The relationship between the orientation of the glenoid and tears of the rotator cuff.

Our aim was to determine the most repeatable three-dimensional measurement of glenoid orientation and to compare it between shoulders with intact and torn rotator cuffs. Our null hypothesis was that glenoid orientation in the scapulae of shoulders with a full-thickness tear of the rotator cuff was the same as that in shoulders with an intact rotator cuff. We studied 24 shoulders in cadavers, 12 with an intact rotator cuff and 12 with a full-thickness tear. Two different observers used a three-dimensional digitising system to measure glenoid orientation in the scapular plane (ie glenoid inclination) using six different techniques. Glenoid version was also measured. The overall precision of the measurements revealed an error of less than 0.6 degrees. Intraobserver reliability (correlation coefficients of 0.990 and 0.984 for each observer) and interobserver reliability (correlation coefficient of 0.985) were highest for measurement of glenoid inclination based on the angle obtained from a line connecting the superior and inferior points of the glenoid and that connecting the most superior point of the glenoid and the most superior point on the body of the scapula. There were no differences in glenoid inclination (p = 0.34) or glenoid version (p = 0.12) in scapulae from shoulders with an intact rotator cuff and those with a full-thickness tear. Abnormal glenoid orientation was not present in shoulders with a torn rotator cuff.

Formation and actions of cyclic ADP-ribose in renal microvessels.

Recent studies indicated that cyclic ADP-ribose (cADPR) serves as a second messenger for intracellular Ca(2+) mobilization in a variety of mammalian cells. However, the metabolism and actions of cADPR in the renal vasculature are poorly understood. In the present study, we characterized the enzymatic pathway of the production and metabolism of cADPR along the renal vascular tree and determined the role of cADPR in the control of intracellular [Ca(2+)] and vascular tone. The high performance liquid chromatographic analyses showed that cADPR was produced and hydrolyzed along the renal vasculature. The maximal conversion rate of nicotinamide guanine dinucleotide (NGD) into cyclic GDP-ribose (that represents ADP-ribosyl cyclase activity for cADPR formation) was 8.69 +/- 2.39 nmol/min/mg protein in bulk-dissected intrarenal preglomerular vessels (n = 7) and 4.35 +/- 0.13, 2.23 +/- 0.27, 2.40 +/- 0.19, and 0.31 +/- 0.02 nmol/min/mg protein, respectively, in microdissected arcuate arteries (n = 6), interlobular arteries (n = 6), afferent arterioles (n = 7), and vasa recta (n = 10). The activity of cADPR hydrolase was also detected in the renal vasculature. Using the fluorescence microscopic spectrometry, cADPR was found to produce a large rapid Ca(2+) release from beta-escin-permeabilized renal arterial smooth muscle cells (SMCs). In isolated, perfused, and pressurized small renal arteries, cADPR produced a concentration-dependent vasoconstriction when added into the bath solution. The vasoconstrictor effect of cADPR was completely blocked by tetracaine, a Ca(2+)-induced Ca(2+) release (CICR) inhibitor. These results suggest that an enzymatic pathway for cADPR production and metabolism is present along the renal vasculature and that cADPR may importantly contribute to the control of renal vascular tone through CICR.