A comparison of animated versus static images in an instructional multimedia presentation.

Sophisticated three-dimensional animation and video compositing software enables the creation of complex multimedia instructional movies. However, if the design of such presentations does not take account of cognitive load and multimedia theories, then their effectiveness as learning aids will be compromised. We investigated the use of animated images versus still images by creating two versions of a 4-min multimedia presentation on vascular neuroeffector transmission. One version comprised narration and animations, whereas the other animation comprised narration and still images. Fifty-four undergraduate students from level 3 pharmacology and physiology undergraduate degrees participated. Half of the students watched the full animation, and the other half watched the stills only. Students watched the presentation once and then answered a short essay question. Answers were coded and marked blind. The "animation" group scored 3.7 (SE: 0.4; out of 11), whereas the "stills" group scored 3.2 (SE: 0.5). The difference was not statistically significant. Further analysis of bonus marks, awarded for appropriate terminology use, detected a significant difference in one class (pharmacology) who scored 0.6 (SE: 0.2) versus 0.1 (SE: 0.1) for the animation versus stills group, respectively (P = 0.04). However, when combined with the physiology group, the significance disappeared. Feedback from students was extremely positive and identified four main themes of interest. In conclusion, while increasing student satisfaction, we do not find strong evidence in favor of animated images over still images in this particular format. We also discuss the study design and offer suggestions for further investigations of this type.

Concentrations of salivary testosterone, cortisol, and immunoglobulin A after supra-maximal exercise in female adolescents.

The aim of this study was to examine the effect of supra-maximal exercise on circulating concentrations of salivary testosterone, salivary cortisol, and salivary immunoglobulin A in female adolescents. Nineteen apparently healthy females aged 15-16 years participated in this study. All participants completed 668 s sprints, interspersed with 30 s recovery intervals on a cycle ergometer. Salivary testosterone, cortisol, and immunoglobulin A samples were taken before and 5 min after exercise. Experimental procedures continued over two mornings, at least 3 h after a light breakfast. Participants refrained from performing any strenuous physical activity for at least 24 h prior to the exercise test. None of the participants were engaged in a structured training programme. The group mean (± s) for peak power output was 562 ± 113.0 W. Female adolescents recruited for this study showed no changes in salivary testosterone, cortisol or immunoglobulin A following repeated bouts of supra-maximal cycling (P > 0.05). To date, there has been a paucity of information concerning adolescents' hormonal and mucosal immune function responses to supra-maximal exercise. Our data provide further guidance with regard to physical activities and sports prescription for female adolescents. Further research, on a larger sample of females, is required to elucidate the physiological significance of these findings.

Contributions of alpha 1-adrenoceptors, alpha 2-adrenoceptors and P2x-purinoceptors to neurotransmission in several rabbit isolated blood vessels: role of neuronal uptake and autofeedback.

1. The roles of autofeedback and neuronal uptake in neurotransmission produced by electrical field stimulation in several rabbit isolated blood vessels were examined. 2. Blocking drugs were used to separate the possible purinergic and noradrenergic contributions to the end organ response: prazosin, antagonist at postjunctional alpha 1-adrenoceptors; rauwolscine and yohimbine, antagonists at pre- and postjunctional alpha 2-adrenoceptors; alpha,beta-methylene ATP, desensitizing agent at postjunctional P2x-purinoceptors. In addition to desensitizing postjunctional P2x-purinoceptors, alpha,beta-methylene ATP potentiated the noradrenergic component of the nerve-induced responses. 3. In the presence of an intact neuronal uptake mechanism, the vessels showed different contributions of purinergic (via P2x-purinoceptors) and noradrenergic (via alpha 1-adrenoceptors and alpha 2-adrenoceptors) components to the end organ response to nerve stimulation: saphenous artery (approximately equal contributions from P2x-purinoceptors and alpha 1-adrenoceptors), ileocolic artery (mainly P2x-purinoceptors with a smaller contribution from alpha 1-adrenoceptors), plantaris vein (mainly alpha 1-adrenoceptors with a small contribution from alpha 2-adrenoceptors and P2x-purinoceptors) and saphenous vein (alpha 1-adrenoceptors). 4. The presence of alpha 2-adrenoceptor-mediated autofeedback could be demonstrated for both purinergic and noradrenergic components of the nerve-induced responses in the artery preparations. In the veins, potentiation of nerve-induced responses by alpha 2-adrenoceptor antagonists could not be studied due to blockade of postjunctional alpha 2-adrenoceptor-mediated vasoconstriction. 5. Blockade of neuronal uptake with cocaine potentiated the noradrenergic component of the nerve-induced responses. Both alpha 1-adrenoceptor- and alpha 2-adrenoceptor-mediated components were potentiated, with a relatively greater potentiation of the alpha 2-adrenoceptor-mediated component. In the case of saphenous vein an alpha 2-adrenoceptor-mediated component which was previously absent was uncovered.6. Blockade of neuronal uptake with cocaine had no effect or reduced the purinergic component of responses, the latter effect presumably due to enhanced alpha 2-adrenoceptor-mediated autofeedback.7. In the presence of cocaine, nerve-induced responses in the saphenous vein were biphasic. Rauwolscine potentiated the first phase and inhibited the second phase thus demonstrating effects of pre- and postjunctional alpha 2-adrenoceptor-mediated activation in the same preparation.8. In conclusion, neuronal uptake and autofeedback processes play important and complex interacting parts in determining the relative contributions of alpha 1,- and alpha 2-adrenoceptors and P2.-purinoceptors in the end organ response to neurotransmission in blood vessels.

The effect of ethanol on responses of the isolated rabbit ileocolic artery.

Antagonist drugs were used to separate the purinergic and adrenergic contributions involved in the sympathetic vasopressor responses produced by electrical field stimulation in the ileocolic artery of the rabbit. Blocking drugs were applied either alone or in various combinations and sequences. The effect of ethanol was studied in conditions of alpha-adrenoceptor blockade, P2x purinoceptor desensitisation, or in the absence of antagonists. From these studies it is concluded that ethanol has a selective potentiating effect on alpha-adrenoceptor-mediated responses.

Different sensitivities of rabbit isolated blood vessels exhibiting co-transmission to the slow calcium channel blocker, nifedipine.

1. Antagonist drugs were used to separate the purinergic and adrenergic contributions as well as the adrenoceptor sub-types involved in the sympathetic vasoconstrictor responses produced by electrical field stimulation in rabbit isolated ileocolic and proximal saphenous arteries. Blocking drugs were applied either alone or in various combinations and sequences. 2. Nifedipine attenuated vasoconstrictor responses to sympathetic nerve stimulation both in the presence and in the absence of alpha-adrenoceptor blocking agents. However in the presence of alpha,beta-methylene ATP, nifedipine produces at best only a small attenuation of the vasoconstrictor response. 3. These results suggest that the purinergic component of the response to sympathetic nerve stimulation, at least in these tissues, can be antagonized by nifedipine, whereas the alpha 1-adrenoceptor-mediated response is relatively resistant.

Noradrenaline-ATP corelease and cotransmission following activation of nicotine receptors at postganglionic sympathetic axons.

In rabbit mesenteric arteries, nicotine-evoked vasoconstrictor responses were markedly reduced by prazosin, slightly reduced after desensitization by alpha, beta-methylene ATP, and abolished by combined treatment with prazosin and alpha, beta-methylene ATP. In guinea-pig vasa deferentia preincubated with [3H]noradrenaline, nicotine elicited contractions as well as an overflow of tritium and of ATP. The contractions were greatly reduced by prazosin and abolished after additional desensitization by alpha, beta-methylene ATP. The nicotine-induced overflow of tritium was not changed by either treatment. The overflow of ATP was decreased by prazosin but not diminished further after additional desensitization by alpha, beta-methylene ATP. Activation of prejunctional nicotine receptors elicits a corelease of noradrenaline and ATP which leads to cotransmission in both tissues.

Nucleotides as cotransmitters in vascular sympathetic neuroeffector transmission.

Postganglionic sympathetic cotransmission by noradrenaline (NA) and adenosine 5'-triphosphate (ATP) was studied in isolated arteries from rabbits using as tools alpha-adrenoceptor antagonists and alpha, beta-methylene-ATP which first activates and then desensitizes purine P2X receptors. In the pulmonary artery, NA was the only chemical signal responsible for neurogenic vasoconstriction. In sharp contrast, ATP was the only signal eliciting electric as well as mechanical postjunctional responses in small jejunal arteries. Mixed adrenergic and purinergic transmission was found in the largest ramus caecalis of the ileocolic artery. The purinergic component prevailed in short pulse trains and early in long trains, whereas the adrenergic component prevailed in the late phases of long (20 s) trains. Prejunctional alpha 2-adrenergic autoinhibition markedly depressed purinergic as well as adrenergic transmission as soon as a latency of about 2 s was exceeded.

Presynaptic alpha 2-autoinhibition in a vascular neuroeffector junction where ATP and noradrenaline act as co-transmitters.

1. alpha 2-Autoinhibition of transmitter release was investigated in the largest rami caecales of the rabbit ileocolic artery. Vasoconstriction, elicited by electrical field stimulation or by exogenous agonists, was measured as an increase in perfusion pressure. 2. Short periods of electrical stimulation elicited monophasic vasoconstriction, whereas longer periods (greater than 10 s) produced biphasic vasoconstriction. Prazosin had no significant effect on the first component of the biphasic vasoconstriction elicited by electrical stimulation, but did reduce the second component at higher frequencies. alpha, beta-Methylene ATP significantly attenuated the first component whilst the second component was relatively resistant. 3. The alpha 2-adrenoceptor antagonist yohimbine did not change responses evoked by very short pulse trains (less than 2 s) but enhanced responses to longer pulse trains. When vasoconstriction was biphasic, both phases were potentiated by yohimbine. 4. The results indicate that the vasoconstriction elicited by brief trains of sympathetic nerve impulses is mainly or exclusively mediated by ATP, whereas at longer pulse trains a noradrenergic component comes into play. The potentiation produced by yohimbine is due to interruption of presynaptic alpha 2-adrenoceptor-mediated autoinhibition of transmitter release. The autoinhibition affects both purinergic and adrenergic components of sympathetic neurotransmission.

Selective blockade by nifedipine of 'purinergic' rather than adrenergic nerve-mediated vasopressor responses in the pithed rat.

1. Nifedipine can attenuate pressor responses to sympathetic nerve stimulation both in the presence and in the absence of alpha-adrenoceptor blocking agents. 2. In the presence of alpha,beta-methylene ATP, nifedipine produces only a small attenuation of the vasopressor response. 3. Nifedipine attenuates the vasopressor response produced by intravenous bolus administration of alpha,beta-methylene ATP. 4. The results suggest that the purinergic component of the vasopressor response to stimulation of the sympathetic outflow in the rat is subject to blockade by nifedipine, whereas the alpha-adrenoceptor-mediated response to co-transmitter noradrenaline is relatively resistant.

Blockade of vasopressor and vas deferens responses by alpha,beta-methylene ATP in the pithed rat.

1. The pressor responses produced by the intravenous administration of alpha,beta-methylene ATP were tachyphylactic. 2. alpha,beta-Methylene ATP can attenuate pressor responses to sympathetic nerve stimulation both in the presence and in the absence of alpha-adrenoceptor blocking agents. 3. alpha,beta-Methylene ATP has no effect on the pressor responses produced by bolus injections of noradrenaline. 4. In the presence of alpha-adrenoceptor blocking agents, alpha,beta-methylene ATP further attenuates contractions of the vas deferens produced by nerve stimulation. 5. The results, together with previous data, suggest that the vasopressor response to stimulation of the sympathetic outflow in the rat is partly purinergic and partly alpha-adrenergic and that this occurs as co-transmission. The same applies to rat vas deferens, confirming in vitro data. The pithed rabbit had an alpha-blocker-resistant vasopressor nerve-mediated response but this was resistant to alpha,beta-methylene ATP.

Difference in the potency of alpha 2-adrenoceptor agonists and antagonists between the pithed rabbit and rat.

The subtypes of alpha-adrenoceptors which mediate pressor responses to sympathomimetic agonists or to nerve stimulation in pithed rabbits have been classified according to the effects of 'selective' antagonists and a comparison has been made, for the alpha 2-subtype, with corresponding responses in the rat. In the rabbit the dose-response curve for phenylephrine was shifted to the right in parallel by prazosin (1 mg kg-1) and was unaffected by rauwolscine (1 mg kg-1). The dose-response curve for noradrenaline was shifted to the right by prazosin (1 mg kg-1) and was shifted to a smaller extent by rauwolscine (1 mg kg-1) or imiloxan (10 mg kg-1). After rauwolscine, prazosin produced a rightward shift larger than when given alone. After prazosin, rauwolscine produced a rightward shift larger than when given alone. The responses to pressor nerve stimulation at low frequencies (less than 1 Hz) could be reduced by prazosin, rauwolscine or imiloxan but those at a higher frequency could be reduced only by prazosin. These results indicate that the responses to noradrenaline or to nerve stimulation are mediated by both alpha 1- and alpha 2-adrenoceptors. Low doses or frequencies have a proportionately greater component which is alpha 2. Responses to noradrenaline after prazosin (1 mg kg-1), were sufficiently sensitive to rauwolscine to be considered as predominantly alpha 2. A comparison was therefore made of such responses in the rat and rabbit. They were produced by a lower dose per unit body weight in the rat whereas this was less marked for the alpha 2-adrenoceptor agonist guanabenz. In the rabbit they were more susceptible to blockade by rauwolscine but were less sensitive to Wy 26703 than in the rat. This demonstrates that the alpha 2-adrenoceptors mediating pressor responses in vivo, like those in other tissues in vitro, are different in rat and rabbit, with regard to antagonists.