Preconditioning human cardiomyocytes and endothelial cells.

J Thorac Cardiovasc Surg

Department of Clinical Biochemistry, Toronto Hospital, Ontario, Canada.

Published: January 1998

Background: The effects of simulated "ischemia" and "reperfusion" were evaluated in cell cultures of human ventricular cardiomyocytes and human saphenous vein endothelial cells.

Methods: Myocyte and endothelial cell cultures were exposed to a low volume (1.5 ml) of either hypoxic (oxygen tension = 16 mm Hg) or anoxic (oxygen tension = 0 mm Hg) phosphate-buffered saline solution for 90 minutes ("ischemia") followed by 30 minutes of simulated "reperfusion." Cell injury was evaluated by trypan blue exclusion. Next, the effects of a preconditioning stimulus were evaluated by a brief (10 minute) exposure to hypoxic or anoxic ischemia and 10 minutes of reperfusion before prolonged (90 minutes) anoxic ischemia. Finally, the effects of anoxic preconditioning on intracellular lactate accumulation and extracellular lactate and acid release were assessed.

Results: "Ischemia" and "reperfusion" resulted in greater injury to endothelial cells than to cardiomyocytes. In both cell types, anoxic ischemia resulted in greater injury than hypoxic ischemia. Preconditioning reduced cell injury in myocytes but not in endothelial cells. Endothelial cells produced more lactate than cardiomyocytes under normoxic conditions. Ischemia increased lactate accumulation and release in cardiomyocytes but not endothelial cells. Preconditioning reduced lactate accumulation and release in cardiomyocytes but not endothelial cells.

Conclusions: Endothelial cells were more susceptible to the same period of simulated ischemia than cardiomyocytes. Preconditioning protected cardiomyocytes but not endothelial cells from a subsequent prolonged period of ischemia and reperfusion.

Download full-text PDF

Source
http://dx.doi.org/10.1016/s0022-5223(98)70459-3DOI Listing

Publication Analysis

Top Keywords

endothelial cells
28
cardiomyocytes endothelial
16
anoxic ischemia
12
lactate accumulation
12
endothelial
10
cardiomyocytes
8
"ischemia" "reperfusion"
8
cell cultures
8
oxygen tension
8
cell injury
8

Similar Publications

Development of Electrospinning Setup for Vascular Tissue-Engineering Application with Thick-Hierarchical Fiber Alignment.

Tissue Eng Regen Med

January 2025

College of Materials Science and Engineering, Hunan University, Changsha, 410072, People's Republic of China.

Background: Tissue engineering holds promise for vascular repair and regeneration by mimicking the extracellular matrix of blood vessels. However, achieving a functional and thick vascular wall with aligned fiber architecture by electrospinning remains a significant challenge.

Methods: A novel electrospinning setup was developed that utilizes an auxiliary electrode and a spring.

View Article and Find Full Text PDF

Objectives: To explore the role of berberine (BBR) in ameliorating coronary endothelial cell injury in Kawasaki disease (KD) by regulating the complement and coagulation cascade.

Methods: Human coronary artery endothelial cells (HCAEC) were divided into a healthy control group, a KD group, and a BBR treatment group (=3 for each group). The healthy control group and KD group were supplemented with 15% serum from healthy children and KD patients, respectively, while the BBR treatment group received 15% serum from KD patients followed by the addition of 20 mmol/L BBR.

View Article and Find Full Text PDF

Parthenolide improves sepsis-induced coagulopathy by inhibiting mitochondrial-mediated apoptosis in vascular endothelial cells through BRD4/BCL-xL pathway.

J Transl Med

January 2025

Department of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.

Background: Sepsis is a systemic inflammatory syndrome that can cause coagulation abnormalities, leading to damage in multiple organs. Vascular endothelial cells (VECs) are crucial in the development of sepsis-induced coagulopathy (SIC). The role of Parthenolide (PTL) in regulating SIC by protecting VECs remains unclear.

View Article and Find Full Text PDF

Gold(I) N-heterocyclic carbene complexes show strong proapoptotic, antioxidant and anti-inflammatory effects in A2780 and endothelial cells.

Chem Biol Interact

January 2025

Institute of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Schwarzspanierstrasse 17, 1090 Vienna, Austria. Electronic address:

A series of eight gold(I) N-heterocyclic carbene (NHC) complexes [Au(IMes)(HLn)] based on 1,3-bis(2,4,6-trimethylphenyl)imidazol-2-ylidene (IMes) and 7-azaindole derivatives (HLn), where n = 1-8 for HL1 = 5-flouro-7-azaindole, HL2 = 5-bromo-7-azaindole, HL3 = 3-chloro-7-azaindole, HL4 = 3-iodo-7-azaindole, HL5 = 5-bromo-3-chloro-7-azaindole, HL6 = 5-bromo-3-iodo-7-azaindole, HL7 = 4-chloro-2-methyl-7-azaindole and HL8 = 7-azaindole, was prepared, characterised and studied for their in vitro anti-cancer and anti-inflammatory effects. The complexes showed significant cytotoxicity on human ovarian cancer cell lines (A2780, IC ≈ 8-19 μM and A2780R, IC ≈ 8-19 μM) and lowered toxicity in normal HaCat and MRC-5 cells. Cellular effects of the selected complexes 1 and 7 were evaluated in A2780 cells using flow cytometry.

View Article and Find Full Text PDF

The interactive toxic effect of homocysteine and copper on cardiac microvascular endothelial cells during ischemia-reperfusion injury.

Chem Biol Interact

January 2025

Department of Thoracic Surgery, The 1st Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, Jiangxi, PR China; Jiangxi Hospital of China-Japan Friendship Hospital, National Regional Center for Respiratory Medicine, Nanchang 330000, Jiangxi, PR China; Jiangxi Institute of Respiratory Disease, The 1st Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330000, Jiangxi, PR China. Electronic address:

Hyperhomocysteinemia (HHcy) is associated with the development and progression of chronic cardiovascular diseases through the deleterious effects of high levels of homocysteine (Hcy) on the cardiovascular system. However, the exact mechanism of action of Hcy on the acute injury of the cardiovascular system following ischemia/reperfusion (I/R) remains unclear. The present study demonstrated that copper mobilization occurs during cardiac I/R, and the interactive toxic effect of Hcy and mobile Cu during cardiac I/R induces necroptosis of cardiac microvascular endothelial cells (CMECs) and thus enhances cardiac dysfunction.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!