scholarly journals Cerebral Blood Flow Restoration and Reperfusion Injury After Ultraviolet Laser–Facilitated Middle Cerebral Artery Recanalization in Rat Thrombotic Stroke

Stroke ◽  
2002 ◽  
Vol 33 (2) ◽  
pp. 428-434 ◽  
Author(s):  
Brant D. Watson ◽  
Ricardo Prado ◽  
Alexander Veloso ◽  
J-P. Brunschwig ◽  
W. Dalton Dietrich
1995 ◽  
Vol 80 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Andreas Weyland ◽  
Heidrun Stephan ◽  
Frank Grune ◽  
Wolfgang Weyland ◽  
Hans Sonntag

1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P<0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.


2000 ◽  
Vol 8 (5) ◽  
pp. 1-4 ◽  
Author(s):  
Emanuela Keller ◽  
Thorsten Steiner ◽  
Javier Fandino ◽  
Stefan Schwab ◽  
Werner Hacke

Object Moderate hypothermia has been reported to be effective in the treatment of postischemic brain edema. The effect of hypothermia on cerebral hemodynamics is a matter of controversial discussion in literature. Clinical studies have yet to be performed in patients with ischemic stroke after induction of hypothermia. Methods Measurements during mild hypothermia (33–34°C) were made in six patients with severe ischemic stroke involving the middle cerebral artery territory. Hypothermia was induced as soon as possible and maintained for 48 to 72 hours. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were estimated by a new double-indicator dilution method. Measurements of CBF were made during normothermia, immediately after induction of hypothermia, at the end of hypothermia, and after rewarming. A total of 19 measurements of CBF and jugular bulb O2 saturation were made. Immediately after induction of hypothermia, CBF decreased in all patients. During late hypothermia, CBF improved in patients who survived but remained diminished in the two patients who died. Reduced CMRO2 levels were observed during all phases of hypothermia in all but one case. Conclusions Preliminary oberservations indicate that moderate hypothermia seems to reduce CMRO2 Immediately after induction of hypothermia, CBF may decrease in all patients. During late hypothermia CBF seems to recover in patients with good outcome but remains diminished in patients who die. Serial bedside CBF measurements with the new double-indicator dilution technique may be useful to describe cerebral hemodynamic characteristics in patients with severe ischemic stroke during hypothermia.


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