SUMMARY In eight humans with coarctation, fresh aortic tissue was examined pharmacodynamically. In four of these patients, and in 12 additional patients, the aorta above and below the coarctation was studied morphologically and compared with eight control aortas. By in vitro stimulation with potassium (127 mM), noradrenaline (18 usM), and prostaglandin F,. (28 M), postcoarctational aortic ring preparations-showed a significantly greater contractility than precoarctational rings (p < 0.05). Volumetric analysis showed significantly more collagen (p < 0.01) and less smooth muscle mass (p < 0.01) in the aorta above than below the coarctation. No significant differences were found between sections from the arch and distal to the ligamentum arteriosum in the normal aortas.We conclude that the precoarctational aortic wall is more rigid than the postcoarctational wall. (25-30°C) and transported to the laboratory, where they were cleaned of connective tissue and cut into rings. The macroscopically identified coarctation was isolated in one ring preparation, and two preparations of about the same weight were isolated above and below the stenosis. MethodThe isometric tension changes in both rat and human ring segments were recorded by the "ring" method described by Bevan and Osher7 and others.8-'0 The ring preparations were mounted in 30-ml jacketed organ baths that contained Krebs solution ( fig. 1). The temperature of the solution was maintained at 37°C and was constantly aerated with 95% oxygen and 5% carbon dioxide. The isometric contractions were recorded using Grass Ft 03 transducers connected to a Beckman R6 11 polygraph.During a 1-2-hour period, the resting length was adjusted (by stepwise depression of the rod) ( fig. 1) to the level at which maximal contraction force by depolarization could be generated. During this period, anesthetics possibly left in the tissue were also washed out. The resulting resting length -and corresponding resting tension -for a ring preparation were kept constant throughout the experiment, and a drug was not applied before the resting tension was reached again.The repeated isometric contractions were induced by potassium depolarization (127 mM) until responses were reproducible. Thereafter, the responses to supra-

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Myocardial catecholamine concentrations were determined in endomyocardial biopsies from patients with heart failure to assess if tissue catecholamine levels relate to the severity of myocardial damage or the aetiology of the underlying disease. Methodological studies revealed a good reproducibility of catecholamine determinations in biopsies; the variance between paired biopsies was below 17% when myocardial catecholamines were related to non-collagen protein (NCP). Myocardial norepinephrine (in pg micrograms-1 NCP) levels were comparable in patients with dilated cardiomyopathy (DCM, 5.3 +/- 3.4, n = 22) and in patients with coronary or valvular heart disease (5.6 +/- 4.7, n = 14). In both groups, a significant reduction of myocardial norepinephrine was found (controls 12.0 +/- 3.4, P less than 0.0006). In a subgroup of patients with heart failure and a LVEF less than 30% (3.9 +/- 3.5, n = 17) myocardial norepinephrine content was lower than in patients with heart failure and LVEF of 31-55% (6.6 +/- 3.4, n = 19) (both P less than 0.05 against controls: 12.0 +/- 3.4, n = 16). A correlation between myocardial norepinephrine and LVEF was found in DCM (P less than 0.001, r = 0.70). The loss of myocardial norepinephrine is a characteristic feature of heart failure. It is independent of the origin of failure, but correlates with the impairment of LV function.