did not increase sufficiently in the nimodipine-treated group to achieve statistical significance. These data suggest that the improved neurological outcome associated with nimodipine treatment following global cerebral ischemia does not relate to reduced levels of the prostaglandin precursor arachidonate.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 416-420 |
| Number of pages | 5 |
| Journal | Journal of Neurosurgery |
| Volume | 69 |
| Issue number | 3 |
| State | Published - 1988 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Clinical Neurology
- Neuroscience(all)
Cite this
Effects of nimodipine on the production of thromboxane A2 following total global cerebral ischemia. / Haddon, W. S.; Prough, Donald; Kong, D.; Petrozza, P.
In: Journal of Neurosurgery, Vol. 69, No. 3, 1988, p. 416-420.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of nimodipine on the production of thromboxane A2 following total global cerebral ischemia
AU - Haddon, W. S.
AU - Prough, Donald
AU - Kong, D.
AU - Petrozza, P.
PY - 1988
Y1 - 1988
N2 - To clarify the contribution of vasoconstrictor prostaglandins to the hypoperfusion state typically following total global cerebral ischemia, 14 mongrel dogs were subjected to 11 minutes of global cerebral ischemia. They were then randomly assigned to receive either no treatment or an intravenous bolus of the calcium channel blocker nimodipine, 10 μg/kg, 15 minuts after ischemia followed by a continuous infusion of nimodipine, 1.0 μg/kg/min. Thromboxane (Tx) A2 production, as measured by cerebral venous levels of TxB2 (the stable metabolite of TxA2) increased similarly in the two groups. In contrast to previous studies, mean postischemic cerebral blood flow did not increase sufficiently in the nimodipine-treated group to achieve statistical significance. These data suggest that the improved neurological outcome associated with nimodipine treatment following global cerebral ischemia does not relate to reduced levels of the prostaglandin precursor arachidonate.
AB - To clarify the contribution of vasoconstrictor prostaglandins to the hypoperfusion state typically following total global cerebral ischemia, 14 mongrel dogs were subjected to 11 minutes of global cerebral ischemia. They were then randomly assigned to receive either no treatment or an intravenous bolus of the calcium channel blocker nimodipine, 10 μg/kg, 15 minuts after ischemia followed by a continuous infusion of nimodipine, 1.0 μg/kg/min. Thromboxane (Tx) A2 production, as measured by cerebral venous levels of TxB2 (the stable metabolite of TxA2) increased similarly in the two groups. In contrast to previous studies, mean postischemic cerebral blood flow did not increase sufficiently in the nimodipine-treated group to achieve statistical significance. These data suggest that the improved neurological outcome associated with nimodipine treatment following global cerebral ischemia does not relate to reduced levels of the prostaglandin precursor arachidonate.
UR - http://www.scopus.com/inward/record.url?scp=0023714359&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0023714359&partnerID=8YFLogxK
M3 - Article
VL - 69
SP - 416
EP - 420
JO - Journal of Neurosurgery
JF - Journal of Neurosurgery
SN - 0022-3085
IS - 3
ER -