Experimental CNS ischemia

@article{Zivin1984ExperimentalCI,
  title={Experimental CNS ischemia},
  author={J A Zivin and J A Venditto},
  journal={Neurology},
  year={1984},
  volume={34},
  pages={469 - 469}
}
We tested three serotonin antagonists-lysergic acid diethylamide (LSD), 2-bromolysergic acid diethylamide (BOL), and cinanserin — for effects on experimental spinal cord ischemia in the rabbit. Blood fiow to spinal cord was obstructed. Drugs were administered before or after initiation of occlusion, and flow was later restored. When LSD was given 5 minutes after the onset of occlusion, the duration of ischemia required to produce neurologic abnormality was prolonged, but this protection was… 
Serotonin Antagonists Reduce Central Nervous System Ischemic Damage
TLDR
There is a compelling case for the utility of serotonin antagonists in the emergency therapy of such problems as cardiac arrest to prevent cerebral damage while the cardiac status is stabilized, and possibly for stroke-in-evolution to prevent continued progressive extension of damage.
Cyproheptadine reduces or prevents ischemic central nervous system damage
TLDR
The results suggest that serotonin antagonists reduce isChemic CNS damage; cyproheptadine may be a potential treatment for ischemic stroke.
Studies of the influence of biogenic amines on central nervous system ischemia.
TLDR
It is found that it is possible to study biochemical and morphological aspects of spinal cord ischemia in great detail using a combination of quite precise techniques, but at this level of resolution there were no substantial changes in biogenic amine concentrations in severely ischemic or marginally perfused tissue after the durations of ischemIA that cause the onset of irreversible tissue damage.
Effects of ketanserin and mianserin on delayed neuronal death induced by cerebral ischemia in Mongolian gerbils
TLDR
Administration of ketanserin and mianserin led to better passive avoidance and prevented the delayed neuronal death induced by cerebral ischemia in gerbils and the effects of these drugs are not mediated by serotonergic and cholinergic systems.
The serotonin antagonist mianserin improves functional recovery following experimental spinal trauma
TLDR
In acute studies, mianserin at 1 mg/kg was associated with the preservation of posttraumatic spinal cord blood flow at T‐12 as well as a pronounced alteration in postmortem spinal serotonin content and metabolism, in contrast to vehicle control treatments, which lend further support to a serotonergic hypothesis of secondary spinal cord injury.
Effects of lodoxamide tromethamine on paraplegia that occurs after infrarenal aortic occlusion in the rabbit.
TLDR
Results suggest lodoxamide may be useful in alleviating ischemic damage to the spinal cord in animals treated with this antioxidant.
Comparison of a serotonin antagonist, opioid antagonist, and TRH analog for the acute treatment of experimental spinal trauma.
TLDR
All agents displayed similar and significant efficacies with respect to Tarlov and Rivlin-Tator measures of motor recovery and preservation of raphe-spinal fibers below the lesion site, and none of the agents were effective for preserving the central gray matter or myelin staining in the white matter in slices of tissue from the site of injury.
Ischemia‐Induced Extracellular Release of Serotonin Plays a Role in CA1 Neuronal Cell Death in Rats
TLDR
It is suggested that serotonin plays a detrimental role, mediated by 5-HT2 receptors, in the development of ischemic damage.
Inhibitory Mechanisms in Cerebral Ischemia: a Brief Review
TLDR
In conclusion, inhibitory mechanisms that may be important in cerebral ischemia are summarized, experimental evidence for their potential efficacy is provided, and such medications have few side-effects and are in clinical use for other indications.
Effect of the Serotonin Antagonist Ketanserin on the Hemodynamic and Morphological Consequences of Thrombotic Infarction
  • W. Dietrich, R. Busto, M. Ginsberg
  • Medicine
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 1989
TLDR
Data are consistent with the hypothesis that 5-HT is involved in the widespread hemodynamic consequences of experimentally induced thrombotic infarction, and can be inhibited without altering final infarct size.
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