Early effects of nimodipine on intracanial and cerebral perfusion pressures in cerebral anoxia after out-of-hospital cardiac arrest

Gueugniaud, Pierre‐Yves; Gaussorgues, P.; Garcia-Darennes, F; Bancalari, G; Roux, H; Robert, Dominique; Petit, Paul

doi:10.1016/0300-9572(90)90003-w

Cited by 29 publications

(2 citation statements)

References 14 publications

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“…Nimodipine is a lipophilic calcium antagonist that can easily pass through the blood brain barrier and reach a high concentration in cerebrospinal fluid. Studies have shown that nimodipine could increase cerebral perfusion pressures [ 23 ] and improve cognition by reducing neuronal damage [ 18 ]. Nimodipine can dilate the cerebral vessels specifically and have almost no effect on peripheral vessels.…”

Section: Discussionmentioning

confidence: 99%

Pretreatment with nimodipine reduces incidence of POCD by decreasing calcineurin mediated hippocampal neuroapoptosis in aged rats

Zhang

Bao³

et al. 2018

BMC Anesthesiol

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BackgroundCalcineurin (CaN) having a high expression in hippocampal neurons is closely related to apoptosis. Pretreatment with nimodipine can lower the apoptosis rate of hippocampal neuron to reduce the incidence of postoperative cognitive dysfunction (POCD). However, the relationship between cerebral protective effect of pretreatment with nimodipine and CaN is controversial in the literature. The aim of this study is to evaluate the relationship between neuroprotective effect of nimodipine and CaN on POCD in aged rats.MethodsNinety-six 18-month-old male Sprague-Dawley rats were randomly assigned into 4 groups (n = 24 each): control group (Group C), nimodipine group (Group N), surgery group (Group S) and nimodipine + surgery group (Group N + S). In Group N and Group N + S, nimodipine 1 mg/kg was intraperitoneally injected, while the equal volume of normal saline was given instead in Group S. 30 min later, Group N and Group C inhaled pure oxygen for 2 h, and Group S and N + S inhaled 3% sevoflurane for 2 h when exploratory laparotomy was performed. Morris water maze test was performed on 1 day before operation and 1, 3 and 7 days after operation. After the end of Morris water maze test at 1 day before operation and 1 and 7 days after operation, 8 rats were sacrificed, brains were removed and hippocampal tissues were obtained for detection of apoptosis in hippocampal neurons, cytoplasmic calcium ([Ca2+]i), and hippocampal CaN and caspase-3 expression.ResultsCompared with the 1st day before operation, the escape latency, apoptosis rate, [Ca2+]i, expression of CaN and caspase-3 increased significantly, but the frequency of crossing the original platform decreased dramatically in Group S and N + S(P<0.05). In addition, the escape latency, apoptosis rate, [Ca2+]i, and expression of CaN and caspase-3 decreased markedly, but the frequency of crossing the original platform increased significantly in Group N + S as compared with Group S (P<0.05).ConclusionsPretreatment with nimodipine reduces the incidence of POCD by decreasing CaN mediated hippocampal neuroapoptosis in aged rats.

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Section: Discussionmentioning

confidence: 99%

Pretreatment with nimodipine reduces incidence of POCD by decreasing calcineurin mediated hippocampal neuroapoptosis in aged rats

Zhang

Bao³

et al. 2018

BMC Anesthesiol

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“…In spite of causing cerebral vasodilatation and increased cerebral blood flow, initiation of intravenous nimodipine therapy (10 /-tg/kg initially then 30 to 60 /-tg/kg/h for 5 days) within 10 minutes of successful resuscitation after cardiac arrest reduced intracranial pressure; the mean peak value was 17.3mm Hg compared with 22.8mm Hg in the control group who did not receive nimodipine (p < 0.01; Gueugniaud et al 1990). …”

Section: Effects On Cerebral Blood Flowmentioning

confidence: 96%

Nimodipine

Wadworth¹,

McTavish²

1992

Drugs & Aging

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Nimodipine is a dihydropyridine calcium antagonist which dilates cerebral blood vessels and increases cerebral blood flow in animals and humans. Preliminary findings reveal its potential benefit for the treatment of a wide range of cerebrovascular disorders, particularly for prophylaxis and treatment of delayed ischaemic neurological deficits resulting from cerebral vasospasm in patients with subarachnoid haemorrhage. Studies involving patients aged up to 79 years have confirmed these preliminary findings by showing that nimodipine reduces the incidence of severe ischaemic deficit after subarachnoid haemorrhage. Initial results from studies of patients with acute ischaemic stroke indicate that nimodipine, started within 72 hours of onset, improved recovery, particularly in patients over 65 years. However, other investigators have found no marked difference in 6-month mortality or morbidity rates of stroke patients aged up to 97 years. Findings from other studies suggest that nimodipine may improve symptoms of cognitive dysfunction in elderly patients. Nimodipine is well tolerated by both younger and older patients. The most frequently reported adverse event has been hypotension. Thus, nimodipine therapy offers important benefits as part of the approach to management of patients with subarachnoid haemorrhage and has potential in other cerebral disorders, including stroke and impaired cognitive function, although confirmation of initial results in patients with cerebral impairment are required.

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Prognostic significance of early intracranial and cerebral perfusion pressures in post-cardiac arrest anoxic coma

et al. 1991

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The prognosis of prolonged cardiac arrests is generally related to brain damage due to the cerebral anoxia. A neurological worsening leading to irreversibility is sometimes associated with an increase in intracranial pressure. We studied for 5 years the early intracranial and cerebral perfusion pressures in 84 patients with deep anoxic coma after cardiac arrest. Intracranial pressure monitoring was set up as soon as possible with an extradural screw over a period of 6 days. No complications occurred using this technique. We recorded the percentage of patients suffering from intracranial pressure peaks over 15 mmHg (a), over 25 mmHg (b) or cerebral perfusion pressures drops under 50 mmHg (c). We obtained during the 1st day of monitoring: (a) 46.4%, (b) 21.4%, (c) 39%; during the 2nd day: (a) 73.6%, (b) 26.3%, (c) 55.9%. Eight patients (9.5%) were still alive after a couple of months, 4 of whom had no neurological sequelae; among the 76 non-survivors 63 (82.9%) had died because of cerebral anoxic damage. A daily comparison between survivors and non-survivors points out that the survivors' intracranial pressures were always lower than in the non-survivors and the survivors' cerebral perfusion pressures higher than in the non-survivors. Moreover, none of the patients showing intracranial peak pressures over 25 mmHg survived without after-effects. It is clear that many patients suffer early periods of high intracranial pressures and low cerebral perfusion pressures leading to a bad neurological prognosis. Intracranial pressure monitoring may allow assessment of patients' neurological status and prognosis after cardiac resuscitation.

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Early effects of nimodipine on intracanial and cerebral perfusion pressures in cerebral anoxia after out-of-hospital cardiac arrest

Cited by 29 publications

References 14 publications

Pretreatment with nimodipine reduces incidence of POCD by decreasing calcineurin mediated hippocampal neuroapoptosis in aged rats

Pretreatment with nimodipine reduces incidence of POCD by decreasing calcineurin mediated hippocampal neuroapoptosis in aged rats

Nimodipine

Prognostic significance of early intracranial and cerebral perfusion pressures in post-cardiac arrest anoxic coma

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