We applied trains of stimuli to the vagosympathetic trunks of anesthetized dogs and studied the time courses of the resultant chronotropic and inotropic responses. These responses were maximum soon after the onset of the test stimulus train but then declined over the next 1-5 min despite continued stimulation. The fade ratio was defined as the magnitude of this decline divided by the magnitude of the maximum response. For both inotropic and chronotropic responses, maximum increased with stimulation frequency, but the fade ratio did not change. In some experiments, conditioning stimulus trains of variable duration were applied before a standard rest period, after which the test stimulus train was applied. The longer the conditioning period, the lower was the subsequent fade ratio of the inotropic responses to the test stimulation train. In other experiments, a conditioning train of 2 min was applied, and then variable rest periods were interposed before the test train was applied. The longer the rest period, the greater were the subsequent maximum and fade ratios of the inotropic responses to the test stimulus train. These results indicate that some factor persists well after the cardiac responses to a given stimulus, and this factor affects the next response to an identical vagal stimulation. The chronotropic responses faded about three times faster than the inotropic responses. Thus different mechanisms may account for the fade of the inotropic and chronotropic responses.

No abstract

SUMMARY When identical, successive single vagal stimulations, separated in time (T) by 2-60 seconds, are applied in the dog, the peak change in atrioventricular conduction time for the second stimulus, AAV 2 , is less than that of the first, AAV,, that is, the ratio AAV 2 /AAV, < 1.0 (the mean minimum AAV 2 /AAV, = 0.52). It was further determined that at any one given T, the actual value of AAVj/AAV, also was a function of the first stimulus amplitude. The same dependence of A AV 2 /AAV, on the first stimulus amplitude was found when the amplitude was varied either by (1) changing the number of vagal fibers stimulated for both the first and second response, but at a constant AD (the delay in the cardiac cycle at which the stimulus was given), or (2) by stimulating the same number of fibers but changing AD for both the first and second response. Also the same characteristic of AAV 2 /AAV, plotted vs. T was found either (1) when both the first and second responses were produced by stimulation of the same nerve, or (2) when stimulation of the nerve from one side produced the first response and the alternate side the second response. These data suggest that the reason for this AAVj/AAV, time-dependent effect lies in changes in receptor responsiveness or in acetylcholine inactivation, but not in mechanisms purely internal to the nerve terminal associated with synthesis, storage, or release of acetylcholine.WHEN A TEST stimulus is applied to the vagus nerve after a conditioning stimulus, the increment in cardiac cycle length or atrioventricular conduction time produced by the test stimulus may be considerably less than that produced by the first (conditioning) stimulus. This has been found both for a single stimulus 1 and for pulse trains. 2 -3 In this study these conditioning phenomena were explored in an effort to analyze the mechanism by which they are produced. MethodsExperiments were conducted on 18 mongrel dogs (10-15 kg) of both sexes; 16 yielded satisfactory results (in the other two dogs the responses to a repeated standard test stimulation of the vagus decayed to too great an extent with time to be usable). The dogs were anesthetized with morphine sulfate (2 mg/kg, im), followed 30 minutes later by chloralose dissolved in polyethylene glycol (75 mg/kg, iv).Both cervical vagosympathetic trunks were dissected free from surrounding tissues, crushed, and ligated centrally. Either the left trunk, or both left and right trunks, were connected to a bipolar shielded electrode (Grass) at a point distal to the ligature. /9-Adrenoreceptors were blocked with propranolol (1.0 mg/kg, iv) to abolish the effects of stimulation of cardiac adrenergic fibers contained in the vagosympathetic trunk. Adequacy of blockade was confirmed in selected dogs at 1-hour intervals by noting the absence of cardiac responses to periodic maximal stimulation of the right stellate ganglion. The heart was paced continually throughout the experiment at a rate just above the spontaneous rate; usually the paced cycle length ranged from 400 to 550...

The National Health Service has undergone significant reforms in recent years. A consequence of these reforms has been to recast the relationship between service providers (Trusts) and educational providers (University Departments). This relationship is increasingly formalized through contractual processes and the ability of University Departments to respond promptly to identified needs within Trusts may become inhibited. As a Trust employee the Educational Facilitator can provide practice-led educational initiatives utilizing the resources found within the clinical environment. Such initiatives would be in accord with Trust objectives and be put into operation with ease. The current role of the educational facilitator is explored with key role components and functional areas identified. The paper concludes with a consideration of the role in the development of professional knowledge and strategies for knowledge development.

No abstract