Dynamic heterogeneity of cerebral hypoperfusion after prolonged cardiac arrest in dogs measured by the stable xenon/CT technique: a preliminary study

Mild hypothermia after cardiac arrest in dogs does not affect postarrest multifocal cerebral hypoperfusion.

“…In contrast, in our other recent studies, deep resuscitative hypothermia induced with reperfusion from cardiac arrest worsened brain damage,18 whereas mild resuscitative hypothermia mitigated brain damage37 [7][8][9][10][11][12][13][14][15][16][17][18][19] more so than moderate resuscitative hypothermia.20 Impaired microcirculatory reperfusion with low temperatures is one of the several explanations that remain to be studied.…”

Mild hypothermia after cardiac arrest in dogs does not affect postarrest multifocal cerebral hypoperfusion.

“…In contrast, in our other recent studies, deep resuscitative hypothermia induced with reperfusion from cardiac arrest worsened brain damage,18 whereas mild resuscitative hypothermia mitigated brain damage37 [7][8][9][10][11][12][13][14][15][16][17][18][19] more so than moderate resuscitative hypothermia.20 Impaired microcirculatory reperfusion with low temperatures is one of the several explanations that remain to be studied.…”

Post-cardiac arrest syndrome: Epidemiology, pathophysiology, treatment, and prognostication: A Scientific Statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke (Part 1)

“…These results do not rule out the potential presence of regional microcirculatory reperfusion deficits that have been observed in animal studies despite adequate CPP (Wolfson et al, 1992;Sterz et al, 1992). Overall, it is likely that the CPP necessary to maintain optimal cerebral perfusion will vary among individual post-cardiac arrest patients at various time points after ROSC.…”

Upregulation of serum and glucocorticoid-regulated kinase 1 exacerbates brain injury and neurological deficits after cardiac arrest

“…The major challenge in developing new therapies to manage brain injury after CA stems from the fact that CA-induced brain injuries involve multiple pathological processes, such as hypoperfusion, neuroinflammation, and cell death (23,24,26). These complicated mechanisms can ultimately result in severe neurological deficits.…”

Mild hypothermia after cardiac arrest in dogs does not affect postarrest multifocal cerebral hypoperfusion.

“…In contrast, in our other recent studies, deep resuscitative hypothermia induced with reperfusion from cardiac arrest worsened brain damage,18 whereas mild resuscitative hypothermia mitigated brain damage37 [7][8][9][10][11][12][13][14][15][16][17][18][19] more so than moderate resuscitative hypothermia.20 Impaired microcirculatory reperfusion with low temperatures is one of the several explanations that remain to be studied.…”

Post-cardiac arrest syndrome: Epidemiology, pathophysiology, treatment, and prognostication: A Scientific Statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke (Part 1)

“…These results do not rule out the potential presence of regional microcirculatory reperfusion deficits that have been observed in animal studies despite adequate CPP (Wolfson et al, 1992;Sterz et al, 1992). Overall, it is likely that the CPP necessary to maintain optimal cerebral perfusion will vary among individual post-cardiac arrest patients at various time points after ROSC.…”

Upregulation of serum and glucocorticoid-regulated kinase 1 exacerbates brain injury and neurological deficits after cardiac arrest

“…The major challenge in developing new therapies to manage brain injury after CA stems from the fact that CA-induced brain injuries involve multiple pathological processes, such as hypoperfusion, neuroinflammation, and cell death (23,24,26). These complicated mechanisms can ultimately result in severe neurological deficits.…”

Mild hypothermia after cardiac arrest in dogs does not affect postarrest multifocal cerebral hypoperfusion.

“…In contrast, in our other recent studies, deep resuscitative hypothermia induced with reperfusion from cardiac arrest worsened brain damage,18 whereas mild resuscitative hypothermia mitigated brain damage37 [7][8][9][10][11][12][13][14][15][16][17][18][19] more so than moderate resuscitative hypothermia.20 Impaired microcirculatory reperfusion with low temperatures is one of the several explanations that remain to be studied.…”

Post-cardiac arrest syndrome: Epidemiology, pathophysiology, treatment, and prognostication: A Scientific Statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke (Part 1)

“…These results do not rule out the potential presence of regional microcirculatory reperfusion deficits that have been observed in animal studies despite adequate CPP (Wolfson et al, 1992;Sterz et al, 1992). Overall, it is likely that the CPP necessary to maintain optimal cerebral perfusion will vary among individual post-cardiac arrest patients at various time points after ROSC.…”

Upregulation of serum and glucocorticoid-regulated kinase 1 exacerbates brain injury and neurological deficits after cardiac arrest

“…The major challenge in developing new therapies to manage brain injury after CA stems from the fact that CA-induced brain injuries involve multiple pathological processes, such as hypoperfusion, neuroinflammation, and cell death (23,24,26). These complicated mechanisms can ultimately result in severe neurological deficits.…”