Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
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J. Cereb. Blood Flow Metab. · May 2009
Deep hypothermia markedly activates the small ubiquitin-like modifier conjugation pathway; implications for the fate of cells exposed to transient deep hypothermic cardiopulmonary bypass.
Various cardiovascular operations are performed during conditions of deep hypothermic circulatory arrest. Here we investigated the effects of deep hypothermia on the small ubiquitin-like modifier (SUMO) conjugation pathway using a clinically relevant animal model of deep hypothermic cardiopulmonary bypass (DHCPB). ⋯ Activation of the SUMO conjugation pathway is believed to protect neurons from damage caused by low blood flow. This pathway may, therefore, play a key role in defining the outcome of cells exposed to DHCPB.
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J. Cereb. Blood Flow Metab. · May 2009
Propofol anesthesia does not alter regional rates of cerebral protein synthesis measured with L-[1-(11)C]leucine and PET in healthy male subjects.
We report regional rates of cerebral protein synthesis (rCPS) in 10 healthy young males, each studied under two conditions: awake and anesthetized with propofol. We used the quantitative L-[1-(11)C]leucine positron emission tomography (PET) method to measure rCPS. The method accounts for the fraction (lambda) of unlabeled leucine in the precursor pool for protein synthesis that is derived from arterial plasma; the remainder comes from proteolysis of tissue proteins. ⋯ Intersubject variances and patterns of regional variation were also similar under both conditions. In propofol-anesthetized subjects, rCPS varied regionally from 0.98+/-0.12 to 2.39+/-0.23 nmol g(-1) min(-1) in the corona radiata and in the cerebellum, respectively. Our data indicate that the values, variances, and patterns of regional variation in rCPS and lambda measured by the L-[1-(11)C]leucine PET method are not significantly altered by anesthesia with propofol.
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J. Cereb. Blood Flow Metab. · May 2009
Early metabolic characteristics of lesion and nonlesion tissue after head injury.
We defined lesion and structurally normal regions using magnetic resonance imaging at follow-up in patients recovering from head injury. Early metabolic characteristics in these regions of interest (ROIs) were compared with physiology in healthy volunteers. Fourteen patients with severe head injury had positron emission tomography within 72 h, and magnetic resonance imaging at 3 to 18 months after injury. ⋯ There was considerable heterogeneity between and within patients. Although irreversibly damaged tissue is characterized by marked derangements in physiology, a more detailed analysis shows acute changes in physiology and physiologic relationships within regions of the brain that appear structurally normal at follow-up. Such pathophysiological derangements may result in selective neuronal loss and impact on functional outcome.
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J. Cereb. Blood Flow Metab. · May 2009
Comparative StudyCritical closing pressure: comparison of three methods.
Critical closing pressure (CCP) is an arterial pressure threshold below which small arterial vessels collapse. Our aim was to compare different methods to estimate CCP in the cerebrovascular circulation using the relationships between transcranial Doppler flow velocity (FV), laser-Doppler flux (LDF), and arterial blood pressure (ABP). A total of 116 experiments in rabbits were analyzed retrospectively. ⋯ Critical closing pressures obtained from FV waveform and CA correlated with mean ICP before CA (R=0.40; P=0.001). In conclusion strong correlation exists between CCP values obtained by means of FV and LDF during cardiac arrest. However, predictions of CCP using TCD waveform analysis show substantial differences from values of CCP recorded during cardiac arrest.
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J. Cereb. Blood Flow Metab. · May 2009
When hypothermia meets hypotension and hyperglycemia: the diverse effects of adenosine 5'-monophosphate on cerebral ischemia in rats.
Mild hypothermia renders potent neuroprotection against acute brain injury. Recent reports show that adenosine 5'-monophosphate (AMP) plays a role in thermoregulation and induces hypothermia in mice. Therefore, this study sought to determine whether AMP induces hypothermia in rats and to study its collective effects on cerebral ischemia induced by 2-h middle cerebral artery occlusion. ⋯ In addition, western blots showed early dephosphorylation and degradation of AMP-activated kinase in the ischemic cortex in AMP-treated rats. Taken together, our findings suggest that AMP induces hypothermia in rats, probably by limiting cellular access to glucose. However, the potential neuroprotection of AMP-mediated hypothermia against ischemia was overwhelmed by the detrimental effects of hypotension and hyperglycemia, thus making AMP an unlikely agent for inducing hypothermia to protect the brain against ischemic injury.