Can Streptokinase Produce Beneficial Effects Additional to Coronary Recanalization? Quantitative Microvascular Analysis of Critically Injured Reperfused Myocardium

Woo, Kam S.; Armiger, Lois C.; White, Harvey D.; Norris, R. M.

doi:10.1006/mvre.2000.2236

Cited by 9 publications

(8 citation statements)

References 29 publications

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“…23,29 Our findings suggest a novel mechanism, namely an inducible defect in local endogenous fibrinolytic activity, favouring local thrombus formation in the pathophysiology of microvascular obstruction and re-infarction. In support of this hypothesis, streptokinase reduces myocardial congestion and improves microvascular perfusion in a canine model of IR injury 30 and acutely improves indices of coronary microvascular perfusion when administered immediately following primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction. 31 …”

Section: Discussionmentioning

confidence: 78%

Ischaemia–reperfusion injury impairs tissue plasminogen activator release in man

Pedersen¹,

Barnes²,

Schmidt³

et al. 2011

European Heart Journal

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AimsIschaemia–reperfusion (IR) injury causes endothelium-dependent vasomotor dysfunction that can be prevented by ischaemic preconditioning. The effects of IR injury and preconditioning on endothelium-dependent tissue plasminogen activator (t-PA) release, an important mediator of endogenous fibrinolysis, remain unknown.Methods and resultsIschaemia–reperfusion injury (limb occlusion at 200 mmHg for 20 min) was induced in 22 healthy subjects. In 12 subjects, IR injury was preceded by local or remote ischaemic preconditioning (three 5 min episodes of ipsilateral or contralateral limb occlusion, respectively) or sham in a randomized, cross-over trial. Forearm blood flow (FBF) and endothelial t-PA release were assessed using venous occlusion plethysmography and venous blood sampling during intra-arterial infusion of acetylcholine (5–20 µg/min) or substance P (2–8 pmol/min). Acetylcholine and substance P caused dose-dependent increases in FBF (P<0.05 for all). Substance P caused a dose-dependent increase in t-PA release (P<0.05 for all). Acetylcholine and substanceP-mediated vasodilatation and substanceP-mediated t-PA release were impaired following IR injury (P<0.05 for all). Neither local nor remote ischaemic preconditioning protected against the impairment of substance P-mediated vasodilatation or t-PA release.ConclusionIschaemia–reperfusion injury induced substanceP-mediated, endothelium-dependent vasomotor and fibrinolytic dysfunction in man that could not be prevented by ischaemic preconditioning.Clinical Trial Registration Information: Reference number: NCT00789243, URL:

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Section: Discussionmentioning

confidence: 78%

Ischaemia–reperfusion injury impairs tissue plasminogen activator release in man

Pedersen¹,

Barnes²,

Schmidt³

et al. 2011

European Heart Journal

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“…It has been demonstrated that streptokinase (SK) inhibits red-cell aggregation and reduces platelet aggregation in vitro. It has also been shown histopathologically, in an open-chest model of anterior descending artery occlusion and reperfusion, that SK results in improved perfusion of the microvasculature in severely ischemic myocardium to which blood flow has been restored [68,69].…”

Section: Ic Thrombolyticsmentioning

confidence: 96%

Intracoronary pharmacotherapy in the management of coronary microvascular dysfunction

Kunadian

Zorkun

Williams

et al. 2008

J Thromb Thrombolysis

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Although percutaneous coronary intervention restores optimal epicardial blood flow in most cases, abnormal myocardial perfusion may still persist. This might be as a result of macro and microembolization, neutrophil plugging, vasoconstriction, myocyte contracture, local intracellular and interstitial edema, intramural haemorrhage, and endothelial blistering. Local delivery of intracoronary pharmacotherapy via the coronary arteries may increase local drug concentration several fold, and may improve drug efficacy. Several pharmacological agents such as adenosine, calcium channel blockers, alpha blockers, beta2 receptor activators, vasodilators, antithrombotics, and antiplatelet agents have been used to treat coronary microvascular dysfunction. This article reviews the results of trials of intracoronary pharmacotherapy to date.

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“…Related to this finding, the authors have used streptokinase to reduce myocardial congestion and improve microvascular perfusion in a canine model of IRI. 44,45 Others Many other agents have been examined in an attempt to attenuate IRI. These agents, as listed by Wang et al 6 include recombinant human BCL2 protein, ethyl pyruvate, low-level laser therapy, PARP inhibition, ketamine, recombinant human VEGF165 protein, activated protein C, adenosine A3receptor-selective agonist, bortezomib, MRS2693, hypertonic saline, cariporide, grape seed proanthocyanidin extract, Wisconsin solution, frequency ultrasound, erythropoietin, resveratrol, vitamin E, amino acid peptides, statins, and hyperbaric oxygen.…”

Section: Thrombosismentioning

confidence: 99%

“…Related to this finding authors have used streptokinase to improves microvascular perfusion in a canine model of IRI. 44,45 PRACTICAL IMPLICATIONS By defining the cellular/molecular events occurring with IRI, we can begin to strategize an approach to limit tissue damage. This may well take the form of a multitargeted approach where anticipated sequences of physiological changes are anticipated and modulated.…”

Section: Phase 2avimmediate Reperfusion Phase: Ros Generation Mitochmentioning

confidence: 99%

“…Preconditioning has resulted in improved microvascular perfusion and reduces leukocyte-EC interaction and cell apoptosis in skeletal muscle as reported by many authors in rat hindlimb, cremaster muscle, and pig latissimus dorsi muscle flaps. 12,44,45 Practical applications may be important in elective surgical procedures. In microsurgery, after the isolation of the tissue transfer flap, before the division of the vascular pedicle, manipulation of the pedicle with intermittent restriction of flow causing conditioned ischemia or remotely restricting blood flow (pressure cuff ) in nonoperated limbs before replantation may provide protection against reperfusion injury.…”

Section: Preconditioning and Postconditioningmentioning

confidence: 99%

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Ischemia-Reperfusion Injury

Widgerow

2014

Annals of Plastic Surgery

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Ischemia-reperfusion injury forms the basis of tissue damage and cellular apoptosis in many pathologic and traumatic processes. The tissue damage follows a natural progression of cellular and metabolic events initiated by an ischemic episode. Ischemia causes intracellular/extracellular changes principally resulting in increased intracellular calcium, pH changes, and adenosine triphosphate depletion that end in cell death if the process is not interrupted. This interruption takes the form of reperfusion, characterized by a "flushing" of tissues with toxic metabolites, principally reactive oxygen species. The immediate effect is mitochondrial pore permeability, complement activation, cytochrome release, cytokine activation, inflammation, edema, neutrophil platelet adhesion, capillary plugging, and thrombosis. This sets the stage for the long recognized "no-reflow" phenomenon and progressive tissue death. Current recognition of cellular "cross-talk" and molecular events have introduced new logical strategies to sequentially combat the events occurring in relation to ischemia-reperfusion injury. These include mechanical preconditioning and pharmacological preconditioning and postconditioning strategies. It is likely that success in reversing or limiting tissue damage will be found in a sequential multitargeted approach using a combination of these strategies-clinical trials in this regard are sorely needed.

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Can Streptokinase Produce Beneficial Effects Additional to Coronary Recanalization? Quantitative Microvascular Analysis of Critically Injured Reperfused Myocardium

Cited by 9 publications

References 29 publications

Ischaemia–reperfusion injury impairs tissue plasminogen activator release in man

Ischaemia–reperfusion injury impairs tissue plasminogen activator release in man

Intracoronary pharmacotherapy in the management of coronary microvascular dysfunction

Ischemia-Reperfusion Injury

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