Influence of ACE Inhibition on Myocardial Damage, the Kallikrein-Kinin System and Hemostasis during Cardiopulmonary Bypass Surgery

Walter, Thomas; Helber, Uwe; Bail, D. H. L.; Heller, W.; Hm, Hoffmeister

doi:10.1055/s-2002-32409

Cited by 10 publications

(7 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Few studies have examined the role of interventions destined at decreasing systemic oxidative stress during clinical CPB; in this regard, it is possible that angiotensinconverting enzyme inhibitors, angiotensin-1 blockers, and statin drugs could play a role in improving systemic and myocardial outcomes [76][77][78][79], although clinical studies involving angiotensin-converting enzyme inhibitors have so far been disappointing [80,81].…”

Section: Free-radicalsmentioning

confidence: 99%

Vasomotor dysfunction after cardiac surgery

Ruel

Khan

Voisine

et al. 2004

European Journal of Cardio-Thoracic Surgery

106

View full text Add to dashboard Cite

Cardiopulmonary bypass and cardioplegic arrest, which allow for support of the circulation and stabilization of the heart during cardiac procedures, are still used for the vast majority of cardiac operations worldwide. However, in addition to a well-recognized systemic inflammatory response, cardiopulmonary bypass and cardioplegic arrest elicit complex, multifactorial vasomotor disturbances that vary according to the affected organ bed, with reduced vascular resistances in the skeletal muscle and peripheral circulation, and increased propensity to spasm in the cardiac, pulmonary, mesenteric and cerebral vascular beds. This article outlines the nature, mechanistic basis, and clinical correlates of the vasomotor alterations encountered in patients undergoing cardiac surgery using cardiopulmonary bypass and cardioplegic arrest.

show abstract

Section: Free-radicalsmentioning

confidence: 99%

Vasomotor dysfunction after cardiac surgery

Ruel

Khan

Voisine

et al. 2004

European Journal of Cardio-Thoracic Surgery

106

View full text Add to dashboard Cite

show abstract

“…On the other hand, in another study, hexamethonium abolished the protection provided by intramesenteric bradykinin infusion [ 119 ]. Regarding bradykinin, it is worth mentioning that it is degraded rapidly by angiotensin-converting enzyme (ACE) [ 136 ], while ACE inhibitors and angiotensin-1 receptor antagonists [ 63 ] mimic its cardioprotective effects. The role of adenosine in RIC cardioprotection is still controversial, being confirmed in a mouse model [ 120 ], but not a porcine model [ 48 ].…”

Section: The Mechanisms Of Cardioprotection By Remote Ischaemic Condimentioning

confidence: 99%

Neural mechanisms in remote ischaemic conditioning in the heart and brain: mechanistic and translational aspects

et al. 2018

View full text Add to dashboard Cite

Remote ischaemic conditioning (RIC) is a promising method of cardioprotection, with numerous clinical studies having demonstrated its ability to reduce myocardial infarct size and improve prognosis. On the other hand, there are several clinical trials, in particular those conducted in the setting of elective cardiac surgery, that have failed to show any benefit of RIC. These contradictory data indicate that there is insufficient understanding of the mechanisms underlying RIC. RIC is now known to signal indiscriminately, protecting not only the heart, but also other organs. In particular, experimental studies have demonstrated that it is able to reduce infarct size in an acute ischaemic stroke model. However, the mechanisms underlying RIC-induced neuroprotection are even less well understood than for cardioprotection. The existence of bidirectional feedback interactions between the heart and the brain suggests that the mechanisms of RIC-induced neuroprotection and cardioprotection should be studied as a whole. This review, therefore, addresses the topic of the neural component of the RIC mechanism.

show abstract

“…In clinical trials to date, studies have tended to concentrate upon adenosine, in particular, and to a much lesser extent, bradykinin. The trails on the latter are limited in both size and outcome [71–74].…”

Section: Therapeutic Strategies 2: Harnessing the Cell's Endogenous Pmentioning

confidence: 99%

There is More to Life than Revascularization: Therapeutic Targeting of Myocardial Ischemia/Reperfusion Injury

Bell¹,

Yellon²

2010

Cardiovascular Therapeutics

View full text Add to dashboard Cite

Ischemic heart disease is the world's leading cause of death, and while clinical advances have meant improved and more rapid revascularization, there remains a significant element of myocardial death that thus far has not been successfully targeted in clinical practice, namely lethal reperfusion injury. Ischemia-reperfusion injury has been the subject of intense research over the last 40 years and our appreciation of the mechanisms of cellular death and salvage have increased immensely over this time, to the extent that a number of clearly identifiable therapeutic targets can now be subjected to clinical trials, as the basic science translates into potentially effective therapies in patients presenting with acute coronary syndromes.In this review, we aim to provide an overview of current evidence regarding the mechanisms of lethal reperfusion injury and endogenous protection, how cardioprotective pharmacological manipulations have been approached to date, and to indicate where therapies may be targeted in the future.

show abstract

Influence of ACE Inhibition on Myocardial Damage, the Kallikrein-Kinin System and Hemostasis during Cardiopulmonary Bypass Surgery

Abstract: Reduction of ischemic injury during CPB is not achieved with ACE inhibitors. However, treatment of patients with ACE inhibitors before and during CPB is fully feasible without side effects affecting the kallikrein contact phase or significant influence on hemostasis.

Cited by 10 publications

References 17 publications

Vasomotor dysfunction after cardiac surgery

Vasomotor dysfunction after cardiac surgery

Neural mechanisms in remote ischaemic conditioning in the heart and brain: mechanistic and translational aspects

There is More to Life than Revascularization: Therapeutic Targeting of Myocardial Ischemia/Reperfusion Injury

Contact Info

Product

Resources

About