Mesenchymal stem cells (MSCs) have been reported to improve
survival of cardiomyocytes (CMCs) and overall regeneration of
cardiac tissue. Despite promising preclinical results, interactions
of MSCs and CMCs, both direct and indirect, remain unclear. In
this study, porcine bone marrow MSCs and freshly isolated
porcine primary adult CMCs were used for non-contact co-culture
experiments. Morphology, viability and functional parameters of
CMCs were measured over time and compared between CMCs
cultured alone and CMCs co-cultured with MSCs. In non-contact
co-culture, MSCs improved survival of CMCs. CMCs co-cultured
with MSCs maintained CMCs morphology and viability in
significantly higher percentage than CMCs cultured alone. In
viable CMCs, mitochondrial respiration was preserved in both
CMCs cultured alone and in CMCs co-cultured with MSCs.
Comparison of cellular contractility and calcium handling,
measured in single CMCs, revealed no significant differences
between viable CMCs from co-culture and CMCs cultured alone.
In conclusion, non-contact co-culture of porcine MSCs and CMCs
improved survival of CMCs with a sufficient preservation of
functional and mitochondrial parameters.
A patent ductus arteriosus (DA) was maintained in newborn rats (Wistar strain) by administering prostaglandin E2 (PG E2) in doses of 15 /ig.kg'1 at 30 min intervals up to 300 min after birth. In the control animals, the DA was functionally closed 300 min after birth. The lumen was blocked by clustered endothelial cells at various stages of degeneration. Elastic membranes of the media had disintegrated into irregular fragments and the smooth muscle cells were contracted. Cytoplasm excrescences formed on their surface as a result of contraction protruded as hernias into adjacent muscle cells and into endothelial cells. The smooth muscle cells degenerated. The administration of PG E2 inhibited contraction of the smooth muscle cells and so also the development of degenerative changes; 300 min after birth the DA was fully patent, the elastic membranes were structurally intact, regularly organized and continuous. The smooth muscle cells had the character of synthesizing cells with richly developed granular endoplasmic reticulum. The intima and its endothelial lining were likewise free from structural changes. The ultrastructural image of the wall of the DA correspondent to the state 10 min after birth, when the DA was fully patent. The administration of PG E2 did not induce any ultrastructural changes indicative of injury to the wall of the DA.
Propofol is a short-acting hypnotic agent used in human medicine for sedation and general anesthesia. Its administration can be associated with serious cardiovascular side-effects that include decrease in arterial blood pressure and cardiac output. The aim of the present study was to evaluate propofol effects on mitochondrial respiration, myocardial contractility and electrophysiology in the same samples isolated from the heart ventricles of adult rats. Mitochondrial oxygen consumption was
measured in permeabilized samples dissected from free walls of
both ventricles using high-resolution respirometry. State LEAK was determined with malate and glutamate. Active respiration was induced by ADP (state PI) and further by succinate, a Complex II substrate (PI+II). Rotenone was injected to measure state PII. Antimycin A, a Complex III inhibitor was used to determine residual oxygen consumption (ROX). N,N,N',N'-tetramethyl-p-phenylenediamine dihydrochloride and ascorbate
were injected simultaneously for respirometric assay of cytochrome c oxidase activity (CIV). Isometric contractions and membrane potentials were determined on multicellular preparations isolated from right and left ventricles. Propofol concentrations used ranged from 0.005 to 0.5 mmol/l. All
respiratory parameters were significantly higher in the left control ventricles compared to the right ones. Propofol significantly decreased Complex I activity at concentration 0.025 mmol/l and papillary muscle contraction force at 0.1 mmol/l. Propofol did not affect action potential duration at any concentration studied. Our study suggests that mechanisms contributing to the impaired myocardial contraction during propofol anesthesia might include also mitochondrial dysfunction manifested by compromised
activity of the respiratory Complex I.