SUMMARY1. Activity of the paraventricular nucleus neurones was recorded by micro-electrodes during resting conditions and while various osmotic, chemical, direct and indirect neural stimuli were applied. This activity was correlated with evidence of oxytocin release by recording milk ejection responses.2. Seventy-four per cent of all paraventricular nucleus neurones were osmosensitive in that firing was augmented following close arterial injection of hypertonic solutions (1 ml. lM-NaCl in 10-15 sec). A very few neurones showed decreased activity and in twenty-two per cent no change at all occurred following injection. Evidence indicated that the observed depressions ofcellular firing rate were due to other than osmotic stimulation.3. In post-partum cats an osmotically-induced neurone discharge increase was accompa'hied by a milk ejection response equivalent to that produced by 2-3 m-u. of oxytocin. 4. Paraventricular neurones were also sensitive to acetylcholine. Intracarotid injections of ,tg of acetylcholine greatly increased discharge rates and caused a very definite milk ejection response.5. Stimulation of the nipples by gentle suction, but not by electrical shock, and distension of the uterus in post-partum cats increased unit discharge in the paraventricular nucleus and evoked a milk ejection response.6. Neurones of the paraventricular nucleus, unlike those of the supraoptic nucleus, did not appear to be specifically responsive to electrical stimulation of skin and muscle afferent or of central nervous structures. Such stimuli did cause slight augmentations or depressions in firing rates of cells within and adjacent to the paraventricular nuclei, but many neurones were unaffected. Stimuli such as those applied appeared to have
Persisting alternation in mechanical response of the ventricle, pulsus alternans, develops when the heart is driven above certain rates. This critical rate varies, but tends to occur between rates of 200 and 300 beats/min. The ventricle can be driven slightly faster (10–20 beats/min) by direct than by indirect drive, through atrial electrodes, without showing pulsus alternans. There is a rate "threshold" for persisting alternation which represents the rate limits of compensation. Alternation appears at lower rates but the contractile process can gradually accelerate and alternation disappears even in denervated hearts and after adrenalectomy. Slower progressive accelerations delay onset of pulsus alternans and compensation occurs more quickly than when stepwise rate changes are made. Fast drives above the threshold for pulsus alternans can produce some additional acceleration of the contraction-relaxation process: if the rate is reduced to a level which previously produced a persisting alternation, pulsus alternans does not occur for a number of seconds. The resemblances of these phenomena to "treppe" and "postextrasystolic potentiation" and implications relative to catecholamine release and action are discussed.
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