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Results for “Reperfusion”

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PubMed1996

Heart rate variability during the first 24 hours of successfully reperfused acute myocardial infarction: paradoxic decrease after reperfusion.

Heart rate variability (HRV) was evaluated during the first 24 hours of hospitalization in 36 patients with acute myocardial infarction. Reperfusion was achieved by 60 minutes in 21 patients (group M1) and by 130 minutes in the remaining 15 (group M2). Mean 24-hour HRV measures were not significantly different between groups M1 and M2. Hourly spectral analysis revealed a decrease in total power (0.01 to 1.0 Hz) from 0 to 8 hours to 9 to 16 and 17 to 24 hours in groups M1 (7.04 +/- 0.27 to 6.94 +/- 0.28 and 6.52 +/- 0.18; p = 0.0006) and in group M2 (6.88 +/- 0.30 to 6.57 +/- 0.23 and 6.40 +/- 0.15; p = 0.002). Total power decreased immediately after reperfusion: in group M1 it decreased during the second hour (7.32 +/- 0.96 to 6.42 +/- 1.2; p = 0.001) and in group M2 during the third (7.47 +/- 1.2 to 6.73 +/- 1.4; p = 0.049) and fourth hours (7.47 +/- 1.2 to 6.48 +/- 1.4; p = 0.029). Mean change in total power in the second hour was -11.6% in group M1 and +3.9% in group M2 (p = 0.0001) and in the third hour, +14.5% in group M1 and -8.6% in group M2 (p = 0.006). During the remaining 21 hours, there was no significant difference in hourly change in total power between groups. Similar changes were noted in high-frequency power, but the ratio of low-frequency to high-frequency power was unchanged. In acute myocardial infarction, HRV is higher during the early phase and decreases as hours progress. Reperfusion causes an immediate, transient, and seemingly paradoxic decrease in HRV, probably because of an abrupt decrease in parasympathetic tone.

Anistreplase↗

PubMed2004

Protective role of melatonin given either before ischemia or prior to reperfusion on intestinal ischemia-reperfusion damage.

Tissue injury resulting from ischemia-reperfusion is of fundamental importance. Experimental evidence suggests that the generation of reactive oxygen species is significantly responsible for this type of injury. In the present study, besides investigating the protective role of melatonin on tissue damage caused by intestinal ischemia-reperfusion, the protective activity of this compound was also analyzed in both pre- and post ischemia melatonin-treated rats. The activities of the main antioxidative enzymes, catalase, superoxide dismutase and glutathione peroxidase in the intestine showed significant (P < 0.05) increases in melatonin-treated animals that were subjected to ischemia/reperfusion compared with those subjected only to ischemia/reperfusion. Also, results clearly indicate that the level of malondialdeyhde, an index of lipid peroxidation, decreased significantly (P < 0.05) when rats subjected to intestinal/reperfusion were given melatonin either before ischemia or before reperfusion.

Animals↗

PubMed1989

Arachidonic acid metabolism and cerebral blood flow in the normal, ischemic, and reperfused gerbil brain. Inhibition of ischemia-reperfusion-induced cerebral injury by a platelet-activating factor antagonist (BN 52021).

Cerebral ischemia and ischemia-reperfusion induced cerebral injury results in the accumulation of free fatty acids and diacylglycerols as a result of increased activity of phospholipases A and C. We have evaluated the incorporation of 14C arachidonic acid into the whole brain and synaptoneurosomes, the effect of cerebral ischemia on 14C incorporation, and the effect of a PAF antagonist (BN 52021) on cerebral blood flow, free fatty acids, diacylglycerols, and polyphosphoinositides. Peak incorporation of 14C arachidonic acid into the whole brain and synaptoneurosomal fractions occurred 30 minutes following intraventricular injection. Peak incorporation into cerebellar synaptoneurosomal fractions was at 60 minutes following intraventricular injection. Turnover in phospholipid pools was similar in the whole brain and synaptoneurosomes (PI greater than PC greater than PE). Considering phosphatidylinositol content in the gerbil brain, the specific activity of 14C arachidonic acid was 22 times greater in PI than PC. Five minutes of bilateral carotid artery ligation resulted in decreased phosphatidylinositol and polyphosphoinositols. Bilateral carotid artery ligation resulted in systemic arterial hypertension, complete forebrain ischemia (CBF less than 7 ml/100 gm/min) and a 20% to 50% reduction in midbrain CBF. Reperfusion resulted in cerebral reactive hyperemia and systemic hypotension. BN 52021 inhibited the maturation of ischemia-reperfusion induced cerebral injury. Cerebral blood flow was improved. Free fatty acids were decreased, suggesting inhibition of phospholipase A activity. Decreased DAG pools with increased PIP2 pools suggest a possible coinhibition of phospholipase C.

Animals↗

PubMed1999

[Effects of reperfusion on neuronal changes and macrophagic response after transient focal ischemia--reperfusion of brain in rats].

Male SD rats(n = 29) were subjected to 2 hours' middle cerebral artery occlusion and were killed at various times of reperfusion (0.5-48 hours). The histological features of neuronal changes, the macrophagic response and the relationship between them were investigated. The neurons underwent acute changes(shrinking or swollen), and the pyknotic apoptotic neurons were occasionally seen within 3 hours. The number of apoptotic neurons increased with recirculation time. The scattered red neurons and ghost cells were first found at 6 hours of reperfusion. Many apoptotic neurons, apoptotic bodies were detected in the penumbra of ischemic core at 48 hours. Lectin histochemistry with GSI-B4 was performed to observe the macrophage. The results showed the active microglia and macrophage from meninges presented at 12 hours. The macrophages from parenchyma vessels appeared at 24 hours. Reactive microglia and extrinsic macrophage aggregated into the band of macrophage which phagocytized the apoptotic neurons. The results indicate that, firstly, it is important to prevent the neuronal apoptosis and reduce the volume of infarct in stroke patients; secondly, irreversible neuronal lesions simultaneously stimulate microglial activation and the presence of extrinsic macrophages from meninges was earlier than the appearance of the macrophages from parenchyma blood-monocytes. The authors also suggest that the data on the neuronal changes over time after ischemia and reperfusion be useful reference materials for selecting the most timely medication to treat cerebral infarction.

Animals↗

PubMed1998

[Effect of Daflon 500 mg on reperfusion damage following ischemia and reperfusion of striated muscle].

The results of the current study indicate that Daflon 500 mg effectively reduces permeability for macromolecules induced by ischemia-reperfusion, thus reducing postischemic edema formation in the early reperfusion period. The inhibitory effect of Daflon 500 mg on leukocyte emigration may account for the reduction of edema formation in the postischemic tissue and favor the therapeutic use Daflon 500 mg of reperfusion-injury.

Animals↗

PubMedDate not supplied

The effect of prophylactic melatonin administration on reperfusion damage in experimental testis ischemia-reperfusion.

AIM: Torsion of testis, which is a urologic emergency case, is generally treated by surgical detorsion procedure. However, the resulting reperfusion and both ipsilateral and contralateral testis damage caused thereby are important problems. This study aims at investigating the administration of prophylactic melatonin in order to reduce free radical damage that is caused due to reperfusion after experimental testis torsion-detorsion procedure. MATERIAL AND METHOD: The rats used in the study were allocated to four groups, each containing 10 rats. Rats in Group I had six hours of torsion (ischemia) followed by orchiectomy. Rats in Group II had six hours of torsion, then received melatonin (10 mg/kg/IM) and after that had detorsion (reperfusion). Rats in Group III had detorsion after six hours of torsion and serum physiologic administration (the same volume as melatonin). Torsion and/or detorsion procedures were not applied in Group IV (control). Ipsilateral, contralateral testis and plasma Malondialdehyde (MDA) levels were determined in all groups. RESULTS: Tissue and plasma MDA levels in the group which had detorsion were found to be significantly higher than those in the group that had orchiectomy only (p<0.02). Ipsilateral and contralateral testis MDA levels were identified to be significantly lower in the group receiving prophylactic melatonin in comparison to the group receiving serum physiologic (p<0.02). Plasma and contralateral MDA levels correlated positively with MDA levels identified in ipsilateral testis in all groups (rs=+0.89, n=40, p=0.000). CONCLUSION: In cases where testis torsion is identified, administration of melatonin just before torsion may reduce local and systemic free radical damage.

Animals↗

PubMed1987

Effects of nicainoprol on reperfusion arrhythmia in the isolated working rat heart and on ischemia and reperfusion arrhythmia and myocardial infarct size in the anesthetized rat.

The effect of the novel antiarrhythmic agent nicainoprol on coronary occlusion and reperfusion arrhythmia was investigated in isolated working rat hearts and in anesthetized rats. In isolated working rat hearts nicainoprol (10(-6) M, 5 X 10(-6) M and 10(-5) M) induced concentration-related protection against reperfusion arrhythmia without changing the cardiodynamics, with the exception of a decrease in heart rate at the highest concentration. Enzyme levels (lactate dehydrogenase and creatine kinase) in the coronary venous effluent, and cardiac tissue concentrations of glycogen, lactate, ATP and creatine phosphate were not affected by nicainoprol. Given to anesthetized rats, nicainoprol (5 and 10 mg/kg i.v.) reduced dose dependently in the early post occlusion (0-30 min) period, the percentage of animals with premature ventricular complexes (PVCs) and ventricular tachycardia while completely preventing the occurrence of ventricular fibrillation. In the reperfusion period no animal treated with 5 mg/kg and 12% of the rats treated with 10 mg/kg showed PVCs (the only form of arrhythmia observed in this period) versus 60% of the control rats. Both doses of nicainoprol induced a decrease in heart rate, blood pressure and myocardial oxygen consumption. The ratio of infarct mass to ventricular mass was significantly reduced by 20% at a dose of 5 mg/kg and by 28% at the dose of 10 mg/kg. Nicainoprol could be useful in the prevention and treatment of arrhythmias associated with acute myocardial infarction.

Anesthesia↗

PubMed1985

Reperfusion injury induced by augumented oxygen uptake in the initial reperfusion period. Possible efficacy of extreme hemodilution.

This study was designed to investigate the relationship between myocardial oxygen consumption and oxygen-induced myocardial injury. Dog hearts were exposed to 40 min normothermic ischemia and then reperfused for 10 min with three oxygenated perfusates containing different hemoglobin concentrations and with moderate hemodilution. The experimental groups consist of a moderate hemodilution group (Group M) receiving 8 g/dl of hemoglobin, an extreme hemodilution group (Group E) given 4 g/dl of hemoglobin, and a hemoglobin-free autologous plasma group (Group F). Hearts in the non-ischemic control group (Group C) were also perfused with moderate hemodilution throughout. In Group C, Group M and Group E, the O2 tension of perfusates was maintained at about 100 mmHg and in Group F, at over 300 mmHg. Oxygen extraction at 5 min after reperfusion in Group C was 14%, in Group M and Group E less than 10%, but in Group F 70%. Oxygen consumption in Group F was more than twice that in Group E and surpassed that in Group C. Group M also showed a significant increase in oxygen consumption compared with Group E at 5 min after reperfusion. Among the ischemic groups, Group E showed improvement of left ventricular function almost comparable to Group C accompanied by a rapid decrease in myocardial lactate, improved preservation of myocardial adenine nucleotides and prevention of myocardial lipid peroxidation. In contrast, Group F showed persistently higher values of lipid peroxides and lactate, the poorest recovery of adenine nucleotides, and impairment of left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗

PubMed1992

Reperfusion of hibernating myocardium: contractile function, high-energy phosphate content, and myocyte injury after 3 hours of sublethal ischemia and 3 hours of reperfusion in the canine model.

Hibernating myocardium has been defined as a persistent impairment of contractile function resulting from reduced coronary blood flow that can be partially or completely resolved once coronary perfusion is restored. In fact, recent clinical reports have documented a dramatic improvement in contractile function after relief of chronic sublethal ischemia. To investigate the phenomenon of sublethal ischemia followed by reperfusion, we assessed myocyte morphology, high-energy phosphate content, and regional contractile function in dogs undergoing (1) 3 hours of subtotal coronary artery occlusion (CO) and 3 hours of reflow or (2) 3 hours of total CO followed by reflow, in which myocyte viability was maintained by extensive collateral perfusion during ischemia (total CO/negligible necrosis). Data were compared with findings in a third group of dogs with total CO and low collateral blood flow during ischemia, in which large confluent infarcts developed. Endocardial blood flow averaged 30 +/- 6% (p less than 0.01) and 27 +/- 4% (p less than 0.01) of baseline preocclusion values during ischemia in the groups with subtotal CO and total CO/negligible necrosis, versus 3 +/- 1% of baseline values in dogs with total CO/confluent necrosis. Both the subtotal CO and total CO/negligible necrosis groups exhibited only mild-to-moderate reversible myocyte injury (assessed by electron microscopy) and had essentially no necrosis: infarct size was 1 +/- 1% (p less than 0.01) and 4 +/- 2% (p less than 0.01) of the risk region in the subtotal CO and total CO/negligible necrosis groups, versus 55 +/- 9% of the risk region in the total CO/confluent necrosis group. Furthermore, myocardial high-energy phosphate stores were in part preserved in all dogs that underwent sublethal ischemia: endocardial adenosine triphosphate (ATP) content was 55 +/- 11% (p less than 0.01) and 56 +/- 8% (p less than 0.01) versus 11 +/- 2% of baseline values in the subtotal CO, total CO/negligible necrosis, and total CO/confluent necrosis groups, respectively. At 3 hours post occlusion, segment shortening averaged +21 +/- 10% of baseline values in dogs with subtotal CO, (p less than 0.01 versus both total CO groups), -29 +/- 9% in dogs with total CO/negligible necrosis, and -36 +/- 13% in dogs with total CO/confluent necrosis. Reperfusion after sublethal ischemia produced an acute improvement in contractile function in both the subtotal CO and total CO/negligible necrosis groups.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗

PubMed1989

Hyperoxia during reperfusion is a factor in reperfusion injury.

Imposition of ischemia should result in accumulation of lactic acid with an attendant drop in pH. Subsequent reperfusion would result in hyperoxia, in the affected tissue, due to the Bohr Effect. O2- should therefore be produced in greater than normal amounts, due to this transient hyperoxia, and may contribute to reperfusion injury. Tissue acidification, during extreme exercise or in diabetes mellitus, may similarly lead to hyperoxia and to tissue damage by O2-.

Free Radicals↗

PubMed2003

Can the ischemia-reperfusion syndrome in transplanted kidneys procured from non-heart-beating donors be influenced by adding selenium into the reperfusion solution? An experimental study.

The ischemic-reperfusion syndrome significantly influences the function of a kidney transplanted from a non-heart-beating donor (NHBD). The animal model of a NHBD was used to monitor the influence of exogenous addition of selenium into the reperfusion solution (HTK, Custodiol) with respect to the formation of free oxygen radicals at 0 to 120 minutes after the NHBD transplantation. This maneuvers produced a statistically significant decrease in malondialdehyde concentration, an indicator of free oxygen radicals in the venous blood of the transplanted kidney. The augmentation of the antioxidative capacity of the preservation solution might be a possible route to improve the function of kidneys transplanted from NHBDs.

Animals↗

PubMed2006

Interstitial lactic acidosis in the graft during organ harvest, cold storage, and reperfusion of human liver allografts predicts subsequent ischemia reperfusion injury.

BACKGROUND: The impact of the process of liver transplantation on glucose metabolism in the graft was studied using microdialysis. METHODS: Microdialysis catheters were inserted into 15 human livers to monitor metabolic changes that took place during organ harvest, the process of backtable preparation of the graft, and following implantation in the recipient where it remained in situ for 48 hours. The cannula was perfused with isotonic solution and hourly samples of perfusate were collected and analyzed. RESULTS: Six livers showed serum biochemical evidence of ischemia/reperfusion (IR) injury with 24 hours aspartate transaminase (AST) levels >2000 IU/L (Group A) whereas the remaining patients showed little evidence of IR injury (Group B). In Group A, lactate levels in the donor microdialysate rose to >6 mM (P < 0.05), were significantly higher during backtable preparation of the liver (>15 mM; P < 0.03), and took longer to normalize in the recipient following implantation (18 vs. 8 hours, P < 0.03) than lactate levels of the livers of patients in Group B who did not develop ischemia reperfusion injury. No significant differences were observed in glucose, pyruvate, or glycerol concentrations between the two groups. CONCLUSIONS: Interstitial lactic acidosis in the donor allograft is associated with significant reperfusion injury on implantation.

Acidosis, Lactic↗

PubMed1989

New reperfusion devices: the Kensey catheter, the atherolytic reperfusion wire device, and the transluminal extraction catheter.

Substantial interest exists in the development of reperfusion and recanalization devices that would aid in the management of both peripheral vascular and coronary artery occlusive disease. Several of these devices are now in multicenter investigative trials. The atherolytic reperfusion wire incorporates a 0.035-inch guide wire with a modified tip to recanalize the lumen through the totally obstructed vascular segment. Clinical experience in the initial 12 patients has been successful. The Kensey catheter, a high-speed rotational recanalization device, has been used in 110 patients in a multicenter trial. Technical success has been reported in 77% of the patients and clinical success in 55% of the patients, with follow-up periods of 3 months to 1 year. The transluminal extraction catheter (TEC) is a torque-controlled atherectomy catheter that incorporates an aspiration device into a distal rotational cutter. Consequently, distal embolization has not been a clinical problem in the 95 patients treated with the TEC catheter for peripheral vascular disease. Technical success has been accomplished in 87 (92%) patients. Three-month follow-up studies in 16 patients showed that restenosis occurred in four, two of whom had undergone combined atherectomy and angioplasty.

Angioplasty, Balloon↗

PubMed2002

Time course of lung ischemia-reperfusion-induced ICAM-1 expression and its role in ischemia-reperfusion lung injury.

Upregulation of intercellular adhesion molecule-1 (ICAM-1) expression is an important mechanism underlying ischemia-reperfusion (I/R) induced neutrophil activation and tissue injury in other organs. However, I/R of the lungs has not been shown to upregulate ICAM-1 expression. We determined the time course profile of lung I/R-induced ICAM-1 expression and assessed the role of ICAM-1 in mediating neutrophil sequestration, transmigration, and I/R injury in the isolated blood-perfused rat lungs. I/R had a biphasic effect on ICAM-1 expression, an early downregulation and a late-phase upregulation. Superoxide dismutase and neutrophil depletion prevented the early ICAM-1 downregulation. The late-phase ICAM-1 upregulation coincided with the I/R-induced increase in pulmonary microvascular leakage index. ICAM-1 monoclonal antibody (MAb) reversed the I/R-induced increase in pulmonary microvascular leakage index, with control antibody being ineffective. Neither I/R nor ICAM-1 MAb affected lung MPO activity and circulating neutrophil count. Lung I/R significantly increased bronchoalveolar lavage fluid neutrophil count and the GSSG-to-(GSSG+GSH) ratio. ICAM-1 MAb blocked the I/R-induced increase in GSSG-to-(GSSG+GSH) ratio but had no effect on bronchoalveolar lavage fluid neutrophil count. Our results demonstrated that lung I/R up- and downregulates ICAM-1 expression depending on the duration of reperfusion. ICAM-1 upregulation is an important mechanism of I/R-induced pulmonary endothelial injury.

Animals↗

PubMedDate not supplied

Albumin infusion after reperfusion prevents gut ischemia-reperfusion-induced gut-associated lymphoid tissue atrophy.

BACKGROUND: Our recent study clarified that gut ischemia-reperfusion (I/R) causes gut-associated lymphoid tissue (GALT) mass atrophy, a possible mechanism for increased morbidity of infectious complications after severe surgical insults. Because albumin administration reportedly reduces hemorrhagic shock-induced lung injury, we hypothesized that albumin treatment prevents GALT atrophy due to gut I/R. METHODS: Male mice (n = 37) were randomized to albumin, normal saline, and sham groups. All groups underwent jugular vein catheter insertion. The albumin and normal saline groups underwent 75-minute occlusion of the superior mesenteric artery. During gut ischemia, all mice received normal saline infusions at 1.0 mL/h. The albumin group was given 5% bovine serum albumin in normal saline at 1.0 mL/h for 60 minutes after reperfusion, whereas the normal saline group received 0.9% sodium chloride at 1.0 mL/h. The sham group underwent laparotomy only. Mice were killed on day 1 or 7, and the entire small intestine was harvested. GALT lymphocytes were isolated and counted. Their phenotypes (alphabetaTCR, gammadeltaTCR, CD4, CD8, B220) were determined by flow cytometry. RESULTS: On day 1, the gut I/R groups showed significantly lower total lymphocyte and B cell numbers in Peyer's patches and the lamina propria than the sham group. However, the albumin infusion partially but significantly restored these cell numbers. On day 7, there were no significant differences in any of the parameters measured among the 3 groups. CONCLUSIONS: Albumin infusion after a gut ischemic insult may maintain gut immunity by preventing GALT atrophy.

Albumins↗

PubMed2003

Can ischemia-reperfusion syndrome in transplanted kidneys procured from non-heart-beating donors be influenced by adding selenium into the reperfusion solution? An experimental study.

Ischemia-reperfusion syndrome significantly influences the function of a kidney transplanted from a non-heart-beating donor (NHBD). An animal model of NHBD was used to monitor the influence of the exogenous addition of selenium in the perfusion solution (HTK, Custodiol) on the generation of free oxygen radicals between 0 and 120 minutes after transplantation of the NHBD organ. During this interval, the malondialdehyde concentration, an indicator of free oxygen radicals in the venous blood of the transplanted kidney, significantly decreased. The augmentation of the anti-oxidant capacity of the preservation solution might represent a possible improvement in the function of kidneys transplanted from NHBDs.

Animals↗

PubMedDate not supplied

[Prevention of myocardial reperfusion injury by increasing artificial trans-membrane sodium gradient in "calcium paradox" and post-ischemic reperfusion].

An effect of the high sodium gradient during "calcium paradox" and postischemic reperfusion has been studied. A decrease of Na/Ca exchange by high sodium gradient (200 mM NaCl in the perfusion solution) resulted in the reduction of myoglobin release from the heart during "calcium paradox". High sodium concentration solution (200 mM) increased protective effect of ATP during "calcium paradox". Exogenous phosphocreatine (100 mumol/mol) increased myoglobin release from the heart. During perfusion of the heart by high sodium concentration, phosphocreatine efficiently decreased myoglobin release from the heart during "calcium paradox". Exogenous ATP (as Na-pump activator) and high Na+ concentration solution (180 mM) prevented the LDH release from the myocardium, decreased ATP hydrolysis, inhibited Ca influx, maintained total adenine nucleotides, phosphate potential, energy charge of the cardiomyocytes.

Adenine Nucleotides↗

PubMed1999

Effect of time of 7E3 administration on rt-PA-induced reperfusion: study in a canine model of thrombus-based occlusion-reperfusion.

Chimeric version of the murine monoclonal antibody, 7E3 has been proposed for the early restoration of coronary artery patency during thrombolytic therapy. We determined the optimal time for administration of 7E3 during recombinant tissue plasminogen activator (rt-PA)-induced thrombolysis using a canine model of coronary artery thrombosis. After 30 min of thrombotic occlusion, microspheres were injected to assess regional myocardial blood flow, followed by a 90-min rt-PA infusion. Dogs were randomized to three groups wherein 7E3 (0.8 mg kg(-1), i.v.) was administered either 5 min before rt-PA (Group I), at the first evidence of thrombolysis (Group II), or after the completion of rt-PA infusion (Group III). Hemodynamic parameters were monitored for 6 h after which infarct size was estimated. Time to occlusion/reperfusion was similar in all groups. In the rt-PA alone group, 78% arteries reoccluded after 60 min of reperfusion. The incidence of reocclusion was lower in Groups II (25%, P = 0.04) and III (0%. P < 0.01). All arteries (100%) were patent at the end of the protocol in Group III vs 50% remaining patent in Group I (P = 0.01). Arterial patency was maintained longer in Group III (301 min, n = 10), compared with Groups I (124 min, n = 5) and II (124 min, n = 6). Arterial flow was greater in Group III (82%) compared with Groups I (27%) and II (35%) (P < 0.01). Regional myocardial blood flow and infarct size were similar in all groups. The data indicate that the time of administration of 7E3 in conjunction with rt-PA-induced thrombolysis influences patency status. The experimental results suggest that in the absence of aspirin and heparin, optimal thrombolysis is obtained when 7E3 is administered after the completion of rt-PA infusion regimen.

Animals↗