Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertonic (3.0%) saline (HS) resuscitation from hemorrhagic shock is associated with less cerebral edema and lower intracranial pressure (ICP) compared to normal saline (NS) and 10% Dextran 40 (D-40). The effect of HS resuscitation on cerebral blood flow (CBF) is unknown. Beagle dogs with a head injury underwent shock and resuscitation, receiving either NS (N = 6), HS (N = 6), or D-40 (N = 6). CBF (via a microsphere technique) and ICP were measured at baseline (BL) and at end shock (ES) after infusion of shed blood and test fluid (ER) and 2 hours after resuscitation (LR). CBF was determined globally (GCBF), and for the right (RCBF) and left (LCBF) cerebral hemispheres. ICP values (+/- SEM) at BL and ES were 10.8 +/- 1.31 mmHg and 8.0 +/- 1.67 mmHg, respectively, for all groups. GCBF, RCBF and LCBF at BL were 29.4 +/- 5.04, 26.7 +/- 4.93 and 26.6 +/- 4.50 ml 100 g-1 min-1, respectively. ES values for CBF were not significantly different from BL. Global and hemispheric CBF values were not different between groups at times measured. ICP was significantly lower in animals receiving HS. Therefore, lower ICP following HS resuscitation is not associated with alteration in CBF.
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PMID:Cerebral blood flow following hypertonic saline resuscitation in an experimental model of hemorrhagic shock and head injury. 279 Mar 1

The effects of prostacyclin, nimodipine, and verapamil on local cerebral pH (LCpH) and CBF (LCBF) in middle cerebral artery (MCA)-occluded rats were compared with those in controls and others receiving nimodipine carrier. LCpH and LCBF were determined simultaneously by a double-label autoradiographic technique. The infusions were intravenous, started 15 min following the occlusion, and ended at decapitation 4 h postocclusion. The dosages were 0.5 micrograms/kg/min for nimodipine, 40 micrograms/kg/min for verapamil, and 5 ng/kg/min for prostacyclin. Cortical LCpH in the MCA territory of control and carrier-infused rats varied between 6.72 +/- 0.05 and 6.76 +/- 0.05 (means +/- SEM). These values were significantly lower than the LCpH in the same structures in the contralateral hemisphere (7.09 +/- 0.06; p less than 0.05). LCBF on the side of occlusion varied between 54 +/- 5 ml/100 g/min for the parietal and 57 +/- 7 ml/100 g/min for the sensorimotor cortex, while on the contralateral side, LCBF in these same structures was 190 +/- 18 and 191 +/- 4 ml/100 g/min, respectively. LCpH was not modified by prostacyclin treatment following MCA occlusion, but the pH in the structures that were acidotic in the controls became indistinguishable from contralateral values in nimodipine- and verapamil-treated animals. In contrast, LCBF was statistically higher than controls in many structures only in rats treated with prostacyclin. This suggested that the correction of LCpH produced by calcium blockers was not related to an effect they had on blood flow. Animals receiving calcium blockers tended to have smaller areas of infarction. These results may have therapeutic implications in cerebral ischemia.
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PMID:Cerebral acidosis in focal ischemia: II. Nimodipine and verapamil normalize cerebral pH following middle cerebral artery occlusion in the rat. 379 3