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Di Pumpo et al. Vessel Plus 2018;2:41 I http://dx.doi.org/10.20517/2574-1209.2018.38 Page 3 of 8

Table 1. Difference between early and late preconditioning
Early preconditioning Late preconditioning
It begins early It begins 12-24 h after ischemia
Duration of 1-2 h Duration of 72 h
It is due to the accumulation of adenosine It is due to gene up-regulation

flurane and sevoflurane. The opening of the canal would lead to the reduction of the swelling of the inter-
membrane space after ischemia, preserving the structure and mitochondrial function. Depolarization of the
+
+
mitochondrial inner membrane also prevents the opening of the mPTP and inhibits the exchange of Na -H ,
attenuating Ca overload and cellular edema . Interferences have been described with the apoptotic cascade
2+
[5]
mediated by Bcl-2-associated death promoter and Bcl-2-associated X proteins and caspases 9, in addition to
activation of nitric oxide endothelial synthase [5,20,21] which may give a cardioprotective effect. Also reactive
oxygen species (ROS) have an important task: the opening of the KATP channels causes an increase in the
intracellular concentrations of ROS, at the same time, the production of ROS can also precede and cause the
opening of the KATP channels. Activators of the KATP channel and sevoflurane may attenuate the overpro-
duction of ROS during reperfusion. Therefore, halogenates, in order to achieve preconditioning, must cause
ROS production. Preconditioning, in turn, allows a reduction of ROS excess, during reperfusion [21,22] . Volatile
anesthetics also reduce platelet adhesion to the vascular wall after ischemia .
[23]
Regarding the late preconditioning, it is due to cardioprotective proteins that are expressed after the trans-
lation of the first genes induced by cardiac preconditioning. The most common genes expressed virtually
by any type of stress conditioning include antioxidants such as superoxide dismutase, glutathione peroxi-
dase and heme oxygenase, genes associated with cell defense [heat shock proteins(HSP) such as HSP70 and
[24]
HSP10, aldose reductase, Bcl-xS] and cycloid-oxygenase 2 .

Ischemic preconditioning is the process implemented by the myocardial tissue at the cellular level that pro-
vides myocardial protection against the damage due to the ischemia/reperfusion phenomenon in the cardiac
[25]
tissue .
After administration of volatile agents, the systolic function improves because we have a reduction in myo-
cardial oxygen consumption due to depression of myocardial contractility and improvement of blood flow in
[26]
several capillary beds .
Human studies have shown that volatile anesthetics can reduce mortality, but also the use of mechanical
ventilation in cardiac patients, especially coronary artery bypass grafting (CABG). In contrast, total intrave-
nous anesthesia (TIVA) (and more specifically propofol) has not shown any significant benefit compared to
[28]
[27]
halogenated agents. The studies of Fortis et al. and Schilling et al. have shown that halogenates lead to a
reduction of the inflammatory response in acute lung injury. In addition, the volatile agents cause neuropro-
[30]
[29]
tection after brain damage , reduce hepatic damage and the incidence of acute renal injury after an isch-
[31]
emic insult . As a result, volatile anesthetics can also play an important role in preventing cardiac surgery
complications.
CLINICAL IMPLICATIONS
In 2011, there was an international consensus conference that included volatile agents among the few drugs
[10]
that would decrease perioperative mortality in cardiac surgery . Volatile anesthetics (desflurane, isoflurane
and sevoflurane) have pharmacological characteristics that generate cardiac protection, unlike the drugs
used for TIVA.

Indeed, the 2007 Landoni meta-analysis showed a reduction in perioperative cardiac troponin release and
[32]
reduced mortality in patients receiving volatile anesthetics compared to patients receiving a TIVA .