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Ghrelin is an acylated peptide recently isolated from rat and human stomach that potently stimulates GH release in vivo and in vitro in rats and humans. Ghrelin specifically activates the receptor for the growth hormone secretagogues (GHS) and it has been proposed that it may be the endogenous ligand mimicked by these synthetic compounds. Ghrelin is primarily produced in endocrine cells of the stomach, and to a lesser extent, in other peripheral tissues, including the pituitary. Although ghrelin is the most potent GH-secretagogue so far identified, its circulating levels do not correlate with those of GH either in physiological and pathological conditions. Because of these and many other observations, it may be postulated that ghrelin is not physiologically involved in the regulation of growth hormone secretion. Nonetheless, ghrelin may serve as a very useful model for the development of more potent synthetic GHS, which may be therapeutically useful for the treatment of human GH deficiency.

A 34-year-old woman without heart disease had an acute pulmonary edema after a grand mal seizure. Neurogenic pulmonary edema is characterized by the primary role played by the central nervous system in its pathogenesis, usually in the absence of cardiopulmonary disease. We believe that the initiating mechanism was a marked, although brief, generalized vasoconstriction, followed by a shift of blood from the peripheral vascular bed to the pulmonary vascular bed. We stress the need of treating the underlying neurologic disease as the only regional way of preventing the recurrence of pulmonary edema.

To obtain information on endocardial activation-sequence, unipolar recordings at seven left ventricular and six right ventricular points were performed in a 37-year-old man suffering from cardiomyopathy and tachycardia-dependent left bundle branch block (LBBB). Results were as follows: 1) the recovery time was longer in anterior than in posterior portion of left bundle branch fibers; 2) an high posterior left ventricular point was directly activated via posterior left bundle branch fibers; 3) the directly activated left ventricular zone was too small and relatively too late excited in respect of the right interventricular septum, from which the stimulus reached the left septum, to mask the LBBB electrocardiographic pattern; 4) in the presence of tachycardia-dependent LBBB the duration of left ventricular endocardial activation was about twice (62 msec) that found in the absence of tachycardia-dependent LBBB (28 msec).

To obtain information on normal left ventricular activation, endocardial recordings with an electrode catheter were made a seven left ventricular sites in ten patients undergoing diagnostic heart catheterization. All the patients had: 1) sinus rhythm; 2) normal duration and shape of the QRS complex of left chest leads; 3) normal left ventriculography, i.e. normal volume and contractility of the left ventricle. The earliest left ventricular endocardial activation was recorded at septal and/or posterior level, i.e. at the septum (6 to 16 msec, average 9.7 msec, after the onset of intracardiac QRS complex) in seven patients; at the posterior wall (0 to 4 msec, average 2.6 msec, after the onset of intracardiac QRS complex) in three patients (in one of these, the earliest activation occurred at the posterior wall and apex simulaneously). If the earliest activation occurred at the left interventricular septum, the next excited point was found on the posterior wall or at the apex, and vice versa. The latest part to be activated was on the lateral free wall in seven patients; on the posterior wall in two patients; at the apex in the last one.