PMID- 19078915
OWN - NLM
STAT- MEDLINE
DCOM- 20101012
LR  - 20131121
IS  - 0392-9590 (Print)
IS  - 0392-9590 (Linking)
VI  - 27
IP  - 6
DP  - 2008 Dec
TI  - Effects of pentoxifylline and n-acetylcysteine on injuries caused by ischemia and 
      reperfusion of splanchnic organs in rats.
PG  - 512-21
AB  - AIM: Occlusion and reperfusion of splanchnic arteries cause local and systemic 
      changes due to the release of cytotoxic substances and the interaction between 
      neutrophils and endothelial cells. This study evaluated the role of 
      pentoxifylline (PTX) and n-acetylcysteine (NAC) in the reduction of ischemia, 
      reperfusion shock and associated intestinal injury. METHODS: Sixty rats were 
      divided into 6 groups of 10 animals. Rats in three groups underwent mesenteric 
      ischemia for 30 minutes followed by 120 minutes of reperfusion, and were treated 
      with saline (SAL-5 mL/kg/h), pentoxifylline (PTX-50 mg/kg) or n-acetylcysteine 
      (NAC-430 mg/kg/h). The other 3 groups underwent sham ischemia and reperfusion 
      (I/R) and received the same treatments. Hemodynamic, biochemical and histological 
      parameters were evaluated. RESULTS: No significant hemodynamic or intestinal 
      histological changes were seen in any sham group. No histological changes were 
      found in the lung or liver of animals in the different groups. There was a 
      progressive decrease in mean arterial blood pressure, from mean of 111.53 mmHg 
      (30 minutes of ischemia) to 44.30+/-19.91 mmHg in SAL-I/R, 34.52+/-17.22 mmHg in 
      PTX-I/R and 33.81+/-8.39 mmHg in NAC-I/R (P<0.05). In all I/R groups, there was a 
      progressive decrease in: aortic blood flow, from median baseline of 19.00 mL/min 
      to 2.50+/-5.25 mL/min in SAL-I/R; 2.95+/-6.40 mL/min in PTX-I/R and 3.35+/-3.40 
      mL/min in NAC-I/R (P<0.05); in the heart rate, from mean baseline of 311.74 bpm 
      to 233.33+/-83.88 bpm in SAL-I/R, 243.20+/-73.25 bpm in PTX-I/R and 
      244.92+/-76.05 bpm in NAC-I/R (P<0.05); and esophageal temperature, from mean 
      baseline of 33.68 degrees C to 30.53+/-2.05 degrees C in SAL-I/R, 30.69+/-2.21 
      degrees C in PTX-I/R and 31.43+/-1.03 degrees C in NAC-I/R (P<0.05). In the other 
      hand, there was an attenuation of mucosal damage in the small intestine of the 
      animals receiving PTX, and only in the ileum of the animals receiving NAC. No 
      changes were found in ileum or plasma malondialdehyde levels in any group. 
      CONCLUSIONS: PTX was more efficient in reducing histological lesions than NAC, 
      but neither treatment prevented hemodynamic changes during splanchnic organs I/R.
FAU - Cerqueira, N Freire
AU  - Cerqueira NF
AD  - Department of Veterinary Surgery and Anesthesiology, School of Veterinary and 
      Animal Science, Universidade Estadual Paulista, Sao Paulo, Brazil. 
      nereidef@zipmail.com.br
FAU - Hussni, C A
AU  - Hussni CA
FAU - Yoshida, W Bonetti
AU  - Yoshida WB
FAU - Sequeira, J Lopes
AU  - Sequeira JL
FAU - Padovani, C R
AU  - Padovani CR
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Italy
TA  - Int Angiol
JT  - International angiology : a journal of the International Union of Angiology
JID - 8402693
RN  - 0 (Free Radical Scavengers)
RN  - SD6QCT3TSU (Pentoxifylline)
RN  - WYQ7N0BPYC (Acetylcysteine)
SB  - IM
MH  - Acetylcysteine/*pharmacology
MH  - Animals
MH  - Disease Models, Animal
MH  - Free Radical Scavengers/*pharmacology
MH  - Hemodynamics/*drug effects
MH  - Intestinal Mucosa/drug effects/pathology
MH  - Intestine, Small/blood supply/*drug effects/metabolism/pathology
MH  - Male
MH  - Mesenteric Vascular Occlusion/*drug therapy/metabolism/pathology/physiopathology
MH  - Oxidative Stress/drug effects
MH  - Pentoxifylline/*pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - Reperfusion Injury/metabolism/pathology/physiopathology/*prevention & control
MH  - Severity of Illness Index
MH  - Shock/physiopathology/prevention & control
MH  - Splanchnic Circulation/*drug effects
MH  - Time Factors
EDAT- 2008/12/17 09:00
MHDA- 2010/10/13 06:00
CRDT- 2008/12/17 09:00
PHST- 2008/12/17 09:00 [entrez]
PHST- 2008/12/17 09:00 [pubmed]
PHST- 2010/10/13 06:00 [medline]
PST - ppublish
SO  - Int Angiol. 2008 Dec;27(6):512-21.