GS5-2 A novel in vitro model for evaluating the triple play of vascular cell-stent-blood flow(GS5: Tissue Engineering)

Degeneration of articular cartilage (AC) is a common healthcare issue that can result in significantly impaired function and mobility for affected patients. The avascular nature of the tissue strongly burdens its regenerative capacity contributing to the development of more serious conditions such as osteoarthritis. Recent advances in bioprinting have prompted the development of alternative tissue engineering therapies for the generation of AC. Particular interest has been dedicated to scaffold-based strategies where 3D substrates are used to guide cellular function and tissue ingrowth. Despite its extensive use in bioprinting, the application of polycaprolactone (PCL) in AC is, however, restricted by properties that inhibit pro-chondrogenic cell phenotypes. This study proposes the use of a new bioprintable poly(ester urea) (PEU) material as an alternative to PCL for the generation of an in vitro model of early chondrogenesis. The polymer was successfully printed into 3D constructs displaying adequate substrate stiffness and increased hydrophilicity compared to PCL. Human chondrocytes cultured on the scaffolds exhibited higher cell viability and improved chondrogenic phenotype with upregulation of genes associated with type II collagen and aggrecan synthesis. Bioprinted PEU scaffolds could, therefore, provide a potential platform for the fabrication of bespoke, pro-chondrogenic tissue engineering constructs.

Download Full-text

Methods for detecting local intestinal ischemic anaerobic metabolic acidosis by P CO 2

Journal of Applied Physiology ◽

10.1152/jappl.1996.81.4.1834 ◽

1996 ◽

Vol 81 (4) ◽

pp. 1834-1842 ◽

Cited By ~ 54

Author(s):

Ranna A. Rozenfeld ◽

Michael K. Dishart ◽

Tor Inge Tønnessen ◽

Robert Schlichtig

Keyword(s):

Blood Flow ◽

Metabolic Acidosis ◽

Anaerobic Threshold ◽

In Vitro Model ◽

Venous Blood ◽

Flow Reduction ◽

Portal Venous Blood ◽

Vitro Model ◽

Arterial Plasma

Rozenfeld, Ranna A., Michael K. Dishart, Tor Inge Tønnessen, and Robert Schlichtig. Methods for detecting local intestinal ischemic anaerobic metabolic acidosis by[Formula: see text]. J. Appl. Physiol. 81(4): 1834–1842, 1996.—Gut ischemia is often assessed by computing an imaginary tissue interstitial pH from arterial plasma [Formula: see text] and the[Formula: see text] in a saline-filled balloon tonometer after equilibration with tissue[Formula: see text](P[Formula: see text]). P[Formula: see text] may alternatively be assumed equal to venous[Formula: see text]([Formula: see text]) in that region of gut. The idea is that as blood flow decreases, gut P[Formula: see text] and[Formula: see text] will increase to the maximum aerobic value, i.e., maximum respiratory[Formula: see text]([Formula: see text]). Above a “critical” anaerobic threshold, lactate (La−) generation, by titration of tissue [Formula: see text], should raise P[Formula: see text]above[Formula: see text]. During progressive selective whole intestinal flow reduction in six pentobarbital-anesthetized pigs, we used[Formula: see text] electrodes to test the hypotheses that critical P[Formula: see text]is achieved earlier in mucosa than in serosa and that[Formula: see text], computed using an in vitro model, predicts critical P[Formula: see text]. We defined critical P[Formula: see text] as the inflection of P[Formula: see text]-[Formula: see text]vs. O2 delivery (Q˙o 2) plots. CriticalQ˙o 2for O2 uptake was 12.55 ± 2 ml ⋅ kg−1 ⋅ min−1. Critical P[Formula: see text] for mucosa and serosa was achieved at similar whole intestineQ˙o 2(13.90 ± 5 and 13.36 ± 5 ml ⋅ kg−1 ⋅ min−1, P = NS). Critical P[Formula: see text] (129 ± 24 and 96 ± 21 Torr) exceeded[Formula: see text](62 ± 3 Torr). During ischemia, La− excretion into portal venous blood was matched by K+excretion, causing [Formula: see text] to increase only slightly, despite P[Formula: see text] rising to 380 ± 46 (mucosa) and 280 ± 38 (serosa) Torr. These results suggest that mucosa and serosa become dysoxic simultaneously, that ischemic dysoxic gut is essentially unperfused, and that in vitro predicted[Formula: see text]underestimates critical P[Formula: see text].

Download Full-text