Literature DB >> 18063820

Emboli formation rather than inflammatory mediators are responsible for increased cerebral water content after conventional and assisted beating-heart myocardial revascularization in a porcine model.

Benjamin Bierbach1, Matthias Meier, Walter Kasper-König, Axel Heimann, Beat Alessandri, Georg Horstick, Hellmut Oelert, Oliver Kempski.   

Abstract

BACKGROUND AND
PURPOSE: Emboli and proinflammatory mediators are suspected of generating cerebral edema after coronary surgery. In contrast to cardiopulmonary bypass (CPB), off-pump coronary artery bypass surgery (OPCAB) reduces microemboli count and proinflammatory mediator release but carries the risk of hemodynamic instability. A microaxial blood pump can augment cardiac output.
METHODS: Coronary bypasses were constructed in pigs with CPB and cardioplegia (n=9), OPCAB (n=9), or blood-pump support CAB (n=9). Nine animals underwent sham operation. Embolus count was monitored and regional cerebral blood flow was assessed with microspheres in 21 brain specimens per animal (n=189 per group). Interleukins 6 and 8 and tumor necrosis factor-alpha concentrations were determined. These variables were studied before, during, and for 4 hours after surgery. Finally, cerebral water content was determined.
RESULTS: During CPB and blood-pump CAB, a significant number of emboli were counted in contrast to OPCAB and controls (P<0.05). During CPB, regional cerebral blood flow was affected (32 of 189) and showed reactive hyperemia except in 10 specimens after aortic cross-clamp release. This impairment persisted in 20 specimens. During and after OPCAB, regional cerebral blood flow remained nearly unchanged but showed low flow during (58 of 189) and after (35 of 189) the blood-pump run. A significant increase in proinflammatory mediators was observed only in the CPB group. CPB and blood-pump CAB significantly increased cerebral water content (P<0.05). A strong correlation between embolic load and cerebral water content was observed in all groups. No correlation between proinflammatory mediator release and cerebral water content was detected.
CONCLUSIONS: Emboli formation rather than inflammatory mediators are responsible for increased cerebral water content after conventional and assisted beating-heart myocardial revascularization.

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Year:  2007        PMID: 18063820     DOI: 10.1161/STROKEAHA.107.496620

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  6 in total

1.  Neuroprotective Effects of Resatorvid Against Traumatic Brain Injury in Rat: Involvement of Neuronal Autophagy and TLR4 Signaling Pathway.

Authors:  Yan Feng; Junling Gao; Ying Cui; Minghang Li; Ran Li; Changmeng Cui; Jianzhong Cui
Journal:  Cell Mol Neurobiol       Date:  2016-03-10       Impact factor: 5.046

2.  Poloxamer-188 attenuates TBI-induced blood-brain barrier damage leading to decreased brain edema and reduced cellular death.

Authors:  Hai-Jun Bao; Tao Wang; Ming-Yang Zhang; Ran Liu; Ding-Kun Dai; Yao-Qi Wang; Long Wang; Lu Zhang; Yu-Zhen Gao; Zheng-Hong Qin; Xi-Ping Chen; Lu-Yang Tao
Journal:  Neurochem Res       Date:  2012-09-26       Impact factor: 3.996

3.  Apelin-13 as a novel target for intervention in secondary injury after traumatic brain injury.

Authors:  Hai-Jun Bao; Hai-Yang Qiu; Jin-Xia Kuai; Cheng-Jie Song; Shao-Xian Wang; Chao-Qun Wang; Hua-Bin Peng; Wen-Can Han; Yong-Ping Wu
Journal:  Neural Regen Res       Date:  2016-07       Impact factor: 5.135

4.  Exogenous Hydrogen Sulfide Offers Neuroprotection on Intracerebral Hemorrhage Injury Through Modulating Endogenous H2S Metabolism in Mice.

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Review 6.  Managing the inflammatory response after cardiopulmonary bypass: review of the studies in animal models.

Authors:  Gabriel Romero Liguori; Alexandre Fligelman Kanas; Luiz Felipe Pinho Moreira
Journal:  Rev Bras Cir Cardiovasc       Date:  2014 Jan-Mar
  6 in total

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