Effects of Hemodilution on Long-Term Survival in an Uncontrolled Hemorrhagic Shock Model in Rats

Author(s):  
Harry P. Marshall ◽  
Antonio Capone ◽  
Anita P. Courcoulas ◽  
Brian G. Harbrecht ◽  
Timothy R. Billiar ◽  
...  
2020 ◽  
Vol 25 (4) ◽  
pp. 346-353
Author(s):  
Wangde Dai ◽  
Jianru Shi ◽  
Juan Carreno ◽  
Robert A. Kloner

Background: We investigated whether the cardioprotective, volatile gas anesthetic agent, isoflurane, could improve survival and organ function from hemorrhagic shock in an experimental rat model, compared to standard nonvolatile anesthetic agent ketamine/xylazine. Methods: Sprague Dawley rats (both genders) were randomized to receive either intraperitoneal ketamine/xylazine (K/X, 90 and 10 mg/kg; n = 12) or isoflurane (5% isoflurane induction and 2% maintenance in room air; n = 12) for anesthesia. Blood was withdrawn to maintain mean arterial blood pressure at 30 mm Hg for 1 hour, followed by 30 minutes of resuscitation with shed blood. Rats were allowed to recover and survive for 6 weeks. Results: During the shock phase, the total withdrawn blood volume (expressed as % of estimated total blood volume) to maintain a level of hypotension of 30 mm Hg was significantly higher in the isoflurane group (51.0% ± 1.5%) than in the K/X group (45.3% ± 1.8%; P = .023). Recovery of blood pressure during the resuscitation phase was significantly improved in the isoflurane group compared to the K/X group. The survival rate at 6 weeks was 1 (8.3%) of 12 in rats receiving K/X and 10 (83.3%) of 12 in rats receiving isoflurane ( P < .001). Histology performed at 6 weeks demonstrated brain infarction in the 1 surviving rat receiving K/X; no brain infarction occurred in the 10 surviving rats that received isoflurane. No infarction was detected in heart, lung, liver, or kidneys among the surviving rats. Conclusions: Isoflurane improved blood pressure response to resuscitation and resulted in significantly higher long-term survival rate.


2015 ◽  
Vol 33 (7) ◽  
pp. 965-970 ◽  
Author(s):  
Christian Kleber ◽  
Christopher A. Becker ◽  
Tom Malysch ◽  
Jens M. Reinhold ◽  
Serafeim Tsitsilonis ◽  
...  

1990 ◽  
Vol 10 (2) ◽  
pp. 207-212 ◽  
Author(s):  
Yoichi Yamauchi ◽  
Hiroyuki Kato ◽  
Kyuya Kogure

A new shock model in the rat using hemorrhagic hypotension for production of brain damage is described. Hemorrhagic shock was induced by lowering arterial blood pressure with bleeding. The MABP was maintained at ∼25 mm Hg, accompanied by isoelectric EEG, and then shed blood was retransfused. At 1 week of recovery, morphological and 45Ca autoradiographic changes were examined. No brain damage was observed in rats after 1 min of isoelectric EEG. Mild neuronal damage in the hippocampal CA1 subfield was seen in some animals after 2 min of isoelectric EEG. Severe and consistent neuronal loss in the hippocampal CA1 subfield was recognized after 3 min of isoelectric EEG. Additional damage was also seen in the dentate hilus and the thalamus in some animals. This model can be used to study the pathophysiology of postshock brain damage and to assess new therapies following shock.


2000 ◽  
Vol 28 (7) ◽  
pp. 2465-2474 ◽  
Author(s):  
Akira Takasu ◽  
S. William Stezoski ◽  
Jason Stezoski ◽  
Peter Safar ◽  
Samuel A. Tisherman

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