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Ann Thorac Surg 2000;69:711-715
© 2000 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, South Carolina, USA
Address reprint requests to Dr Spinale, Division of Cardiothoracic Surgery, Medical University of South Carolina, 114 Doughty St, Suite 625, Strom Thurmond Research Building, Charleston, SC 29403
Presented at the Forty-sixth Annual Meeting of the Southern Thoracic Surgical Association, San Juan, Puerto Rico, Nov 4–6, 1999.
Background. Increased synthesis and release of the potent bioactive peptide endothelin-1 (ET-1) occurs during and after cardiac surgery. However, the cellular and molecular basis for the effects of ET-1 on human left ventricular (LV) myocyte contractility remains unknown.
Methods. LV myocyte contractility was examined from myocardial biopsies taken from patients (n = 30) undergoing elective coronary artery bypass. LV myocytes (n = 997, > 30/patient) were isolated using microtrituration and contractility examined by videomicroscopy at baseline and after ET-1 exposure (200 pmol/L). In additional studies, myocytes were pretreated to inhibit either protein kinase C (PKC) (chelerythrine, 1 µmol/L), the sodium/hydrogen (Na/H) exchanger (EIPA, 1 µmol/L), both PKC and the Na/H exchanger, or the ETA receptor (BQ-123, 1 µmol/L), followed with ET-1 exposure.
Results. Basal myocyte shortening increased 37.8 ± 6.3% with ET-1 (p < 0.05). Na/H exchanger, PKC, and dual inhibition all eliminated the effects of ET-1. Furthermore, ETA inhibition demonstrated that ET-1 effects on myocyte contractility were mediated through the ETA receptor subtype.
Conclusions. ET-1 directly influences human LV myocyte contractility, which is mediated through the ETA receptor and requires intracellular activation of PKC and stimulation of the Na/H exchanger.
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