A Comparison of the Cerebral Protective Effects of Isoflurane and Mild Hypothermia in a Model of Incomplete Forebrain Ischemia in the Rat

Sano, Tomoya; Drummond, John C.; Patel, Piyush M.; Grafe, Marjorie R.; Watson, Joseph C.; Cole, Daniel J.

doi:10.1097/00000542-199202000-00011

Cited by 145 publications

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“…Although it has been clearly demonstrated that barbiturates decrease the cerebral metabolic rate for oxygen (CMRO 2 ), the concept that decreasing the CMRO 2 per se is directly related to a neuroprotective effect has been questioned [7,8]. Attempts at assessing brain energy states using 31 P nuclear magnetic spectroscopy suggest that the administration of thiopental before a period of hypothermic circulatory arrest may be detrimental to the preservation of the energy state of the brain [9].…”

Section: Discussionmentioning

confidence: 99%

Pharmacological agents as cerebral protectants during deep hypothermic circulatory arrest in adult thoracic aortic surgery

2002

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SummaryA postal survey was sent to members of the Association of Cardiothoracic Anaesthetists to ascertain current practice in the use of pharmacological agents as cerebral protectants during deep hypothermic circulatory arrest. The response rate was 60%. Eighty-three per cent of respondents used some form of pharmacological agent specifically for cerebral protection. Fifty-nine per cent of respondents used thiopental, 29% used propofol and 48% used a variety of other agents, the most common of these being a steroid. There were variations in the dose and timing of administration of drugs. Few respondents believed that there was a body of evidence to support this use of pharmacological agents. Only 35% of respondents believed there to be sufficient evidence to support the use of thiopental. Similarly, only 11% of respondents believe that there is evidence supporting the use of propofol, and 16% the use of steroids. The above findings demonstrate that it would not be possible to create a 'best practice' set of guidelines at present. A national database of all cases of adult thoracic surgery involving deep hypothermic cardiac arrest, with methodology and outcome, could probably establish such guidelines, evidence based.

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Section: Discussionmentioning

confidence: 99%

Pharmacological agents as cerebral protectants during deep hypothermic circulatory arrest in adult thoracic aortic surgery

2002

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“…The only 2 human outcome studies of barbiturate protection in focal cerebral ischemia were directed by cardiac anesthesiologists, 57,58 one showing protection in cardiac valvular surgery patients 57 and the other showing no protection in patients having coronary artery bypass grafting (CABG), 58 both in patients subjected to cardiopulmonary bypass-assisted circulation and in whom focal cerebral ischemia was suspected. 60 Drummond et al 61 also reported actual exacerbation of ischemic brain injury by etomidate. 38 The theory of metabolic depression as a common link for cerebral protection in neuroanesthesiology scenarios began unraveling on many fronts in the 1990s and afterward.…”

Section: Cerebral Protection By Metabolic Depressant Anestheticsmentioning

confidence: 97%

The History of Neuroanesthesiology

Lanier¹

2012

Journal of Neurosurgical Anesthesiology

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Neuroanesthesiology has a rich history. Although advances in research and clinical practice were cornerstones for the development of this field, other equally critical factors came into play. These include the development of subspecialty societies, formal dissemination of information through textbooks and journal publications, and, most importantly, strong leadership. This article reviews important advances within the subspecialty and many individuals behind those advances. The analysis and speculative synthesis provide insights into the current status of neuroanesthesiology and possible directions for the subspecialty's future.

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“…Cerebral metabolic rate is modestly reduced (29), as is the accumulation of glutamate in the extracellular space (9,41). However, the importance of these effects has been questioned (32,42). In vitro, mild hypothermia reduces calcium uptake by neurons (2,6).…”

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Pharmacological correction of hypothermic P₅₀shift does not alter outcome from focal cerebral ischemia in rats

Wainwright

Sheng²,

Sato³

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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. Pharmacological correction of hypothermic P 50 shift does not alter outcome from focal cerebral ischemia in rats. Am J Physiol Heart Circ Physiol 282: H1863-H1870, 2002; 10.1152/ajpheart.00863.2001.-Hypothermia decreases the arterial PO 2 at which hemoglobin is 50% saturated (P50), increasing hemoglobin O2-binding affinity. We used RSR13, a synthetic allosteric modifier of hemoglobin that increases P 50, to study the role of altered hemoglobin O2-binding affinity in mild hypothermic neuroprotection. RSR13 (150 mg/kg iv) restored P50 to normothermic values. Rats underwent 70 min of middle cerebral artery occlusion (MCAO) at 30.0, 34.0, or 37.5°C with hemoglobin saturation held at 98-100%. The 34.0°C group received RSR13 or vehicle before ischemia. After 7 days of recovery, infarct volumes were reduced in all hypothermic groups, without evidence of a detrimental effect on infarct size or neurological score as a result of P 50 correction. To examine for a beneficial effect of P50 correction, ischemia duration was increased to 120 min in rats maintained at 34.0°C. Correction of P50 by RSR13 did not alter cerebral infarct sizes or neurological scores. The decrease in P 50, caused by mild hypothermia, could not be associated with infarct size or neurological deficit resulting from ischemic brain hypoxia in rats.brain; allosteric modification; hypothermia; RSR13 IN LABORATORY MODELS of focal and global cerebral ischemia, mild (34.0°C) and moderate (30.0°C) hypothermia have been shown to reduce brain injury (8,14,17,30,31). Although the efficacy of induced hypothermia remains unproven in humans sustaining ischemic brain injury, intense investigation continues with the hope of defining conditions where benefits may be obtained (12,20,34,36,43).Mild hypothermia produces multiple effects on the ischemic brain. Cerebral metabolic rate is modestly reduced (29), as is the accumulation of glutamate in the extracellular space (9, 41). However, the importance of these effects has been questioned (32, 42). In vitro, mild hypothermia reduces calcium uptake by neurons (2, 6). Mild hypothermia has no effect on protein synthesis during early recirculation (4) but hastens recovery of protein synthesis several hours after reperfusion (39) and diminishes membranebound protein kinase C activity in selectively vulnerable regions (10). Hypothermia also reduces the cerebral formation of reactive oxygen species and nitric oxide (18,22,23,26). The frequency of peri-infarct spontaneous depolarizations is also decreased in hypothermic rats (11).Hypothermia exerts another biological effect, the significance of which has not been examined. The PO 2 at which 50% of hemoglobin (Hb) binding sites are occupied by oxygen (P 50 ) is reduced in a temperature-dependent fashion. It can be speculated that this effect on Hb O 2 -binding affinity may be either beneficial or detrimental to the ischemic brain. Because hypothermia increases the affinity of Hb for O 2 , release of O 2 into tissue could be reduced. In contrast, when Hb affinity for O 2 is incre...

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A Comparison of the Cerebral Protective Effects of Isoflurane and Mild Hypothermia in a Model of Incomplete Forebrain Ischemia in the Rat

Cited by 145 publications

References 0 publications

Pharmacological agents as cerebral protectants during deep hypothermic circulatory arrest in adult thoracic aortic surgery

Pharmacological agents as cerebral protectants during deep hypothermic circulatory arrest in adult thoracic aortic surgery

The History of Neuroanesthesiology

Pharmacological correction of hypothermic P₅₀shift does not alter outcome from focal cerebral ischemia in rats

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A Comparison of the Cerebral Protective Effects of Isoflurane and Mild Hypothermia in a Model of Incomplete Forebrain Ischemia in the Rat

Cited by 145 publications

References 0 publications

Pharmacological agents as cerebral protectants during deep hypothermic circulatory arrest in adult thoracic aortic surgery

Pharmacological agents as cerebral protectants during deep hypothermic circulatory arrest in adult thoracic aortic surgery

The History of Neuroanesthesiology

Pharmacological correction of hypothermic P50shift does not alter outcome from focal cerebral ischemia in rats

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Pharmacological correction of hypothermic P₅₀shift does not alter outcome from focal cerebral ischemia in rats