Reperfusion Injury In Rabbits Research Articles

Effect of the extract from salvia miltiorrhiza radix (SMR) on skeletal muscle ischemia and reperfusion injury in rabbits

The extract of salvia miltiorrhiza radix (SMR) is a well known Chinese herbal medicine known as danshen. It has been found in several experimental studies, published mostly in China, to have antiox...

Reduction of central nervous system reperfusion injury in rabbits using doxycycline treatment.

Activated leukocytes appear to potentiate central nervous system reperfusion injury, and agents that block leukocyte adhesion have shown neuroprotective efficacy in experimental models. Doxycycline, a tetracycline antibiotic, inhibits leukocyte function in vitro, presumably through divalent cation binding. We used a model of focal central nervous system reperfusion injury to determine the efficacy of doxycycline treatment in preserving neurological function. Rabbits randomly received 10 mg/kg i.v. doxycycline 30 minutes before ischemia (pretreatment group) or 45 minutes after ischemia (posttreatment group) or received phosphate-buffered saline vehicle (control group) followed by 10 mg/kg q 8 hours times two. The average length of reversible spinal cord ischemia required to produce paraplegia (P50) at 18 hours was calculated for each group. For the control group (n = 13), the P50 was 22.8 +/- 2.2 minutes; for the pretreatment group (n = 14), 35.5 +/- 2.4 minutes (P < .01; t = 3.8); and for the posttreatment group (n = 13), 31.4 +/- 4.2 minutes (not significant; t = 1.6). Doxycycline also attenuated postischemic decreases in vivo leukocyte counts and inhibited in vitro leukocyte adhesion. Therapeutic doxycycline levels at 24 hours were confirmed in the plasma and spinal cord. This significant protective effect suggests that doxycycline, a safe and readily available agent, may play a role in reducing clinical central nervous system reperfusion injury.

Prevention of lung reperfusion injury in rabbits by a monoclonal antibody against interleukin-8.

Re-establishing blood flow to ischaemic tissues causes greater injury than that induced during the ischaemic period. This type of tissue injury, reperfusion injury, is involved in frostbite, multiple organ failure after hypovolaemia and in myocardial infarction. Depletion of neutrophils alleviates reperfusion injury, implying a causal role of neutrophil infiltration. Among members of the recently discovered family of chemotactic cytokines (chemokines), interleukin-8 (IL-8) is a major neutrophil chemotactic and activating factor produced by various types of human cells. We investigated its pathophysiological role in a rabbit model of a lung reperfusion injury. Reperfusion of ischaemic lung caused neutrophil infiltration and destruction of pulmonary structure, as well as local production of IL-8. Furthermore, the administration of a neutralizing monoclonal antibody against IL-8 prevented neutrophil infiltration and tissue injury, proving a causal role of locally produced IL-8 in this model.

The effects of normovolemic hemodilution with dextran-40 on acute myocardial ischemia/reperfusion injury in rabbits.

The effects of decreasing blood viscosity by normovolemic hemodilution with dextran-40 or normal saline (NS) on myocardial lipid peroxides, superoxide dismutase, infarct size and left ventricular function during acute myocardial ischemia/reperfusion were studied in rabbits. It was found that normovolemic hemodilution with dextran-40 could decrease the content of ischemic myocardial malondialdehyde and preserve ischemic myocardial superoxide dismutase activity after 1 h of coronary occlusion followed by 1 h of reperfusion. However, after administration of NS only a tendency in this aspect exhibited without statistical significance. Besides, hemodilution with dextran-40 reduced infarct size and improved left ventricular systolic function after 1 h of ischemia followed by 23 h of reperfusion. These results suggest that normovolemic hemodilution with dextran-40 may have anti-injury effect on acute myocardial ischemia/reperfusion to a certain degree.

Leukocyte and Platelet Depletion Can Alleviate Reperfusion Injury in Rabbits

To investigate the effect of leukocyte and platelet depletion on reperfusion injury using a leukocyte-platelet removal filter (LRF), several cardiovascular variables were examined in the rabbits during ischemia followed by reperfusion. The rabbits underwent cytoapheresis with LRF (n=S) and were compared with controls without LRF (n=S). LRF was composed of a nonwoven polyester fabric (1.8,um, 4.6 gm). Removal of leukocytes and platelets by LRF was 98% for both. A period of 30 min equilibration was allowed before any experimental intervention, at which time the diagonal artery was occluded for 20 min and then reperfused. All arrhythmias were defined and quantified in accordance with the Lambeth Convention. Regional wall thickening was examined by a pulsed Doppler dimension system. No significant differences were observed in hemodynamic variables between the two groups; however, rabbits treated with a LRF demonstrated greater regional wall thickening (LRF group: 17.0 ± 0.9%, control group: 11.0 ± 0.3%, p &lt; 0.01), as well as significant improvement in the frequency of ventricular arrhythmias (LRF group: 12.5%, control group: 47.2%, p &lt; 0.01). The data suggest that LRF may help prevent arrhythmias and preserve left ventricular contraction during and after intracoronary thrombolysis.

31P NMR Evaluation of in Vivo Renal Ischemia and Reperfusion Injury in Rabbits and Dogs

³¹P NMR Evaluation of in Vivo Renal Ischemia and Reperfusion Injury in Rabbits and Dogs