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Cartilage has a great capacity to resist compressive force. This quality is related t o its unique composition of proteinpolysaccharide in a mesh-work of collagen fibers. Although cartilage is not grossly altered in appearance in vitro by incubation with enzymes which can deplete proteinpolysaccharide, it becomes less stiff and more flexible. When slices of canine cartilage were incubated in 0.1M Tris-HCI, pH 7.6, 37"C, without prior freezing o r addition of detergents, they spontaneously lost 60% of proteinpolysaccharide by the third day without concomitant loss of collagen. Specimens incubated with trypsin were depleted of 75% proteinpolysaccharide by the first 24 hours and, over a 1-week period, 20% of the collagen, although less than 2% was released during the last 2 days of incubation. Bacterial collagenase resulted in loss of approximately 9% of the total collagen during each day's incubation for 1 week, but the proteinpolysaccharide depletion followed a curve similar to controls. Functional studies, measuring strain under load, indicated that during 24-hour incubations of cartilage treated with trypsin or hyaluronidase these samples had much more evidence of strain than did collagenase-treated specimens. The latter lost actual thickness, however, while the trypsin-treated samples and controls remained the same size, suggesting that collagen has the primary role in determining form of cartilage and may be capable of significant water binding in the absence of proteinpolysaccharide. It is proposed that measurement of compressibility of articular cartilage is a suitable index of its effective proteinpolysaccharide content, and the total volume or thickness can be diminished only by agents capable of removing collagen.

In patients with arterial hypertension and left ventricular hypertrophy, perindopril + indapamide reduced blood pressure and left ventricular mass index and improved resting and hyperaemic myocardial blood flow. Data in rats provide evidence that the improvement in coronary flow observed after treatment is due to reverse remodelling of intramural coronary arterioles and improved microvascular function.

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