Biomedical subjects

A M Scremin

Publications and source records attributed to A M Scremin.

23 records · Page 2Linked to original sources

PubMed1988

Physostigmine enhances blood flow-metabolism ratio in neocortex.

Inhibition of central nervous system cholinesterase with a single pulse of physostigmine induces a pronounced increase of blood flow in the neocortex, cingulate gyrus, claustrum, and amygdala. This phenomenon is not accompanied by an increase in energy metabolism and may help explain the effect of this drug on memory in normal humans and patients with Alzheimer's disease, as well as other conditions. In contrast, a parallel increase of blood flow and metabolism was observed in the superior colliculus, a component of the visual pathways. Prolonged administration of physostigmine lead to persistent vasodilatation in the neocortex, a lessening of this effect in cingulate gyrus, claustrum and amygdala, and an increase in primary olfactory cortex and hippocampus when compared with single pulse administration. Effects of physostigmine on glucose utilization remained essentially the same as with pulse administration.

Animals↗

PubMedDate not supplied

Effects of functional electrical stimulation-induced lower extremity cycling on bone density of spinal cord-injured patients.

Spinal cord-injured (SCI) patients are at increased risk for fractures secondary to neurogenic osteoporosis. Earlier research claimed physical conditioning resulted in a decreased incidence or reversal of neurogenic osteoporosis. This study evaluated the effects of functional electrical stimulation-induced lower extremity cycling (FESILEC) on the bone densities of SCI patients using dual-energy x/ray absorptiometry (DEXA). The study consisted of 12 healthy male SCI patients, aged 23 to 46 (x +/- SD, 34 +/- 6) yr. The patients were post-traumatic, complete, spastic SCI; time postinjury ranged from 2 to 19 (9.7 +/- 5.1) yr. Patients participated in a three-phase training program. Phase 1 consisted of quadriceps strengthening. Phase 2 consisted of progressive sequential stimulation of quadriceps, hamstrings, and gluteal muscles, achieving a rhythmical pedaling motion on the REGYS I ergometer. Phase 3a consisted of 30-min FESILEC sessions. DEXAs were done at baseline and at completion of Phase 3a and Phase 3b. Bone densities were done of the lumbar spine levels 2-4 (L2-4), bilateral trochanters (T), Ward's triangles (WT) and femoral necks (FN). Baseline bone density indicated no difference between L2-4 of ambulatory males and SCI males. Baseline values obtained for T, WT, and FN were, respectively, 71, 82, and 79% of ambulatory values. Results after completion of the Phase 3a training program indicated no statistically significant difference compared with baseline values. There was, however, a positive trend in the lumbar spine post-Phase 3a (L2-4, P=0.056). Eight patients continued the exercise program, using a combination of upper and lower extremity cycling (Phase 3b) for a longer period of time (25 +/- 9 wk). DEXAs done after Phase 3b indicated no change relative to baseline data or data post-Phase 3a. In conclusion, although FESILEC did not significantly increase bone density in the hip parameters of chronic SCI patients, a positive trend was observed in the lumbar spine. Further research with acute intervention, such as FESILEC during the first few months post-SCI, is warranted to further evaluate a treatment regimen to prevent or reduce neurogenic osteopenia.

Absorptiometry, Photon↗

PubMedDate not supplied

Physostigmine-induced cerebral protection against hypoxia.

Physostigmine, at 0.1, 0.2 and 0.3 mg/kg, was tested for effect on the survival of mice exposed to 5% O2-95% N2. Some treated animals survived for one hour under the hypoxic atmosphere (2 out of 14 at 0.1 mg/kg and 8 out of 28 at 0.2 and 0.3 mg/kg), an event never observed in untreated controls. The physostigmine-treated animals that died before the hour showed a dose-related increase in survival time from 4.3 min (untreated controls) to 27.6 min (0.3 mg/kg physostigmine). The effect of physostigmine may be related to its reported ability to increase cerebral blood flow and decrease cerebral oxygen consumption

Animals↗

PubMedDate not supplied

Survival under hypoxia. Age dependence and effect of cholinergic drugs.

Survival under hypoxia (5% O2; 95% N2) was tested in mice 1 day to 50-weeks-old. Survival Rate (ratio of number of animals that survived 30 min under 5% O2 to total number of animals exposed) and the time from onset of exposure until the last gasp (Survival Time) were maximum in newborn animals and decreased as a function of age. Survival Rate and Survival Time were strongly influenced by drugs affecting cholinergic transmission. Atropine decreased the high survival under hypoxia of 1-week-old mice in a dose-related manner. Physostigmine increased survival under hypoxia in mice 3 to 50-weeks-old. This effect was not related to a peripheral action of the drug since it was not mimicked by neostigmine, a cholinesterase inhibitor without central actions. Moreover, peripheral cholinergic blockade with glycopyrrolate, a quaternary cholinergic blocker, did not prevent the protective effect of physostigmine. Since atropine impairs the ability of very young mice to survive hypoxia and physostigmine improves survival at later ages, it is concluded that a central cholinergic mechanism, possibly related to blood flow regulation, plays a significant role in the acute adaptation to hypoxia.

Aging↗

PubMedDate not supplied

Physostigmine induced reversal of ischemia following acute middle cerebral artery occlusion in the rat.

Cerebral cortical ischemia was induced in anesthetized rats by occlusion of the middle cerebral artery (MCA). Cerebral blood flow (CBF) was measured with the H2 clearance technique in the center and periphery of the ischemic territory. A decrease of CBF to about 50% of pre-occlusion values was observed in both areas. Administration of Physostigmine, a cholinesterase inhibitor, at a dose of 0.15 mg/Kg by intravenous route, induced an increase of CBF in the ischemic cortex. This change in CBF reached 120% of pre-occlusion level in the periphery and 80% of pre-occlusion value in the center of the area of distribution of the occluded artery. Although Physostigmine induced an increase in arterial blood pressure, the cerebral hyperemia observed both in normal and ischemic cortex could still be demonstrated after blockade of the pressor effect by bleeding or Phentolamine administration.

Animals↗