Pharmacologic intervention in ischemia‐induced reperfusion injury in the skeletal muscle

Pang, Cho Y.; Forrest, Christopher R.; Mounsey, R A

doi:10.1002/micr.1920140308

Cited by 57 publications

(33 citation statements)

References 67 publications

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“…Our finding here that the cardioprotective effects of PGE1 or PGEO are due to activation of KATP channels and, hence are similar to the cardioprotective effects elicited by ischaemic preconditioning, raises the question whether the anti-ischaemic effects of PGE1 observed in patients with peripheral arterial occlusive disease (PAOD) are also due to activation of KATP channels. Indeed, ischaemic preconditioning also protects against a subsequent more prolonged ischaemic insult in skeletal muscle, by a mechanism that is thought to involve PKC and the activation if KATP channels (Forrest et al, 1992;Pang et al, 1993;1995 …”

Section: Discussionmentioning

confidence: 99%

Reduction by prostaglandin E₁ or prostaglandin E₀ of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

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Ney

Piper

et al. 1995

British J Pharmacology

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1 This study examined whether pretreatment of rabbits with infusions of prostaglandin El (PGEI) or prostaglandin Eo (PGEO) (which were terminated prior to the onset of ischaemia) reduce myocardial infarct size arising from coronary artery occlusion (60 min) and reperfusion (120 min). In addition, we investigated whether the observed cardioprotective effects of these two prostaglandins were due to the activation of ATP-sensitive potassium (KATP) channels. 2 In the anaesthetized rabbit, infarct size (expressed as a percentage of the area at risk) after 60 min of coronary artery occlusion followed by 2 h of reperfusion was 59 + 4% (n = 10). PGEI or PGEo treatment (1.0 ,yg kg-' min-'), administered as 1 h pretreatments (0.05 ml min-', i.v.), significantly reduced infarct size to 44 + 6% (n = 6) or 42 + 1 % (n = 6), respectively. PGE, or PGEo pretreatment resulted in a significant reduction in mean arterial blood pressure, which returned to baseline within 15 min of discontinuation of the infusion (i.e. prior to LAL ligation). 3 The reduction in infarct size afforded by PGE, was abolished by pretreatment of rabbits with the KATP channel blockers, glibenclamide (60 + 4%; n =8) or 5-hydroxydecanoate (58 + 6%; n = 6). Similarly, glibenclamide also largely attenuated the reduction in infarct size afforded by PGEo (52 + 3%; n = 8).4 We propose that a 1 h pretreatment of PGEI or PGEO reduces infarct size by activating protein kinase C resulting in the opening of KATP channels.

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Section: Discussionmentioning

confidence: 99%

Reduction by prostaglandin E₁ or prostaglandin E₀ of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

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Ney

Piper

et al. 1995

British J Pharmacology

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“…5,9,14,29 In this study, group E2 underwent limb ischemia for 6 hours and was treated with 45 mg/kg of intravenous allopurinol. Concannon et al 29 also used this dose and administration route.…”

Section: Effect Of Allopurinolmentioning

confidence: 99%

“…These alterations to mi-crocirculation constitute the no-reflow phenomenon. 3,[5][6][7][8][9] Obstruction is progressive, with thrombus formation in the microcirculation, platelet aggregation, and tissue edema. Irreversible damage and loss of limb or of microsurgical flap can result.…”

Section: Abstract: Warm Ischemia No-reflow Phenomenon Free Radicalsmentioning

confidence: 99%

Study of Warm Ischemia Followed by Reperfusion on a Lower Limb Model in Rats: Effect of Allopurinol and Streptokinase

Cunha

Silva

Nakamoto

et al. 2005

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MC. Study of warm ischemia followed by reperfusion on a lower limb model in rats: effect of allopurinol and streptokinase. Clinics. 2005;60(3):213-20. Prolonged tissue ischemia leads to changes in microcirculation and production of oxygen free radicals. The event eventually responsible for tissue death is the no-reflow phenomenon and its management is a challenge for the surgeon dealing with replantation or transplantation. We introduce a model of warm ischemia and reperfusion of the lower limb of rats with which we studied the effect of allopurinol and streptokinase. METHOD: Section of the lower limb with preservation of vessels and nerves was performed in 110 rats. Femoral vessels clamped for periods of 0, 2, 4, 6, and 8 hours of ischemia were allowed to reperfuse (groups M0, M2, M4, M6, and M8 respectively). Other groups, E1, E2, and E3, received streptokinase, allopurinol, or a combination of the two drugs after 6 hours of ischemia. RESULTS: Viability rates of the ischemic limbs after 7 days were 100% (M0), 80% (M2), 63.6% (M4), 50% (M6), and 20% (M8). In the experimental groups, E1, E2, and E3, viability rates were 67% (E1), 70% (E2), and 70% (E3). Groups M0, M2, M4, M6, and M8 differed among themselves except for groups M4 and M6. Group E1 had a higher rate of limb viability than M6 (control group) but not than M4. Groups E1, E2 and E3 had higher rates of limb viability than M6 but not than M2 or M4. DISCUSSION: The results suggest that increased viability of limbs after 6 hours of ischemia occurs when allopurinol or streptokinase is used. The combination of the two drugs does not appear to produce any additional effect.

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“…The events and molecular basis for each of these three topics are very complex, and previous review articles have discussed each topic separately (1)(2)(3)(4)(5)(6)(7).…”

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confidence: 99%

Skin wound healing, ischemia-reperfusion injury and nerve regeneration: Similarities in the sequential events and molecular basis

Al-Qattan¹

2004

J Plast Surg

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Skin wound healing, ischemia-reperfusion injury and nerve regeneration are three important topics for the hand surgeon. The events and molecular basis for each of these three topics are very complex, and previous review articles have discussed each topic separately. The present review demonstrates and comments on the similarities in the sequential events and molecular basis among skin wound healing, ischemia-reperfusion injury and nerve regeneration.Key Words: Cytokines; Ischemia; Nerve; Reperfusion; Skin; Wound Cicatrisation des lésions cutanées, lésions de reperfusion et régénération des nerfs : ressemblances quant à la séquence d'événements et à la structure moléculaire La cicatrisation des lésions cutanées, les lésions de reperfusion et la régénération des nerfs sont trois éléments importants pour le chirurgien de la main. La séquence d'événements et la structure moléculaire de chacun sont très complexes; les trois sujets ont déjà fait l'objet de discussion dans des articles précédents, mais ils étaient considérés isolément. Les auteurs du présent examen relèvent les ressemblances entre les trois phénomènes quant à la séquence d'événements et à la structure molécu-laire, puis les commentent. S kin wound healing, ischemia-reperfusion injury and nerve regeneration are three important topics for the hand surgeon. The events and molecular basis for each of these three topics are very complex, and previous review articles have discussed each topic separately (1-7).The aim of the present review is to demonstrate and comment on the similarities in the sequential events and molecular basis among skin wound healing, ischemia-reperfusion injury and nerve regeneration. Before commenting on the similarities, a brief account on each topic will be given. SKIN WOUND HEALINGThe inflammatory phase Immediately following skin wounding, cytokines, including interleukin-1 (IL-1), are released by endothelial cells and keratinocytes. Platelets forming the primary hemostatic plug secrete tumour necrosis factor-alpha (TNF-α), platelet derived growth factors (PDGF), transforming growth factor-beta (TGF-β) and fragments of fibronectins (Fn). Within minutes of injury, P-selectin (an adhesion molecule) is expressed on the endothelial cell surface which facilitates preferential neutrophil binding and, hence, neutrophils are the first inflammatory cells that enter the wound. P-selectin expression on the endothelial cell is transient, however, and is followed by endothelial E-selectin expression which is induced by the platelet-derived TNF-α and the keratinocyte-derived IL-1. E-selectin expression occurs 2 h to 6 h following the injury and it facilitates both monocyte and neutrophil binding. Approximately 12 h after injury, IL-1, TNF-α and interferongamma induce endothelial intercellular adhesion molecule (ICAM) and vascular cell adhesion molecule expression with selective recruitment of monocytes and lymphocytes into the wound. Further monocyte migration occurs along chemotactic gradients in response to leukotriene B 4 and Fn. Monocytes i...

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Pharmacologic intervention in ischemia‐induced reperfusion injury in the skeletal muscle

Cited by 57 publications

References 67 publications

Reduction by prostaglandin E₁ or prostaglandin E₀ of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Reduction by prostaglandin E₁ or prostaglandin E₀ of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Study of Warm Ischemia Followed by Reperfusion on a Lower Limb Model in Rats: Effect of Allopurinol and Streptokinase

Skin wound healing, ischemia-reperfusion injury and nerve regeneration: Similarities in the sequential events and molecular basis

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Pharmacologic intervention in ischemia‐induced reperfusion injury in the skeletal muscle

Cited by 57 publications

References 67 publications

Reduction by prostaglandin E1 or prostaglandin E0 of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Reduction by prostaglandin E1 or prostaglandin E0 of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Study of Warm Ischemia Followed by Reperfusion on a Lower Limb Model in Rats: Effect of Allopurinol and Streptokinase

Skin wound healing, ischemia-reperfusion injury and nerve regeneration: Similarities in the sequential events and molecular basis

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Reduction by prostaglandin E₁ or prostaglandin E₀ of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels

Reduction by prostaglandin E₁ or prostaglandin E₀ of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels