Role of bradykinin in cardiac functional protection after global ischemia-reperfusion in rat heart

Brew, Elizabeth C.; Mitchell, Max B.; Rehring, Thomas F.; Gamboni‐Robertson, Fabia; McIntyre, Robert C.; Harken, Alden H.; Banerjee, Anirban

doi:10.1152/ajpheart.1995.269.4.h1370

Cited by 48 publications

(48 citation statements)

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“…Goto, et al have shown in the isolated rabbit heart that PKC inhibitors completely abolished the infarct-sparing effect of exogenously administered BK, 4) and Bugge and Ytrehus reported that PKC blockade markedly reduced the infarct-inhibiting effect of BK in the isolated rat heart. 5) In a study that used the recovery of ventricular function as an endpoint, a PKC inhibitor completely blocked the protective effect of exogenous BK 26) as shown also by our results. A number of studies have sought to elucidate the end-effector of ischemic preconditioning, and have revealed that the mitochondrial K ATP channel is an important mediator.…”

Section: Discussionsupporting

confidence: 85%

“…18) Previous experimental studies in the isolated rat heart have demonstrated that pretreatment with BK for 5 to 10 minutes before the initiation of global ischemia improved postischemic left ventricular function in the isolated rat heart. [26][27][28] Similarly, the work of Feng, et al on the isolated rabbit heart has shown that the infusion of BK for 10 minutes and cardioplegic arrest with BK-enriched St. Thomas' cardioplegia solution before the initiation of global ischemia improved the recovery of ventricular function. 22) In line with these studies, the present results demonstrate that pharmacological preconditioning with two cycles of BK infusion can protect the heart subjected to ischemia and reperfusion.…”

Section: Discussionmentioning

confidence: 94%

“…Myocardial protection by BK: Myocardial protection by exogenously administered BK against ischemia-reperfusion injury has been confirmed by many investigators. In experimental studies, brief administration of BK limited infarct size, [3][4][5][6][7][8] improved postischemic contractile function, 22,[26][27][28] and exhibited antiarrhythmic effects. 29) In clinical studies, intracoronary infusion of BK before PTCA enhanced the tolerance of the heart to subsequent ischemia in a manner analogous to ischemic preconditioning, 17) and the infusion of BK before the initiation of car- 3.3 ± 1.0 0.8 ± 0.3 4.1 ± 1.2 4.5 ± 1.6 2.3 ± 0.4 3.1 ± 2.5 3.4 ± 0.9 3.6 ± 1.0 6.6 ± 1.4 2.6 ± 0.6 9.3 ± 1.4 7.4 ± 1.8 5.6 ± 1.4 8.5 ± 2.7 12.6 ± 2.3 9.2 ± 1.5…”

Section: Discussionmentioning

confidence: 99%

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Pharmacological Preconditioning With Bradykinin Affords Myocardial Protection Through NO-dependent Mechanisms

et al. 2005

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SUMMARYBradykinin (BK) is one of the triggers of ischemic preconditioning. Protein kinase C (PKC) and mitochondrial ATP-dependent potassium (K ATP ) channels are central factors in cardioprotection afforded by BK. However, the role of nitric oxide (NO) in the early phase protection of preconditioning with BK is not well understood. We assessed the signaling pathway of the early phase protection of pharmacological preconditioning afforded by BK. Isolated perfused rat hearts (n = 8/group) were subjected to 30-minute global ischemia and 50-minute reperfusion. Left ventricular systolic pressure (LVSP) was recorded prior to the global ischemia and at the end of reperfusion. Preconditioning with BK was induced by two cycles of 5-minute infusion of BK (0.5 µmol/L) and 5-minute washout prior to the global ischemia. To examine participants in the signaling pathway,arginine methyl ester (L-NAME, 50 µmol/L) was added to the perfusate for 5 minutes prior to the infusion of BK. Pharmacological preconditioning by BK improved postischemic recovery of LVSP (+ 45.1% versus control, P < 0.01). Protection by BK was abolished by coadministration of CH, 5-HD, or L-NAME.BK affords myocardial protection in the early phase of pharmacological preconditioning through a pathway that includes endogenous NO, PKC, and mitochondrial K ATP channels. (Int Heart J 2005; 46: 877-887)

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

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Pharmacological Preconditioning With Bradykinin Affords Myocardial Protection Through NO-dependent Mechanisms

et al. 2005

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“…Furthermore, a recently reported notable effect of bradykinin is that bradykinin is protective in some cases of reperfusion injury of cardiac stenosis or thrombosis (81). Also, a recent interesting report (82) is a study with the mixed-gene kininogen deficient rats, which were produced by back-crossing kininogen-deficient B / N-Ka and normal B / N rats with genetically susceptible Lewis rats for 5-generations.…”

Section: Role Of the Kallikrein-kinin System In Inflammatory Exudate mentioning

confidence: 99%

Roles for the Kallikrein-Kinin System in Inflammatory Exudation and Pain: Lessons From Studies on Kininogen-Deficient Rats

Ueno¹,

Oh‐ishi²

2003

J Pharmacol Sci

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Abstract. Roles for the kallikrein-kinin system in inflammation have been investigated extensively, and many reviews on this topic have been published during the 50 years since the discovery of bradykinin in 1949. Recent progress in the field has been remarkable with the help of experiments using gene-targetted transgenic or knockout mice, which have added further valuable information in addition to previous results obtained from pharmacological and biochemical studies using purified and isolated components of the system. Furthermore, much knowledge has been accumulated as a result of the development of various bradykinin agonists and antagonists. In this review, we focused on the data obtained from the kininogen-deficient rat, which is a natural mutant, and discuss the results in comparison with those from bradykinin receptor knockout mice. These data have clarified that endogenous bradykinin exerts a most important role in inflammatory exudation along with prostanoids, preferentially to histamine, serotonin, or neuropeptides. In inflammatory pain perception also, bradykinin produced in the local perivascular spaces stimulates polymodal pain receptors in conjunction with co-helpers such as prostanoids, vanilloids, and neuropeptides. These important roles are concluded based on consistent results obtained from experiments using several antagonists of bradykinin, kininogen-deficient rats, and bradykinin receptor knockout mice.

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“…10,72,75,76,[103][104][105][106][107][108][109] This protective phenomenon has been termed ischemic preconditioning. 103 Ischemic preconditioning can be mimicked pharmacologically by adenosine, 110,111 alpha-adrenergic agonists, 104 bradykinin, 112 and ATPsensitive potassium channel (K ATP ) agonists. 110 Our group has proposed that the protection afforded by adenosine preconditioning against cardiac ischemia reperfusion injury may be due to reduced TNF production.…”

Section: 30mentioning

confidence: 99%

Bench to Bedside Tumor Necrosis Factor‐alpha: From Inflammation to Resuscitation

Cairns

Panacek

Harken

et al. 2000

Academic Emergency Medicine

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Abstract. Proinflammatory mediators such as tumor necrosis factor-alpha (TNF) have been implicated in the pathophysiology in a number of acute disease states. Tumor necrosis factor-alpha can contribute to cell death, apoptosis, and organ dysfunction. Tumor necrosis factor-alpha can be generated with sepsis or ischemia-reperfusion by activation of cell mitogen-activated protein kinases and nuclear factor kappa B, leading to TNF production. A number of strategies to modulate TNF have been recently explored, including factors directed toward mitogen-activated protein kinases, TNF transcription, anti-inflammatory ligands, heat shock proteins, and TNF-binding proteins. However, TNF may also play an important role in the adaptive response to injury and inflammation. Control of the deleterious effects of TNF and other proinflamatory cytokines represents a realistic goal for clinical emergency medicine. The purpose of this article is to provide a background of relevance to emergency medicine academicians on the production and regulation of TNF, the acute effects of TNF on pathophysiology, and the rationale for therapeutic interventions directed toward TNF and the clinical experience with these strategies. Key words: sepsis; shock; ischemia and reperfusion; therapy; trauma; emergency; review; tumor necrosis factor. ACA-DEMIC EMERGENCY MEDICINE 2000; 7:930-941 I NFLAMMATORY cytokines are known to be important mediators of numerous disease states faced by emergency physicians.1-8 A basic understanding of inflammatory cytokines and their relationship to acute disease is of growing importance to laboratory scientists, clinical researchers, and clinicians. Tumor necrosis factor-alpha (TNF) is a proinflammatory cytokine that has been directly implicated in the pathogenesis of many acute disease states, including sepsis, traumatic injury, cardiac and cerebral ischemia, asthma, and burns. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] Tumor necrosis factor-alpha may also play an important role in the adaptive response to injury and inflammation. 14 The intracellular signal pathways that provoke TNF production have been the subject of intense investigations. 10,17,18 In particular, the discovery of Other therapeutic targets include the activation of endogenous anti-inflammatory strategies such as ligands for the gp130 subunit, the induction of heat shock proteins (HSPs), and infusion of TNF-binding proteins. These approaches hold the promise of directly modulating the destructive role of proinflammatory cytokines, such as TNF, in acute disease states.The purpose of this article is to provide a background of relevance to emergency medicine academicians on the production and regulation of TNF, the acute effects of TNF on pathophysiology, and the rationale for therapeutic interventions directed toward TNF and the clinical experience with these strategies.

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Role of bradykinin in cardiac functional protection after global ischemia-reperfusion in rat heart

Cited by 48 publications

References 0 publications

Pharmacological Preconditioning With Bradykinin Affords Myocardial Protection Through NO-dependent Mechanisms

Pharmacological Preconditioning With Bradykinin Affords Myocardial Protection Through NO-dependent Mechanisms

Roles for the Kallikrein-Kinin System in Inflammatory Exudation and Pain: Lessons From Studies on Kininogen-Deficient Rats

Bench to Bedside Tumor Necrosis Factor‐alpha: From Inflammation to Resuscitation

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