Nimodipine Prevents Transient Cognitive Dysfunction After Moderate Hypoxia in Adult Mice

Haile, Michael; Limson, Fred; Gingrich, Kevin J.; Li, Yong Sheng; Quartermain, David; Blanck, Thomas J. J.; Bekker, Alex

doi:10.1097/ana.0b013e3181920d28

Cited by 21 publications

(12 citation statements)

References 27 publications

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“…It has been shown that a relationship exists between changes in cognitive function and hippocampal damage, and that nimodipine treatment reversed the impairment of shortterm working memory caused by moderate hypoxia in mice. 32 Studies on the effect of nimodipine on rats with vascular dementia are, however, scarce. 18 The present study evaluated the effect of nimodipine treatment on levels of NF-κB, TNF-α and IL-1β in the hippocampus of rats with vascular dementia.…”

Section: Effects Of Nimodipine In a Rat Vascular Dementia Modelmentioning

confidence: 99%

Nimodipine Improves Regional Cerebral Blood Flow and Suppresses Inflammatory Factors in the Hippocampus of Rats with Vascular Dementia

2012

J Int Med Res

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Section: Effects Of Nimodipine In a Rat Vascular Dementia Modelmentioning

confidence: 99%

Nimodipine Improves Regional Cerebral Blood Flow and Suppresses Inflammatory Factors in the Hippocampus of Rats with Vascular Dementia

2012

J Int Med Res

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“…It can expand the cerebral blood vessels, improve the cerebral circulation, and protect the brain. [6,7] Studies have shown that nimodipine could improve cognition in adult mice by reducing neuronal damage [8] and our previous research found pretreatment with nimodipine can prevent postoperative cognitive dysfunction (POCD) on aged rats by reducing hippocampal apoptosis rate. [9] However, its clinical effect remains to be discussed.…”

Section: Introductionmentioning

confidence: 99%

Effects of nimodipine on postoperative delirium in elderly under general anesthesia

Zhou

Yin

et al. 2017

Medicine

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Nimodipine is a clinical commonly used calcium antagonistscan lowering the apoptosis rate of hippocampal neuron to reduce the incidence of postoperative cognitive dysfunction (POCD). This study was designed to evaluate the effects of nimodipine on postoperative delirium in elderly under general anesthesia.Sixty patients shceduced spine surgery under general anesthesia were randomly assigned into 2 groups using a random number table: control group (Group C) and nimodipine group (Group N). In Group N, nimodipine 7.5 μg/(kg × h) was injected continually 30 minutes before anesthesia induction, while the equal volume of normal saline was given in Group C. At 0 minute before injection, 0 minute after tracheal intubation, 1 hour after skin incision and surgery completed (T1–4), blood samples were taken from the radial artery and jugular bulb for blood gas analysis. Cerebral oxygen metabolism-related indicators were calculated at the same time. Concentration of S100β and glial fibrillary acidic protein (GFAP) were tested by ELISA. The incidence of postoperative delirium within 7 days after surgery was recorded.Cerebral oxygen metabolism-related indicators fluctuationed in the normal range in 2 groups at different time points and the difference were not statistically significant. Compared with Group C, S100β and GFAP decreased and incidence of postoperative delirium reduced at T3–4 in Group N, the difference was statistically significant (P<.05).The present study suggests that nimodipine can reduce the development of postoperative delirium in elderly patients under general anesthesia, the reduction of brain injury and improvement of cerebral oxygen metabolism may be involved in the mechanism.

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“…NIMO preserves performance in PA tasks, the radial maze, and the object recognition test after memory disruption induced by exposure to hypoxia 12,26…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, we were interested in examining whether nimodipine (NIMO), an L-type calcium channel blocker that crosses the blood-brain barrier, would reduce the hypotension-induced impairment of learning and memory. Our previous investigation demonstrated that NIMO reversed transient cognitive dysfunction caused by moderate hypoxia in adult mice 12. In this study, we examined cognitive changes in animals subjected to nitroglycerin (NTG)-induced hypotension using a passive avoidance (PA) memory retention paradigm.…”

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confidence: 99%

Nimodipine Prevents Memory Impairment Caused by Nitroglycerin-Induced Hypotension in Adult Mice

Bekker

Haile

et al. 2009

Anesthesia &Amp; Analgesia

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BACKGROUND: Hypotension and a resultant decrease in cerebral blood flow have been implicated in the development of cognitive dysfunction. We tested the hypothesis that nimodipine (NIMO) administered at the onset of nitroglycerin (NTG)-induced hypotension would preserve long-term associative memory. METHODS: The passive avoidance (PA) paradigm was used to assess memory retention. For PA training, latencies (seconds) were recorded for entry from a suspended platform into a Plexiglas tube where a shock was automatically delivered. Latencies were recorded 48 h later for a testing trial. Ninety-six Swiss-Webster mice (30–35 g, 6–8 wk), were randomized into 6 groups 1) saline (control), 2) NTG immediately after learning, 3) NTG 3 h after learning, 4) NTG and NIMO, 5) vehicle, and 6) NIMO alone. The extent of hypotension and changes in brain tissue oxygenation (PbtO2) and in cerebral blood flow were studied in a separate group of animals. RESULTS: All groups exhibited similar training latencies (17.0 ± 4.6 s). Mice subjected to hypotensive episodes showed a significant decrease in latency time (178 ± 156 s) compared with those injected with saline, NTG + NIMO, or delayed NTG (580 ± 81 s, 557 ± 67 s, and 493 ± 146 s, respectively). A Kruskal-Wallis 1-way analysis of variance indicated a significant difference among the 4 treatment groups (H = 15.34; P < 0.001). In a separate group of mice not subjected to behavioral studies, the same dose of NTG (n = 3) and NTG + NIMO (n = 3) caused mean arterial blood pressure to decrease from 85.9 ± 3.8 mm Hg sem to 31.6 ± 0.8 mm Hg sem and from 86.2 ± 3.7 mm Hg sem to 32.6 ± 0.2 mm Hg sem, respectively. Mean arterial blood pressure in mice treated with NIMO alone decreased from 88.1 ± 3.8 mm Hg to 80.0 ± 2.9 mm Hg. The intergroup difference was statistically significant (P < 0.05). PbtO2 decreased from 51.7 ± 4.5 mm Hg sem to 33.8 ± 5.2 mm Hg sem in the NTG group and from 38.6 ± 6.1 mm Hg sem to 25.4 ± 2.0 mm Hg sem in the NTG + NIMO groups, respectively. There were no significant differences among groups. CONCLUSION: In a PA retention paradigm, the injection of NTG immediately after learning produced a significant impairment of long-term associative memory in mice, whereas delayed induced hypotension had no effect. NIMO attenuated the disruption in consolidation of long-term memory caused by NTG but did not improve latency in the absence of hypotension. The observed effect of NIMO may have been attributable to the preservation of calcium homeostasis during hypotension, because there were no differences in the PbtO2 indices among groups.

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Nimodipine Prevents Transient Cognitive Dysfunction After Moderate Hypoxia in Adult Mice

Abstract: NIMO reverses the disturbance of short-term working memory caused by moderate hypoxia in mice. The results may have implications for cognitive changes linked to Ca homeostasis in the postoperative period.

Cited by 21 publications

References 27 publications

Nimodipine Improves Regional Cerebral Blood Flow and Suppresses Inflammatory Factors in the Hippocampus of Rats with Vascular Dementia

Nimodipine Improves Regional Cerebral Blood Flow and Suppresses Inflammatory Factors in the Hippocampus of Rats with Vascular Dementia

Effects of nimodipine on postoperative delirium in elderly under general anesthesia

Nimodipine Prevents Memory Impairment Caused by Nitroglycerin-Induced Hypotension in Adult Mice

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