Improved Long-term Survival with Remote Limb Ischemic Preconditioning in a Rat Fixed-Pressure Hemorrhagic Shock Model

2019 ◽  
Vol 33 (2) ◽  
pp. 139-147 ◽  
Author(s):  
Wangde Dai ◽  
Jianru Shi ◽  
Juan Carreno ◽  
Sharon L. Hale ◽  
Robert A. Kloner
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 Blood was withdrawn to maintain mean arterial blood pressure at 30 mm Hg for 1 hour, followed by 30 minutes of resuscitation with shed blood.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 Results: During the shock phase, the total withdrawn blood volume (expressed as % of estimated total blood volume) to maintain a level of hypotension of 30 mm Hg was significantly higher in the isoflurane group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 ◽  
...  

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Wangde Dai ◽  
Jianru Shi ◽  
Juan Carreno ◽  
Sharon Hale ◽  
Robert A Kloner

Background: We further examined the protective effects of experimental bilateral lower limb remote ischemic preconditioning (RIPC) in rats undergoing experimental hemorrhagic shock. Methods: Sprague Dawley rats (both genders) were randomized into RIPC (n= 26) or control group (n= 27), and anesthetized with intraperitoneal ketamine/xylazine. RIPC was induced by 4 cycles of inflating small bilateral pressure cuffs to 200 mmHg around the femoral arteries for 5 minutes, followed by 5 minute deflation of the cuffs. Hemorrhagic shock was induced by withdrawing blood from the carotid artery. Target mean blood pressure of 30 mmHg was maintained for 30 minutes followed by reinfusion of shed blood within the next 30 min. Rats remained anesthetized for another 30 min before recovery; endpoints were survival at 72 hours and 6 weeks. Results: The % of estimated total blood volume withdrawn to maintain a level of 30 mmHg was similar in the RIPC group (41.7 ± 1.0 %) and control group (41.9 ± 1.0 %). Recovery of blood pressure during the early resuscitation phase was significantly improved in the RIPC group. The diastolic internal dimension of the left ventricle (echocardiogram), which indicates circulating intravascular blood volume, was significantly larger in the RIPC group at 1 hour after initiation of shed blood reinfusion (5.8 ± 0.1 mm) compared to 5.4 ± 0.1mm in the control group (p=0.04). Left ventricular fractional shortening was comparable between RIPC (50.9 ± 1.9 %) and control group (49.6 ± 1.8 %; p=0.64) at 1 hour after initiation of resuscitation. At 48 hours after shock, BUN was within normal range in the RIPC group (17.3 ± 1.2 mg/dl); but elevated in the control group (22.0 ± 1.7 mg/dl). At 72 hours after hemorrhagic shock injury, 6 of 27 (22.2 %) rats in the control group and 13 of 26 (50 %, p = 0.047) rats in the RIPC group survived. At 6 weeks, 5 of 27 (18.5 %) rats in the control group and 13 of 26 (50 %; p = 0.021) rats in the RIPC group survived. RIPC significantly increased survival rate at both 72 hours and 6 weeks. Conclusions: RIPC improved recovery of blood pressure and maintained more circulating intravascular blood volume in the early phase of resuscitation, improved BUN, and markedly and significantly improved short and long term survival in rats subjected to hemorrhagic shock.


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

Sign in / Sign up

Export Citation Format

Share Document