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Microcirculation, endothelium, and lymphatics最新文献

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Contractile and metabolic function following an ischemia-reperfusion injury in skeletal muscle: influence of oxygen free radical scavengers. 骨骼肌缺血再灌注损伤后的收缩和代谢功能:氧自由基清除剂的影响
Microcirculation, endothelium, and lymphatics Pub Date : 1989-06-01
J W Long, J L Laster, R P Stevens, W P Silver, D Silver
{"title":"Contractile and metabolic function following an ischemia-reperfusion injury in skeletal muscle: influence of oxygen free radical scavengers.","authors":"J W Long,&nbsp;J L Laster,&nbsp;R P Stevens,&nbsp;W P Silver,&nbsp;D Silver","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Skeletal muscle contraction and metabolism was evaluated using an in vivo, intact autoperfused canine hindlimb model during 7 hours of reperfusion following 4 hours of complete ischemia, with and without bolus administration of superoxide dismutase (SOD) and catalase (CAT) at the start of reperfusion. Contractile tension of paw dorsiflexion during reperfusion demonstrated small but statistically non-significant increases of recovery towards pre-ischemic baseline with SOD/CAT (i.e. 43% +/- 10 vs 32% +/- 9 with muscle-stimulated tetanic tension). Oxygen utilization by the hindlimb rose during reperfusion from a baseline in the control group of 2.4 +/- 0.3 ml 02/min to 5.4 +/- 1.1 during the first 10 minutes and plateaued at 3.5 +/- 1.3 by the first hour with no differences in the SOD/CAT group. Lactate clearance was prompt (increase from a pre-ischemia value of zero to 0.93 +/- .14 mM/min by 5 minutes and return to near-zero by 1 hour in controls) exhibiting no sustained anaerobic metabolism and was not affected by SOD/CAT. These finding demonstrate irreversible loss of 60-70% of skeletal muscle contraction with preservation of aerobic metabolic capacity at 225% of basal activity. Bolus administration of SOD/CAT at the start of reperfusion offered no significant improvement in metabolic or contractile function. These observations, in a model simulating the in vivo setting, necessitate evaluating alternate ischemia reperfusion conditions and modified free-radical inhibitor protocols before any clinical benefit can be assumed.</p>","PeriodicalId":18718,"journal":{"name":"Microcirculation, endothelium, and lymphatics","volume":"5 3-5","pages":"351-63"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13780267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Participation of the complement system in ischemia/reperfusion injury. 补体系统在缺血再灌注损伤中的作用。
Microcirculation, endothelium, and lymphatics Pub Date : 1989-06-01
B Rubin, A Smith, A Romaschin, P Walker
{"title":"Participation of the complement system in ischemia/reperfusion injury.","authors":"B Rubin,&nbsp;A Smith,&nbsp;A Romaschin,&nbsp;P Walker","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Reperfusion of ischemic skeletal muscle is associated with an early infiltration of WBC, a process mediated by locally generated chemotactic factors. We present evidence that selective activation of the alternative complement cascade occurs in response to skeletal muscle ischemia/reperfusion injury. Complement activation may result in the generation of peptides which are chemotactic for neutrophils, and the formation of molecular complexes which injure cell membranes.</p>","PeriodicalId":18718,"journal":{"name":"Microcirculation, endothelium, and lymphatics","volume":"5 3-5","pages":"207-21"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13778674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The reperfusion syndrome. 再灌注综合征。
Microcirculation, endothelium, and lymphatics Pub Date : 1989-06-01
F W Blaisdell
{"title":"The reperfusion syndrome.","authors":"F W Blaisdell","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>When major vascular occlusion is carried out in the presence of systemic shock and there has been obstruction to blood supply of an extremity, restoration of circulation is not without risk. Morbidity and mortality relate directly to the duration and the degree of ischemia and the mass of tissue involved. The initial problem following the onset of ischemia relates to acidosis and hyperkalemia when limbs are reperfused after several hours of ischemia. When ischemia has been present for more than six to eight hours, there will be death of tissue and reperfusion at this point results in the products of dead and devitalized tissue being washed into the systemic circulation. This produces intravascular coagulation and a diffuse inflammatory response with systemic vascular permeability. Respiratory distress syndrome will develop if the ischemic injury is severe. If patients are not adequately monitored and blood volume maintained, renal failure and multiple organ failure will develop in parallel.</p>","PeriodicalId":18718,"journal":{"name":"Microcirculation, endothelium, and lymphatics","volume":"5 3-5","pages":"127-41"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13842475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects of ischemia-reperfusion injury on microvascular permeability in skeletal muscle. 缺血再灌注损伤对骨骼肌微血管通透性的影响。
Microcirculation, endothelium, and lymphatics Pub Date : 1989-06-01
W N Durán, P K Dillon
{"title":"Effects of ischemia-reperfusion injury on microvascular permeability in skeletal muscle.","authors":"W N Durán,&nbsp;P K Dillon","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Microvascular permeability changes (using FITC-dextran 150 clearance as an index) produced by ischemia-reperfusion (I-R) were investigated in the rat cremaster muscle. I-R produced significant sustained increases in microvascular permeability to macromolecules. Pretreatment with dexamethasone and verapamil reduced this I-R effect. Leukopenia also afforded protection to the microcirculation. It was concluded that changes occurring during ischemia are major causative components of the ischemia-reperfusion damage.</p>","PeriodicalId":18718,"journal":{"name":"Microcirculation, endothelium, and lymphatics","volume":"5 3-5","pages":"223-39"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13630596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The impact of energy depletion on skeletal muscle. 能量消耗对骨骼肌的影响。
Microcirculation, endothelium, and lymphatics Pub Date : 1989-06-01
P M Walker, T Lindsay, S Liauw, A D Romaschin
{"title":"The impact of energy depletion on skeletal muscle.","authors":"P M Walker,&nbsp;T Lindsay,&nbsp;S Liauw,&nbsp;A D Romaschin","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Changes in the skeletal muscle adenine nucleotide pool during prolonged periods of normothermic ischemia, followed by reperfusion are a result of an exaggerated breakdown to lipid soluble precursors, the degree of reactive hyperemia, and activities of the salvage and direct pathways for resynthesis. We show that the degree of breakdown of ATP, ADP and AMP, is time dependent, and with restoration of circulation there is washout of these lipid soluble precursors, and no resynthesis of ATP. We demonstrated a relationship between the loss of energy during ischemia, and the degree of resultant necrosis, suggesting that a limit on the effectiveness of therapeutic interventions during reperfusion in reducing the extent of necrosis may exist.</p>","PeriodicalId":18718,"journal":{"name":"Microcirculation, endothelium, and lymphatics","volume":"5 3-5","pages":"189-206"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13778673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Hypothermia and controlled reperfusion: two non-pharmacologic methods which diminish ischemia-reperfusion injury in skeletal muscle. 低温和控制再灌注:两种减轻骨骼肌缺血再灌注损伤的非药物方法。
Microcirculation, endothelium, and lymphatics Pub Date : 1989-06-01
J G Wright, M Belkin, R W Hobson
{"title":"Hypothermia and controlled reperfusion: two non-pharmacologic methods which diminish ischemia-reperfusion injury in skeletal muscle.","authors":"J G Wright,&nbsp;M Belkin,&nbsp;R W Hobson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The mechanisms of ischemia-reperfusion (I-R) injury in skeletal muscle remain controversial. We have previously reported two non-pharmacologic methods to salvage skeletal muscle from I-R injury, post-ischemic hypothermia and controlled reperfusion. In all experiments, both canine gracilis muscles were subjected to six hours of ischemia followed by one hour of reperfusion. Controlled reperfusion was achieved by partially occluding one gracilis artery to limit the rate of reperfusion blood flow to its pre-ischemic rate, while the contralateral artery was allowed to perfuse freely at a normal rate. Post-ischemic hypothermia was achieved by cooling one gracilis muscle to 21 degrees centigrade (hypothermic reperfusion) after 5 hours of warm ischemia, while the opposite gracilis muscle was maintained at ambient temperature (normothermic reperfusion). Both methods resulted in a significant diminution in muscle infarct and edema. The mechanisms by which this is accomplished are currently unknown, but may be related to a diminished inflammatory response to ischemia. This review of these methods suggests that the hyperemic rate of reperfusion blood flow is a significant factor in the pathophysiology of post-reperfusion edema, and that significant control of skeletal muscle reperfusion injury may be achieved by limiting the rate of reperfusion blood flow or by applying post-ischemic hypothermia.</p>","PeriodicalId":18718,"journal":{"name":"Microcirculation, endothelium, and lymphatics","volume":"5 3-5","pages":"315-34"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13778679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Free radical mediated damage in skeletal muscle. 自由基介导的骨骼肌损伤。
Microcirculation, endothelium, and lymphatics Pub Date : 1989-06-01
T Lindsay, A Romaschin, P M Walker
{"title":"Free radical mediated damage in skeletal muscle.","authors":"T Lindsay,&nbsp;A Romaschin,&nbsp;P M Walker","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Skeletal muscle subjected to prolonged ischemia will develop significant injury, however it can withstand periods of ischemia that would be irreversible in other tissues such as brain and heart. Reperfusion injury has been measured and suggested to occur secondary to oxygen free radicals. The increases in vascular permeability and resistance following ischemia/reperfusion can be blunted using free radical scavengers. Also skeletal muscle necrosis can be reduced if these scavengers are provided in high concentration during reperfusion. Recently increases in hydroxy-conjugated dienes, a marker of lipid peroxidation, have been found in reperfused skeletal muscle, providing chemical evidence for free radical injury during reperfusion. These studies have provided some insight into ischemia/reperfusion injury in skeletal muscle, but more investigations are required to detail the mechanisms involved in this injury.</p>","PeriodicalId":18718,"journal":{"name":"Microcirculation, endothelium, and lymphatics","volume":"5 3-5","pages":"157-70"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13843159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mechanisms of postischemic vascular dysfunction in skeletal muscle: implications for therapeutic intervention. 骨骼肌缺血后血管功能障碍的机制:治疗干预的意义。
Microcirculation, endothelium, and lymphatics Pub Date : 1989-06-01
D L Carden, R J Korthuis
{"title":"Mechanisms of postischemic vascular dysfunction in skeletal muscle: implications for therapeutic intervention.","authors":"D L Carden,&nbsp;R J Korthuis","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In 1981, it was first proposed that xanthine oxidase-derived reactive oxygen metabolites contribute to the microvascular and parenchymal cell damage which occurs when ischemic tissues are reperfused. Figure 1 summarizes a scheme that has been proposed to explain the interaction of xanthine oxidase-derived oxidants, neutrophil infiltration, and the microvascular dysfunction which occurs in postischemic tissue. According to this proposal, xanthine oxidase-derived oxidants, produced at the time of reperfusion, initiate the formation and release of proinflammatory agents, which subsequently attract and activate neutrophils. The activated granulocytes adhere to vascular endothelium, extravasate, and release cytotoxic oxidants and/or non-oxidative toxins (e.g. proteases) which contribute to tissue destruction. The objective of this review is to summarize the supportive evidence for this scheme in postischemic skeletal muscle and to identify the components of the mechanism that may be amenable to pharmacologic intervention.</p>","PeriodicalId":18718,"journal":{"name":"Microcirculation, endothelium, and lymphatics","volume":"5 3-5","pages":"277-98"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13843161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Prostaglandins in the management of cardiac and skeletal muscle ischemia. 前列腺素在心肌和骨骼肌缺血治疗中的作用。
Microcirculation, endothelium, and lymphatics Pub Date : 1989-06-01
M Belkin, J Blebea, J G Wright, R W Hobson
{"title":"Prostaglandins in the management of cardiac and skeletal muscle ischemia.","authors":"M Belkin,&nbsp;J Blebea,&nbsp;J G Wright,&nbsp;R W Hobson","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":18718,"journal":{"name":"Microcirculation, endothelium, and lymphatics","volume":"5 3-5","pages":"335-49"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13630601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Ischemia-reperfusion and cell membrane dysfunction. 缺血再灌注和细胞膜功能障碍。
Microcirculation, endothelium, and lymphatics Pub Date : 1989-06-01
M O Perry, G Fantini
{"title":"Ischemia-reperfusion and cell membrane dysfunction.","authors":"M O Perry,&nbsp;G Fantini","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>One to 3 hours of partial skeletal muscle ischemia-reperfusion in dogs and rats causes cell membrane depolarization. Intracellular levels of adenosine triphosphate remain normal, suggesting that direct membrane injury rather than electrogenic pump failure occurs. Membrane depolarization can be prevented by superoxide dismutase and catalase, or by neutrophil depletion. Oxygen free radicals may be one type of mediator causing membrane damage, and it appears that leukocytes release these toxic species.</p>","PeriodicalId":18718,"journal":{"name":"Microcirculation, endothelium, and lymphatics","volume":"5 3-5","pages":"241-58"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13778675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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