(−)‐Epicatechin‐induced relaxation of isolated human saphenous vein: Roles of K+ and Ca2+ channels

In this study, we aimed to investigate relaxant effect of flavanol (?)‐epicatechin on the isolated human saphenous vein (HSV), as a part of its cardioprotective action, and to define the mechanisms underlying this vasorelaxation. (?)‐Epicatechin induced a concentration‐dependent relaxation of HSV pre‐contracted by phenylephrine. Among K⁺ channel blockers, 4‐aminopyridine, margatoxin, and iberiotoxin significantly inhibited relaxation of HSV, while glibenclamide considerably reduced effects of the high concentrations of (?)‐epicatechin. Additionally, (?)‐epicatechin relaxed contraction induced by 80 mM K⁺, whereas in the presence of nifedipine produced partial relaxation of HSV rings pre‐contracted by phenylephrine. In Ca²⁺‐free solution, (?)‐epicatechin relaxed contraction induced by phenylephrine, but had no effect on contraction induced by caffeine. A sarcoplasmic reticulum Ca²⁺‐ATPase inhibitor, thapsigargin, significantly reduced relaxation of HSV produced by (?)‐epicatechin. These results demonstrate that (?)‐epicatechin produces endothelium‐independent relaxation of isolated HSV rings. Vasorelaxation to (?)‐epicatechin probably involves activation of 4‐aminopyridine‐ and margatoxin‐sensitive K_V channels, BK_Ca channels, and at least partly, K_ATP channels. In addition, not only the inhibition of extracellular Ca²⁺ influx, but regulation of the intracellular Ca²⁺ release, via inositol‐trisphosphate receptors and reuptake into sarcoplasmic reticulum, via stimulation of Ca²⁺‐ATPase, as well, most likely participate in (?)‐epicatechin‐induced relaxation of HSV.     

Pediatric renal transplantation—A UNOS database analysis of donor–recipient size mismatch

Background

We used the BSAi (Donor BSA/Recipient BSA) to assess whether transplanting a small or large kidney into a pediatric recipient relative to his/her size influences renal transplant outcomes.

Methods

We included 14 322 single-kidney transplants in pediatric recipients (0–17 years old) (01/2000–02/2020) from the United Network for Organ Sharing database. We divided cases into four BSAi groups (BSAi ≤ 1, 1 < BSAi ≤ 2, 2 < BSAi ≤ 3, BSAi > 3).

Results

There were no differences concerning delayed graft function (DGF) or primary non-function (PNF) rates, whether the grafts were from living or brain-dead donors. In both transplants coming from living donors and brain-dead donors, cases with BSAi > 3 and cases with 2 < BSAi ≤ 3 had similar graft survival (p = .13 for transplants from living donors, p = .413 for transplants from brain-dead donors), and both groups had longer graft survival than cases with 1 < BSAi ≤ 2 and cases with BSAi ≤ 1 (p < .001). The difference in 10-year graft survival rates between cases with BSAi > 3 and cases with BSAi ≤ 1 reached around 25% in both donor types. The better graft survival in transplants with BSAi > 2 was confirmed in multivariable analysis.

Conclusions

There is no significant impact of donor-recipient size mismatch on DGF and PNF rates in pediatric renal transplants. However, graft survival is significantly improved when the donor's size is more than twice the pediatric recipient's size.