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The Ottawa Charter for Health Promotion is used as a conceptual framework to examine the recommendations concerning prevention in the House of Commons' Report "Foetal Alcohol Syndrome: A Preventable Tragedy." Fetal alcohol syndrome cannot be separated from the complex social, physical and economic environments affecting alcohol consumption. For substantial progress to be made in preventing this significant cause of mental handicap, it will be necessary to consider a wide range of preventive actions, beyond public education and mandatory warning labels on alcoholic beverages. A health promotion framework offers a comprehensive, intersectoral approach to this problem.

The consumer-driven Heart Smart Restaurant Program was developed by the Heart and Stroke Foundation of Saskatchewan and the Saskatoon Community Health Unit, with the aim of improving the nutritional quality of food consumed in table-service restaurants. To participate, restaurateurs must agree to provide smoke-free seating and specific more healthful food choices upon request of the customer. The program was evaluated through telephone interviews with 999 individuals in randomly selected households in Saskatoon and Regina. While public awareness of the program was satisfactory, over half of those who knew of the program misunderstood its function, believing that more healthful choices are indicated on the menu. When choosing a restaurant, individuals are not greatly influenced by whether it is Heart Smart, but in Saskatoon, they are more likely to request a more healthful alternative in a Heart Smart restaurant than in others. Implications of these and other findings for future program development and research are discussed.

1. The ability of the selective dopamine receptor agonists, fenoldopam and SKF38393 (D1) and quinpirole and LY163502 (D2), to mimic the effect of dopamine on cockroach salivary gland acinar cells has been investigated. 2. Intracellular recordings of the membrane potential established that all the agonists mimicked dopamine (i.e. they induced a hyperpolarization which was occasionally followed by a depolarization), whether applied by addition to the superfusate or locally by pressure ejection. 3. The rank order of potency of the agonists to induce a hyperpolarization was (equipotent molar ratio relative to dopamine in parentheses): dopamine (1) much much greater than fenoldopam (1000) greater than SKF38393 (3500) greater than LY163502 (13750) greater than quinpirole (35000). 4. The agonists also elicited secretion from the salivary gland when superfused onto the preparation. SKF38393 and quinpirole did not induce the same maximum rate of secretion as dopamine. The rank order of potency of the agonists was (minimum effective concentration in parentheses): dopamine (0.03 microM) much much greater than fenoldopam (4.8 microM) greater than SKF38393 (40.8 microM) greater than quinpirole (132 microM). 5. Both the hyperpolarizing and secretory responses to all the agonists were antagonized by the selective D1 antagonist, (+)-SCH23390, but not the selective D2 antagonist, (+/-)-sulpiride. 6. These results support the idea that the same receptors mediate both the hyperpolarizing and secretory responses, and that they are similar to the mammalian D1 receptor.

The effects of domperidone on the electrical response of the cockroach salivary gland to applied dopamine and to nerve stimulation have been investigated. Dopamine and nerve stimulation induced a hyperpolarization of the salivary gland acinar cells, which was occasionally followed by a depolarization. At 1 and 10 microM domperidone had no effect on the responses; however, at higher concentrations domperidone (50 and 100 microM) potentiated the hyperpolarization induced by both dopamine and nerve stimulation. Domperidone (50 microM) also potentiated the hyperpolarization induced by 5-HT. Thus the potentiation probably results from a post synaptic action independent of either the dopamine or 5-hydroxytryptamine receptor. In addition, domperidone (50 and 100 microM) had two delayed effects; one, presynaptic, led to a reduction in the response to nerve stimulation; the other, postsynaptic, led to the abolition of the depolarizing phase of the response.

1. Intracellular recordings have been made of the hyperpolarization of cockroach salivary gland cells induced by nerve stimulation and dopamine. 2. The relative potency of a number of dopamine antagonists in inhibiting the dopamine- and nerve-mediated hyperpolarization was studied. SCH23390 (10-50 microM), chlorpromazine (0.1-5 microM), haloperidol (10-100 microM) and metoclopramide (1 mM) inhibited the hyperpolarization. 3. In contrast, domperidone and (+/-)-sulpiride potentiated the hyperpolarization induced by both nerve stimulation and dopamine. 4. Apparent dissociation constants (KDapp) were obtained for the blockade of the dopamine-induced hyperpolarization. The rank order of potency (KDapp in parentheses) was as follows: chlorpromazine (0.2 microM); haloperidol (3.3 microM); SCH23390 (4.1 microM); metoclopramide (265 microM); domperidone and (+/-)-sulpiride (inactive). 5. It is concluded that the receptor subserving the dopamine-induced hyperpolarization of the salivary gland acinar cells is the same as that mediating the secretory response to dopamine. In addition these data support our findings, which suggested that this receptor is similar to the D1 dopamine receptor, but distinct from the D2 receptor found in mammalian systems.

1. A study has been made of the potency of a number of dopamine antagonists to inhibit dopamine-induced secretion from the cockroach salivary gland in vitro. 2. Chlorpromazine (0.5-5 microM), SCH23390 (10-100 microM), haloperidol (10-100 microM) and metoclopramide (2 mM) competitively inhibited the secretory response to dopamine. In contrast (+/-)sulpiride (1-100 microM) and domperidone (1-100 microM) had no effect on either basal or dopamine-induced secretion. 3. Apparent dissociation constants (KDapp) were obtained using a 'three point assay'. The rank order of potency (KDapp in parentheses) was as follows: chlorpromazine (0.2 microM) greater than SCH23390 (2.2 microM) greater than haloperidol (17.5 microM) much greater than metoclopramide (1.2 mM). 4. It is concluded that the receptor mediating dopamine-induced secretion in the cockroach salivary gland is similar to the D1/DA1 dopamine receptor and distinct from the D2/DA2 receptor found in mammalian systems.

The effects of Org 9426 (the 2-morpholino, 3-hydroxy, 16N-allyl pyrrolidino analogue of vecuronium) were studied in anaesthetized cats and pigs and in isolated nerve--muscle preparations using tension and intracellular recording techniques. In isolated preparations, the effects of Org 9426 were antagonized by neostigmine. No contracture of the chick muscle preparation occurred. Org 9426 reduced the amplitude of endplate currents (EPC) in rat and snake muscle, but had no major effects on EPC decay characteristics, indicating a lack of endplate channel blocking action. In anaesthetized animals, no fasciculations were observed and the neuromuscular block was associated with tetanic and train-of-four fade and was antagonized by neostigmine. In anaesthetized cats and pigs, Org 9426 was approximately 20% as potent as vecuronium, its onset of action was twice as rapid as that of vecuronium in the cat and its duration of action was similar to that of vecuronium in both cats and pigs. It blocked the bradycardia produced by vagal stimulation only in doses greater than those necessary to produce neuromuscular block (ratios 7.2 in the cat and 4.4 in the pig--10-14% of the corresponding ratios for vecuronium). Ganglion block was seen only at doses several times those producing vagal block. In general the effects of Org 9426 on the cardiovascular system were slight, a small depressor effect occurring at high doses in the cat. The 17-hydroxy analogue, the potential metabolite of Org 9426, was approximately 20 times less potent than Org 9426 and is thus unlikely to contribute to the neuromuscular block produced by the parent compound.

This paper is a review of 105 acute spinal cord injured patients treated on the Roto-Rest Mark I hospital bed during a 42-month period at the South Florida Regional Spinal Cord System at the Jackson Memorial Hospital in Miami and the Miami Veterans Administration Hospital Spinal Cord Injury Center. The authors observed that Kinetic Nursing was effective in reducing commonly occurring complicatings in pulmonary, cardiovascular, skin, musculo-skeletal, nervous, gastro-intestinal, and genito-urinary systems. Of special interest in the patient group was the unique ability to maintain spinal stability while mobilising these acutely injured patients in the Roto-Rest bed.

1 Drugs which release or modify the response to catecholamines were examined for their effect on the permeability of the mouse peritoneal vascular bed to circulating plasma albumin, labelled with Evans blue.2 Phenoxybenzamine, phentolamine, piperoxane, yohimbine or cocaine reduced the extravasation of Evans blue into the peritoneum, an effect which was antagonized by beta-adrenoceptor blocking drugs. The inhibitory effect of desipramine on the extravasation of Evans blue was less completely antagonized by beta-adrenoceptor blockade.3 Inhibition of catecholamine biosynthesis, ganglion blockade or adrenergic neurone blockade antagonized the reduction in dye extravasation by alpha-adrenoceptor blocking agents and cocaine, but had no significant effect on the response to desipramine. The inhibitory effects of alpha-adrenoceptor blocking agents on dye extravasation were not prevented by bilateral adrenalectomy.4 Mice subjected to the procedure for estimation of vascular permeability excreted increased amounts of adrenaline and noradrenaline. Pretreatment with phenoxybenzamine, piperoxane or cocaine further increased catecholamine excretion, but desipramine caused only a small increase in catecholamine excretion which did not correlate with its effect on dye extravasation.5 It is suggested that phenoxybenzamine, phentolamine, piperoxane and cocaine reduce vascular permeability in the mouse peritoneum by releasing and/or potentiating the effects of endogenous catecholamines on beta-adrenoceptors. Endogenous catecholamines do not appear to be involved in the anti-inflammatory activity of desipramine.

The accumulation of 125I-labelled serum albumin and 51Cr-labelled erythrocytes was measured in mouse paw oedema induced by bradykinin or by heating the paw at 46.5 degrees. The extravasating fluid in bradykinin oedema consistently contained 50% of the albumin concentration of plasma, whereas the extravasating fluid induced by thermal injury initially had a low albumin content, but it progressively increased over a period of 30-40 min to equal albumin levels in plasma. Thermal injury also caused the extravascular accumulation of erythrocytes. Errors involved in attempting to measure the albumin content of the additional extravascular fluid in inflammation are discussed. Adrenaline suppressed bradykinin oedema, but potentiated thermal injury. These results do not support the view that bradykinin is the inflammatory mediator in thermally-induced oedema.

The issues of responsibility for health and control of factors influencing health are discussed with regard to workplace health programs. The role of each of the parties involved - workers, unions, management, and the government - can best be understood in relation to the interests they hold in workers' health. A matrix is presented which divides influences on workers' health according to the degree to which they are controlled by employers and workers. This matrix is used to suggest that workplace health promotion and employee assistance programs may represent employer involvement in areas over which they lack legitimate control. These programs are also criticized for their emphasis on behavior and their neglect of work-related causes of ill health and unhealthy behavior. They should be considered supplemental to a work environment which is conducive to both physical and psychosocial health; they will be most effective and appropriate with a high degree of worker involvement and control. Evidence regarding the effects of occupation and class on health and health-related behavior is presented to support the need for a comprehensive, ecological approach to workers' health. Such an approach should take into account the full range of influences and recognize the limits of legitimate control.

1 Thermic oedema induced by heating rat paws at 46.5 degrees C was potentiated by local injection of adrenaline, noradrenaline or high doses of isoprenaline. The pro-inflammatory effect of sympathomimetic amines was antagonized by phenoxybenzamine or phentolamine but not by propranolol.2 The subcutaneous space of heated rat paws was perfused with Tyrode solution and the perfusate collected and assayed for bradykinin, bradykininogen, kinin-forming activity and kininase activity. When adrenaline (0.5 mug/ml) was included in the perfusion fluid, kininase activity of the perfusate was increased by 76% and free bradykinin reduced by 46%.3 Increased vascular permeability induced by injection of bradykinin or kallikrein was reduced by adrenaline or noradrenaline, but isoprenaline had no significant effect.4 Pretreatment with soya bean trypsin inhibitor (SBTI) or heparin did not antagonize the pro-inflammatory effect of adrenaline or thermic oedema per se.5 Potentiation of thermic oedema similar to that induced by sympathomimetic amines was obtained by injecting paws with vasopressin prior to heating, or by applying a ligature to stop blood flow to the paw for the first 15 min of heating.6 Thermistor probes inserted beneath the paw skin showed that sympathomimetic amines increased the internal temperature of heated paws. This was significant, as small changes in temperature had a marked effect on the development of thermic oedema.7 It is suggested that sympathomimetic amines potentiate thermic oedema of rat paws heated at 46.5 degrees C by reducing blood flow to the paw, thereby causing a greater rise in paw temperature and consequently greater injury.

1. The effects of vesamicol (2-(4-phenylpiperidino) cyclohexanol), an inhibitor of acetylcholine storage, and its two optical isomers have been studied on neuromuscular transmission in rat and frog muscle, and on nerve conduction in frog nerve. 2. Racemic vesamicol produced a pre-block augmentation of twitch tension that also occurred in directly-stimulated muscle. This effect is thus at least partially due to an increase in muscle contractility. 3. (-)-Vesamicol was approximately 20 times more potent than (+)-vesamicol in blocking twitches elicited at 1 Hz. This degree of stereoselectivity is similar to that measured for inhibition of acetylcholine uptake by isolated synaptic vesicles. Both enantiomers were equally weak in reducing nerve action potential amplitude in frog nerve. 4. Further studies with the active isomer, (-)-vesamicol, showed that, like that produced by racemic vesamicol, the neuromuscular block was highly frequency-dependent. The block was not reversed by choline or neostigmine, but was partially reversed by 4- or 3,4-aminopyridine. 5. Preliminary electrophysiological studies showed that vesamicol reduced miniature endplate potential amplitude in rapidly-stimulated frog nerve-muscle preparations. Addition of lanthanum ions increased the frequency of miniature endplate potentials and led to the appearance of apparently normal-sized potentials amongst those of reduced amplitude. 6. The results show the close agreement between pharmacological and biochemical observations indicating the suitability of the rat diaphragm as a test model for substances of this nature. The degree of reversibility of the vesamicol-induced neuromuscular block by aminopyridines was unexpected, and it is suggested that in the presence of a drug which greatly increases release, a pool of acetylcholine is capable of being released which is not normally releasable after block of storage by vesamicol. It is also considered possible that the results from the intracellular recording studies may be explained in these terms.