PubMed Health⌕ Search

Biomedical subjects

D G Nehls

Publications and source records attributed to D G Nehls.

25 records · Page 2Linked to original sources

Effect of naloxone on experimental stroke in awake monkeys.

Naloxone has recently been reported to be of benefit in the treatment of central nervous system ischemia. To study the effect of naloxone in an experimental stroke model, we subjected 40 awake monkeys to middle cerebral artery (MCA) occlusion 2 weeks after the placement of a MCA ligature by a transorbital technique. Cerebral blood flow (CBF) was monitored with stereotactically placed H2 electrodes, and the neurological course was serially recorded. Infarct size was determined 2 weeks after MCA occlusion. Twenty animals served as control and received no naloxone; 10 of these underwent permanent occlusion, and 10 underwent 4-hour MCA occlusion. In 25 treatment animals, naloxone was administered in three different intravenous dosages: (a) naloxone, 2-mg/kg bolus 20 minutes postocclusion and 2 mg/kg/hour X 4 hours, in 10 animals with permanent MCA occlusion; (b) naloxone, 10-mg/kg bolus 20 minutes postocclusion and 10 mg/kg/hour X 4 hours, in 10 animals with 4-hour MCA occlusion; and (c) naloxone, 20-mg/kg bolus, in 5 animals with various neurological deficits. MCA occlusion typically produced a moderate deficit: hemiparesis, hemianopsia, and facial paresis. In most instances, naloxone in the 2- and 10-mg/kg dose regimens produced little or no change in the neurological function. CBF decreased after MCA occlusion and was unaffected by naloxone in most cases. Infarct size was not significantly different between the control and treated groups. However, the 20-mg/kg dose consistently produced a nonfunctional, transient increase in total body motor tone in normal and hemiparetic animals. Naloxone did not significantly improve useful neurological function, CBF, or infarct size in an experimental primate stroke model.

Animals↗

Beneficial effects of induced hypertension on experimental stroke in awake monkeys.

The authors performed a controlled study of induced hypertension therapy for treatment of experimental stroke in unanesthetized monkeys. Ten control and 10 treated animals were subjected to a 4-hour occlusion of the middle cerebral artery (MCA) by an implanted tourniquet. Neurological status and local cerebral blood flow (CBF) were monitored serially. Local CBF was determined by hydrogen clearance in and around the elevated 20% to 40% by intravenous infusion of phenylephrine hydrochloride. Neuropathological evaluation was performed after about 2 weeks. A 4-hour occlusion of the MCA in control animals caused moderate stable neurological deficits, moderate stable decreases in local CBF, and medium-sized infarcts. With induced hypertension, five of 10 treated animals showed neurological improvement, and eight exhibited increased CBF in the ischemic zone. Average infarct size tended to be smaller in the treated group, although the difference did not reach statistical significance. Hemorrhagic infarcts were not observed. In four animals, phenylephrine caused cardiac dysrhythmias and hypotension which were reversed by appropriate measures. In this unanesthetized primate model of moderate experimental stroke, induced hypertension had beneficial effects on neurological status, local CBF, and infarct size without causing hemorrhagic infarction. Induced hypertension may be beneficial for some clinical cases of focal cerebral ischemia.

Anesthesia, General↗

Spontaneous regression of arteriovenous malformations.

Spontaneous regression of an arteriovenous malformation (AVM) is quite rare. When a regression does occur, there is usually an associated factor, such as intracranial hemorrhage, operation, radiation therapy, or new neurological deficit. Twenty-one cases of AVM regression identified in the literature are reviewed. An additional case in which the resolution was totally spontaneous is presented. Regressions occurred over intervals ranging from 7 months to 21 years. Several mechanisms for regression are discussed.

Cerebral Angiography↗