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Computer games are a major part of the culture of children and teenagers in many developed countries. Research shows that children of the computer age prefer computer-assisted learning to any other teaching strategy. Health care workers traditionally have used dolls, games, drawings, creative arts, and even videotapes to prepare children for surgery. No studies have been conducted in Israel on using computers to help ailing children in general or to help children preparing for surgery in particular. This article discusses the potential for using computers to educate patients based on a review of the literature and interviews with children and describes the process of computer game development.

1. The release of catecholamines (CA) from rat adrenal incubated in vivo in Locke solution was studied. 2. Acetylcholine-induced release of CA and CA release by 56 mM KCl were inhibited by verapamil and lanthanum chloride which block calcium permeability. 3. CA secretion induced by salbutamol or by theophylline was unaffected by either verapamil or lanthanum chloride. 4. Dantrolene-sodium inhibited the CA secretion induced by theophylline but only partially reduced potassium-induced release of CA. 5. Verapamil enhanced the secretion of CA induced by salbutamol (in a calcium-free medium). 6. Tyramine-induced secretion of CA was unaffected by lanthanum chloride, verapamil or dantrolene-sodium. 7. It is suggested that cyclic adenosine 3',5'-monophosphate-mediated CA secretion (induced by theophylline or salbutamol) depends on release of calcium from intracellular stores, and that CA secretion induced by tyramine is independent of intra- or extracellular calcium.

1 The mechanism involved in catecholamine (CA) release from the cat adrenal gland in response to insulin hypoglycaemia was studied. In intact cats, hypoglycaemia induced an 11 fold increase in adrenomedullary CA secretion. 2 Acute bilateral nephrectomy nearly abolished the increased CA release from the adrenal gland during hypoglycaemia. 3 Infusion of Sar1-Ileu8-Angiotensin II (AII), a competitive AII antagonist, suppressed the adrenomedullary response to the insulin-induced hypoglycaemia. After termination of the antagonist infusion CA secretion from the adrenal medulla increased rapidly, reaching the same level as in insulin-treated cats. 4 Infusion of rabbit anti-angiotensin I antibodies suppressed CA release from the adrenal gland of hypoglycaemic cats. This effect was more prolonged than that of Sar1-Ileu8-AII. 5 These results indicate that CA release from the adrenal medulla of the cat in response to insulin-induced hypoglycaemia, is mediated through the renal reninangiotensin system. Since hypoglycaemia causes sympathetic stimulation through a central mechanism, angiotensin may act through the central nervous system.

1 The effect of alpha-adrenoceptor agonists on membrane adenosine triphosphatase (ATPase) activity was studied in membranes from the bovine adrenal medulla and the rat submaxillary gland. 2 alpha-Adrenoceptor agonists (10(-7) to 10(-5) M) enhanced significantly Na,K-ATPase activity but not Mg-ATPase activity in adrenal medulla. This effect was not observed in membranes from phaeochromyocytoma. Phenylephrine (10(-5) M), naphazoline (10(-5) M) and clonidine (10(-5) M) caused a significant increase of the activity of Na,K-ATPase (but not of Mg-ATPase) in the submaxillary gland. The enhancement became more prominent after ligature of the submaxillary duct but disappeared completely after superior cervical ganglionectomy. Thus, the effect of the alpha-adrenoceptor agonists was due to an action on adrenergic nerve terminals in the submaxillary gland. 3 Phenylephrine and naphazoline did not affect 45Ca uptake but enhanced the rate of 45Ca efflux from adrenal medullary slices in vitro. 4 Phenylephrine enhanced the rate of 45Ca efflux from slices of submaxillary gland (with previous ligation of the duct); this was blocked by phentolamine and sympathetic denervation. Therefore phenylephrine was acting on the adrenergic nerve terminals. 5 It is suggested that the inhibition by alpha-adrenoceptor agonists of the exocytotic release of catecholamines from adrenergic nerve terminals and from chromaffin cells may be due to activation of the sodium pump, which results in enhancement of calcium efflux, causing a reduction of free intracellular Ca2+.

Prostaglandin E2 induced increased catecholamine release in vitro from adrenals of hypophysectomized rats, while in adrenals of intact rats catecholamine release was suppressed by prostaglandin E2.

1. The concentrations of adrenaline and noradrenaline in the adrenal vein and the adrenal gland of the cat were studied in response to different stimuli leading to increased catecholamine (CA) secretion.2. Haemorrhage and hypoglycaemia, but not acute exposure to cold or intravenous administration of cocaine, induced considerable increases in total catecholamine secretion.3. The ratio of the concentration of adrenaline to noradrenaline in adrenal vein plasma during the control period was higher than the ratio in the adrenal gland itself.4. Haemorrhage increased noradrenaline secretion considerably more than adrenaline secretion so that the ratio of the concentration of adrenaline to noradrenaline in adrenal vein plasma was significantly lower than in the adrenal gland itself.5. Hypoglycaemia induced by insulin increased catecholamine secretion, with the adrenaline to noradrenaline ratio significantly higher than in the adrenal gland itself.6. Hypothermia resulted in a fall of the initial high ratio of adrenaline to noradrenaline, to a value similar to that in the adrenal gland.7. Neither cocaine nor changes in adrenal plasma flow affected the adrenaline to noradrenaline ratio in adrenal vein blood.8. It is concluded that preferential release from the adrenal gland of either adrenaline or noradrenaline is possible in vivo in response to different stimuli.