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Results for “Reperfusion”

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PubMed1984

Role of beta-adrenoreceptor antagonism in the prevention of reperfusion ventricular arrhythmias: effects of acebutolol, atenolol, and d-propranolol on isolated working rat hearts subject to myocardial ischemia and reperfusion.

The role of catecholamines in the genesis of ventricular arrhythmias during the reperfusion period following coronary occlusion remains incompletely understood. An isolated rat heart preparation, free from the influence of autonomic innervation or of circulating catecholamines, was used to assess the effects of beta-adrenoceptor blockade. The hearts were prelabeled with tritiated norepinephrine ( NE3H ), and the total radioactivity and that in NE3H were measured in the effluent coronary flow. The left main coronary artery was ligated for 10 minutes after which reperfusion followed. The liberation of NE3H and the development of ventricular tachycardia and fibrillation were monitored throughout. The cardioselective beta-antagonist agent, acebutolol, in a high concentration (1.1 X 10(-4)M), had good beta-antagonist effect in response to the added isoproterenol (10(-6)M); this concentration of acebutolol also suppressed sustained reperfusion ventricular arrhythmias but unexpectedly increased the release of NE3H . Atenolol, another cardioselective agent, did not prevent reperfusion ventricular arrhythmias even in a high concentration of 40 mg/L (1.5 X 10(-4)M). The d-isomer of propranolol, with poorer beta-antagonist properties than the l-isomer, prevented such ventricular arrhythmias in a concentration of 1.3 X 10(-5)M, which was low when compared to that of atenolol. It is proposed that the beta-antagonist activity of the compounds tested could not explain the inhibition of reperfusion ventricular arrhythmias and that another quality such as membrane-stabilizing activity may be involved.

Acebutolol↗

PubMed2005

Ischemic preconditioning decreases the reperfusion-related formation of hydroxyl radicals in a rabbit model of regional myocardial ischemia and reperfusion: the role of K(ATP) channels.

The objective of this study was to assess the effects of ischemic preconditioning (IP) on hydroxyl free radical production in an in vivo rabbit model of regional ischemia and reperfusion. Another goal was to determine whether K(ATP) channels are involved in these effects. The hearts of anesthetized and mechanically ventilated New Zealand White rabbits were exposed through a left thoracotomy. After i.v. salicylate (100 mg/kg) administration, all animals underwent a 30-min stabilization period followed by 40 min of regional ischemia and 2 h of reperfusion. In the IP group, IP was elicited by 5 min of ischemia followed by 10 min of reperfusion (prior to the 40-min ischemia period). Glibenclamide, a K(ATP) channel blocker, was administered prior to the preconditioning stimulus. Infarct size was measured by 2,3,5-triphenyl tetrazolium chloride (TTC) staining. We quantified the hydroxyl-mediated conversion of salicylate to its 2,3 and 2,5-dihydroxybenzoate derivatives during reperfusion by high performance liquid chromatography coupled with electro-chemical detection.IP was evidenced by reduced infarct size compared to control animals: 22% vs. 58%, respectively. Glibenclamide inhibited this cardioprotective effect and infarct size was 53%. IP limited the increase in 2,3 and 2,5-dihydroxybenzoic acid to 24.3 and 23.8% above baseline, respectively. Glibenclamide abrogated this effect and the increase in 2,3 and 2,5-dihydroxybenzoic acid was 94.3 and 85% above baseline levels, respectively, similar to the increase in the control group. We demonstrated that IP decreased the formation of hydroxyl radicals during reperfusion. The fact that glibenclamide inhibited this effect, indicates that K(ATP) channels play a key role in this cardioprotective effect of IP.

Adenosine Triphosphate↗

PubMed1987

Diminution of "reperfusion injury" in reperfused ischemic myocardium by phenothiazines. A quantitative morphological study.

The effect of pretreatment by phenothiazines--Chlorpromazine (CPR) /Spofa/ and Trifluoperazine (TFP) /Smith Kline and French/ on reperfusion injury of ischemic myocardium were studied. Reperfusion of ischemic myocardium following an ischemic period exceeding 40 min resulted in morphological, physiological and biochemical changes identical with those induced by enhanced cytosolic Ca2+ concentration. Left descending coronary ligation was performed on 70 dogs divided into four group. Group I: permanent occlusion (5 dogs--60 min, 5 dogs--120 min, 5 dogs--180 min); group II: 15 dogs (60 min occlusion + 120 min reperfusion); group III: 20 dogs (60 min occlusion, 15 mg CPR, reperfusion 120 min); group IV: 20 dogs (60 min occlusion, 2 mg TFP + 120 min reperfusion). CPR or TFP were administered 30 min after the ligation. The effect of drugs was quantified on tetrazolium stained gross sections and studied from physiological, biochemical and ultrastructural points of view. Treatment of animals with phenothiazines, known as calmodulin inhibitors, considerably improved the ultrastructure of myocytes in area at risk, and allowed for the recovery of at least 60 per cent of injured myocytes after reflow restoration. Ultrastructural findings tightly correlate with physiological and biochemical results.

Adenine Nucleotides↗

PubMed1995

Myocardial recovery during post-ischemic reperfusion: optimal concentrations of Na+ and Ca2+ in the reperfusate and protective effects of amiloride added to cardioplegic solution.

The effects of Na+ and Ca2+ concentrations in the reperfusate on post-ischemic myocardial recovery were examined. Also, the myocardial protective effects of amiloride, an inhibitor of the Na+/Ca2+ and Na+/H+ exchange systems, added to cardioplegic solutions were assessed, using an isolated working rat heart perfusion system. Global myocardial ischemia was induced by 30-min normothermic cardioplegic arrest, using St. Thomas' solution. The concentration of Na+ in the reperfusate varied, stepwise, from 75 to 145 mM/l, and that of Ca2+, from 0.1 to 2.5 mM/l. In this study post-ischemic functional recovery was best at 110mM/l Na+ and 1.2-1.8 mM/l Ca2+ in the reperfusate. A significantly greater post-ischemic functional recovery and a lower creatine kinase release were observed when amiloride was added to the cardioplegic solution. Ca2+ overload via Na+/Ca2+ and Na+/H+ exchange systems would, thus, appear to be due, at least in part, to post-ischemic reperfusion injury.

Amiloride↗

PubMed1991

Reperfusion injury in dog hearts with permanent occlusion of a coronary artery, probably due to reperfusion via collateral vessels.

To clarify whether or not reperfusion injury occurs in the permanent occlusion of a coronary artery, we analyzed quantitatively contraction band necrosis as an indicator of early recanalization, coagulation necrosis, infarct size and measured regional blood flow in dog hearts with collateral circulation. Fifty mongrel dogs were divided into four groups: 15 dogs with a 24-hour occlusion of the left anterior descending coronary artery just distal to the first diagonal branch (permanent occlusion group): 15 dogs a with 3-hour occlusion followed by 24-hour recanalization (recanalization group); 10 dogs with a 2-hour occlusion without recanalization (transient occlusion group); 10 dogs with a 4-hour occlusion without recanalization (transient occlusion group). The regional blood flow in the subepicardium and subendocardium determined by the generated hydrogen gas clearance method was greatly decreased 30 minutes after occlusion (14 + 8%/12 +/- 9%) and was relatively restored from 180 minutes (31 +/- 21%/21 +/- 14%) to 24 hours later (41 + 19%/26 + 16%) in spite of complete occlusion of the coronary artery. The percentage infarct area in the risk area was significantly greater in the permanent occlusion group (60 +/- 26%) than in the recanalization group (35 +/- 31%). Although most of the infarct was occupied by contraction band necrosis in the recanalization group (86 +/- 12%), contraction band necrosis was diffusely seen even in the permanent occlusion group (54 +/- 27%). In both the permanent and recanalization groups, contraction band necrosis was the main histological feature of small infarcts occupying less than 30% of the risk area, while coagulation necrosis was the main feature in very large infarcts occupying more than 80% of the risk area. In the occlusion groups without recanalization, the percentage area of contraction band necrosis in the risk area was 6 +/- 8% after the 2-hour occlusion, 23 +/- 17% after the 4-hour occlusion and 31 +/- 21% after permanent occlusion; the difference between the 4-hour and permanent occlusion groups was not significant. In the permanent occlusion group, the percentage infarct area in the risk area was inversely correlated with regional blood flow during occlusion, an indicator of collateral flow. It was concluded that reperfusion injury occurs even in hearts without recanalization. The pathogenesis may involve reperfusion in the risk area via collateral circulation. Protection against reperfusion injury is important to minimize the infarct size even in hearts with permanent occlusion, although the presence of collateral flow is an important factor in limiting infarct size.

Animals↗

PubMed1995

Ischemia-reperfusion injury of the spinal cord: the influence of normovolemic hemodilution and gradual reperfusion.

Recent studies have suggested that oxygen-derived free radicals play an important role in ischemia-reperfusion injury of the spinal cord. In other organ systems, reperfusion injury has been reduced by limiting the availability of oxygen in the reperfusion phase. The purpose of this study was to test the effect of normovolemic hemodilution and gradual reperfusion on spinal cord function after aortic cross-clamping in 84 New Zealand White rabbits. All animals underwent 21 min of infrarenal aortic cross-clamping in the conscious state by means of a previously placed aortic occlusion device and were randomized to four groups. Group 1 animals were hemodiluted to a mean (s.e.m.) hematocrit of 28(2)% by extracting 25% of the effective blood volume and reinfusing the plasma component after centrifugation concurrently with a volume of normal saline three times that of the discarded red cells. Group 2 animals (controls) were bled similarly but both plasma and red cells were reinfused, resulting in a mean (s.e.m.) hematocrit of 38(2)%. In the next two groups, distal aortic flow was recorded via an implantable Doppler device. After cross-clamping, flow was returned gradually over 45 min in animals of group 3, and abruptly in group 4. Animals were observed for 5 days and neurologic function was graded by an independent observer. Paraplegia at 5 h after clamping occurred in 75% of animals in group 1 versus 32% in group 2 (P < 0.05), and in 33% of group 3 versus 28% in group 4 (not significant). Of those animals showing initial neurologic recovery, delayed-onset paraplegia was seen in 100% in group 1 versus 87% in group 4 (not significant), and in 50% of group 3 versus 92% of group 4 (P < 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Ischemia, reperfusion, and reperfusion injury: role of oxygen free radicals and oxygen free radical scavengers.

Pathologic cellular changes that begin with ischemia may be worsened when an occluded artery is recannulized. Thrombolytic agents--the standard treatment in acute MI--may contribute to these cellular events, collectively termed "reperfusion injury." Highly toxic chemical moieties called oxygen free radicals participate in the injury process. This article discusses the concepts of ischemia, reperfusion, and reperfusion injury and explains the role played by oxygen free radicals in the generation of reperfusion injury. Also described is the use of oxygen free radical scavengers to prevent this injury.

Free Radicals↗

PubMedDate not supplied

Reperfusion strategy after regional ischaemia: comparative study of reperfusion conditions and compositions.

We investigated the effects of pressure, temperature and additives on aortic root reperfusion success. Cardiopulmonary bypass and heart arrest were initiated in mongrel dogs and sudden uncontrolled normothermic (group 1), pressure controlled substrate enriched normothermic (group 2a), pressure controlled unmodified normothermic (group 2b) and pressure controlled unmodified tepid (group 3) reperfusion compared. In group 1, the first cardiac rhythm was ventricular fibrillation, but dogs in the other groups showed spontaneous sinus rhythm. Recovery times were significantly longer and cardiac output levels significantly decreased in group 1 compared with the other groups. Prolonged lactate production and oxygen uptake failure were observed in group 1 compared with the other groups; oxidative stress markers and microscopic studies confirmed significant tissue injury in group 1. All parameters were similar between groups 2a, 2b and 3, indicating that low reperfusion pressure in the first 2 min is the most effective component of reperfusion.

Animals↗

PubMed2006

Thrombus aspiration before primary angioplasty improves myocardial reperfusion in acute myocardial infarction: the DEAR-MI (Dethrombosis to Enhance Acute Reperfusion in Myocardial Infarction) study.

OBJECTIVES: This study sought to test the hypothesis that thrombus removal, with a new manual thrombus-aspirating device, before primary percutaneous coronary intervention (PPCI) may improve myocardial reperfusion compared with standard PPCI in patients with ST-segment elevation acute myocardial infarction (STEMI). BACKGROUND: In STEMI patients, PPCI may cause thrombus dislodgment and impaired microcirculatory reperfusion. Controversial results have been reported with different systems of distal protection or thrombus removal. METHODS: One-hundred forty-eight consecutive STEMI patients, admitted within 12 h of symptom onset and scheduled for PPCI, were randomly assigned to PPCI (group 1) or manual thrombus aspiration before standard PPCI (group 2). Patients with cardiogenic shock, previous infarction, or thrombolytic therapy were excluded. Primary end points were complete (>70%) ST-segment resolution (STR) and myocardial blush grade (MBG) 3. RESULTS: Baseline clinical and angiographic characteristics were similar in the 2 groups. Comparing groups 1 and 2: complete STR 50% versus 68% (p < 0.05); MBG-3 44% versus 88% (p < 0.0001); coronary Thrombolysis In Myocardial Infarction (TIMI) flow grade 3 78% versus 89% (p = NS); corrected TIMI frame count 21.5 +/- 12 versus 17.3 +/- 6 (p < 0.01); no reflow 15% versus 3% (p < 0.05); angiographic embolization 19% versus 5% (p < 0.05); direct stenting 24% versus 70% (p < 0.0001); and peak creatine kinase-mass band fraction 910 +/- 128 mug/l versus 790 +/- 132 mug/l (p < 0001). In-hospital clinical events were similar in the 2 groups. After adjusting for confounding factors, multivariate analysis showed thrombus aspiration to be an independent predictor of complete STR and MBG-3. CONCLUSIONS: Manual thrombus aspiration before PPCI leads to better myocardial reperfusion and is associated with lower creatine kinase mass band fraction release, lower risk of distal embolization, and no reflow compared with standard PPCI. (Thrombus Aspiration Before Standard Primary Angioplasty Improves Myocardial Reperfusion in Acute Myocardial Infarction; http://clinicaltrials.gov/ct/show/NCT00257153).

Angioplasty, Balloon, Coronary↗

PubMed1999

Reperfusion injury revisited: is there a role for growth factor signaling in limiting lethal reperfusion injury?

Myocardial reperfusion injury represents an important therapeutic target. The ability of several peptide growth factors, including transforming growth factor-beta1, insulin, insulin-like growth factor-1, cardiotrophin-1 and fibroblast growth factors, to modify reperfusion injury has been examined in recent studies. The protective effects of these agents may be related to the inhibition of apoptosis, especially during reperfusion, probably through p42/p44 MAP kinase and PI3-kinase/Akt signaling. Growth factor signaling may therefore represent a novel approach for the development of pharmacological strategies that attenuate reperfusion injury in the heart.

Animals↗

PubMed2003

Propofol decreases reperfusion-induced arrhythmias in a model of "border zone" between normal and ischemic-reperfused guinea pig myocardium.

UNLABELLED: We examined the effect of propofol on the main mechanisms involved in ischemia/reperfusion-induced arrhythmias (i.e., spontaneous arrhythmias, conduction blocks, and dispersion of repolarization) in vitro. In a double-chamber bath, guinea pig right ventricular muscle strips were subjected to 30 min of simulated ischemia followed by 30 min of reperfusion (altered zone; AZ) and to standard conditions (normal zone; NZ). Action potential (AP) parameters were recorded in the NZ and AZ. We studied the effects of Intralipid(R) and of propofol at 10(-6), 10(-5), and 2 x 10(-5) M on the occurrence of spontaneous sustained arrhythmias, conduction blocks, and the dispersion of repolarization. In NZ, Intralipid and propofol did not significantly modify the AP parameters. Propofol, but not Intralipid, lessened the ischemia-induced decrease in AP duration (APD) at 90% of repolarization (APD(90)) and attenuated the APD dispersion around the "border zone." Propofol did not modify the occurrence of ischemia-induced arrhythmias. Propofol 10(-6) M, but not Intralipid or propofol at 10(-5) and 2 x 10(-5) M, decreased the occurrence of ischemia-induced conduction blocks. Propofol decreased the occurrence of reperfusion-induced spontaneous sustained arrhythmias. We conclude that, in vitro, propofol attenuated the ischemia-induced APD(90) dispersion around the "border zone" and decreased the occurrence of spontaneous arrhythmias related to myocardial reperfusion injury. IMPLICATIONS: In isolated guinea pig ventricular myocardium propofol, but not Intralipid(R), attenuated the ischemia-induced shortening of action potential and, thus, the dispersion of repolarization and decreased the occurrence of spontaneous ventricular arrhythmia related to reperfusion injury. This result may be important for propofol-based anesthesia in patients at high risk for intraoperative ischemia.

Action Potentials↗

PubMed2000

["Reperfusion collapse" phenomenon during post-ischemic reperfusion in experiment].

Postischemic changes of central and regional hemodynamic while various reperfusion regimens have been studied on animal experimental model. We had revealed that despite vasodilatation, peripheral vascular resistance in the postischemic extremity rises, as a result of reperfusion by the lowered perfusion volume. Such phenomenon has been named as "reperfusion-collapse". In spite of the microcirculation disorders progression there have been no significant rising of the peripheral vascular resistance as well as worsening of the regional hemodynamic indexes in the postischemic limb during reperfusion by either normal or increased perfusion volume.

Acute Disease↗

PubMed1991

Effects of lidocaine on reperfusion arrhythmias and electrophysiological properties in an isolated ventricular muscle model of ischemia and reperfusion.

Transmembrane electrical activity was recorded from endo- and epicardium of isolated segments of guinea pig right ventricles with standard microelectrode techniques. An ECG was also recorded by two electrodes placed at opposite ends of the tissue bath. Regular stimulation was delivered to the endocardium. Tissues were exposed to simulated ischemia for 15 min and then were reperfused with "normal" Tyrode's solution. Rapid sustained or nonsustained ventricular tachycardia, bigeminy or trigeminy with characteristics of transmural reentry occurred in early reperfusion in 14 of 20 hearts (70%). Arrhythmias were accompanied by prolongation of transmural conduction time and abbreviation of endocardial effective refractory period. With lidocaine, at 1, 5, 10 and 50 microM, reperfusion arrhythmias occurred in 53.3, 22.2, 20.8 and 14.3% of hearts, respectively. The decreased incidence of arrhythmias was statistically significant for 5 to 50 microM lidocaine (P less than .01). The antiarrhythmic effect did not correlate with changes in transmural conduction time, endocardial effective refractory period, or endocardial excitability. However, antiarrhythmic concentrations of lidocaine selectively depressed epicardial excitability and significantly increased endo- to epicardial conduction block during late ischemic and early reperfusion periods. Epicardial inexcitability extended to late diastole and conduction block was not restricted to premature beats. Thus, in transmural reentry in which the epicardium is an essential component of the circuit, lidocaine may interrupt the circuit by selectively rendering this component inexcitable.

Action Potentials↗

PubMed1993

Effects of extracellular magnesium manipulation on reperfusion-induced arrhythmias and myocardial ion shifts in isolated ischemic reperfused rat hearts.

Isolated rat hearts were subjected to global ischemia followed by reperfusion, and a reduction in the incidence of reperfusion-induced ventricular fibrillation and ventricular tachycardia was brought about by increasing the extracellular Mg concentration in the perfusion buffer. Thus the incidence of ventricular fibrillation was reduced from its control value of 100% in 1.2 mM Mg to 83% by 2.4 mM Mg (P = N.S.), to 42% by 3.6 mM Mg (P < .05), to 17% by 4.8 mM Mg (P < .001) and to 17% by 9.6 mM Mg (P < .001). The corresponding values for ventricular tachycardia were 100% (control, 1.2 mM Mg) vs. 92% (P = N.S.), 50% (P < .05), 25% (P < .01) and 25% (P < .01), respectively. In further studies, extracellular Ca was reduced by 50% (1.2 mM) in the perfusion buffer just before ischemia and during reperfusion. The incidence of ventricular fibrillation was reduced from its control value of 83% in 1.2 mM Mg to 75% by 1.8 mM Mg (P = N.S.), to 33% by 2.4 mM Mg (P < .05), to 17% by 3.6 mM Mg (P < .01) and to 8% by 4.8 mM Mg (P < .01). The incidence of ventricular tachycardia followed the same pattern. Myocardial Na, K, Ca and Mg were measured by atomic absorption spectrophotometer after the removal of ions from the extracellular space. In controls, 30 min of ischemia resulted in 3- and 4-fold accumulation of myocardial Na and Ca, respectively, and during reperfusion these values were similar to the values for 30-min ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Leukocyte-depleted reperfusion of transplanted human hearts prevents ultrastructural evidence of reperfusion injury.

The present study examines whether leukocyte depletion can prevent postreperfusion ultrastructural injury in transplanted human hearts. Thirty-two patients undergoing orthotopic cardiac transplantation were randomized to receive either enriched, warm, whole blood (Group I; n = 16) or enriched, warm, leukocyte-depleted blood (Group II; n = 16) reperfusion. Donor hearts were arrested with 1 liter of 4 degrees C crystalloid cardioplegia and topically cooled. RV endomyocardial biopsies taken at end-ischemia and following reperfusion were assessed in a blinded fashion and graded according to injury (1 = minimal to 4 = severe). The mean ischemic time (Group I = 142 min, Group II = 153 min) was similar in the two groups. End-ischemic biopsies showed mild-moderate interstitial edema and mild capillary endothelial swelling in both groups with similar injury scores (Group 1 = 1.3 +/- 0.09 (means +/- SEM), Group 2 = 1.25 +/- 0.08). Postreperfusion biopsies in Group I showed nuclear chromatin clumping, moderate mitochondrial swelling, marked capillary endothelial swelling, and marked interstitial edema with a grade of 2.6 +/- 0.14 (P less than 0.001, paired t test). In contrast, postreperfusion biopsies in Group II showed minimal changes with a grade of 1.33 +/- 0.09, P less than 0.0001 in comparison to Group I Leukocyte-depleted reperfusion of human transplanted hearts prevents ultrastructural injury. This may allow safe extension of the ischemic period and result in improved graft function.

Biopsy↗

PubMed1990

Current research views on myocardial reperfusion and reperfusion injury.

This article discusses the types of reperfusion injury, some of the causes of the injury and the possible role of the radical scavengers in protecting against it. The methodological problems that have plagued this field are explored and some answers put forward, although we are sure that further questions will have been raised. There are now reasons to question the use of the tetrazolium staining procedure which has become the "gold standard" for measurements of infarct size. It seems likely that it is adequate only as a screening procedure, and even then will be associated with a troublesome number of false positives. Collateral flow is an important determinant of infarct size and simultaneous measurements of collateral flow are essential in the interpretation of the effects of drugs on infarct size. The limitations of the various animal models are important when relating experimental findings to the clinical condition. After a decade of research, reperfusion injury is itself still under question, and there remains confusion as to the role that oxygen-derived free radicals may play in the ischemic/reperfused myocardium. However, we believe that, from the experimental data available, oxygen derived free radicals are involved in the overall pathophysiology of ischemia and reperfusion, although the full extent remains to be clarified and the therapeutic implications explored.

Animals↗

PubMed1989

Prevention of reperfusion injury in ischemic-reperfused hearts by oxypurinol and allopurinol.

We investigated the effects of the xanthine oxidase inhibitor allopurinol and its metabolite oxypurinol on isolated rabbit hearts. To assess the potential role of these drugs in preventing reperfusion injury, hearts were perfused using Langendorff techniques, held globally ischemic for 3 h at 15 degrees C, and then reperfused. During perfusion, hearts received Krebs-Henseleit solution maintained at 37 degrees C. Aortic perfusion pressure was held constant at 80 cm H2O. Prior to ischemia, hearts were arrested with a constant volume of KCl cardioplegia. Using a left ventricular (LV) balloon, developed pressures were measured prior to and following global ischemia. In addition, coronary circulation (CC) was measured before and after ischemia. All hearts were paced at 260 beats/min. We studied four groups: group 1 received 1 mM allopurinol, group 2 received 1 mM oxypurinol, group 3 received 90 IU/ml superoxide dismutase (SOD) plus 8085 IU/ml catalase (CAT), and group 4 received no treatment and served as a control. Each group consisted of 8 animals. Hearts receiving drug treatment did so during the first 5 min of reperfusion. Displaying all data as a function of LV volume, postischemic values were compared to preischemic values. Multivariate analysis and Tukey tests were used to detect significant differences between groups. When compared to the control group, all drug-treated groups significantly recovered end-diastolic function. Peak systolic pressure decreased significantly in the SOD/CAT group as compared to all other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Allopurinol↗

PubMed1993

Changes of the Cu and Zn contents in lung and liver in intestinal ischemic reperfusion and general ischemic reperfusion in rabbits.

The changes of pulmonary and liver Cu-Zn contents were determined and evaluated in intestinal ischemic reperfusion (IIR) and general ischemic reperfusion (GIR) of rabbits. The contents of pulmonary Zn and liver Cu were found to be lower, and Cu/Zn ratio increased in lung tissue and decreased in liver tissue in IIR. The contents of pulmonary Zn were increased, and the contents of liver Cu were decreased; Cu/Zn ratio also decreased in both tissues in GIR. Pulmonary Cu and liver Zn contents were not changed in IIR and GIR. These results showed that lower or higher Zn in lung tissue and lower Cu in liver tissue were related to the acute tissue injury during IIR and GIR, suggesting that regulating the state of pulmonary Zn and liver Cu should be attempted during the prevention and treatment of both ischemic reperfusions.

Animals↗