Mechanism of hypothalamic control of cardiac component of sinus nerve reflex.

The modulatory influence of hypothalamic structures on sinus nerve induced bradycardia was investigated in anaesthetized cats. Stimulation of the hypothalamic defence area inhibits the bradycardia produced by sinus nerve stimulation both in intact animals and also in animals with the spinal cord sectioned at C1 or C6. This inhibition was accompanied in the normal animal by an increased sympathetic discharge and by a sustained inspiration or tachypnoea. The same respiratory effects were noted in a spontaneously breathing C6 spinal animal, while an artificially ventilated C1 spinal animal still displayed a powerful central inspiratory drive in its recurrent laryngeal electroneurogram. The presence of central inspiratory activity was found to be an absolute impediment to the development of bradycardia. If this activity was eliminated by simultaneous stimulation of the superior laryngeal nerve, it was possible to obtain bradycardia during combined sinus nerve and hypothalamic defence area stimulation, though this bradycardia was modified by the presence of sympathetic discharge. The level of sympathetic neural discharge affects the magnitude of the bradycardia produced by sinus nerve stimulation. The bradycardia was less with normal or augmented level of sympathetic activity and was greater if this activity was reduced or absent. A lesion just caudal to the mammillary bodies disclosed a tonic hypothalamic influence both on respiration and on sympathetic discharge; stimulation of the sinus nerve produced a much more powerful bradycardia after the lesion. The existence of a respiratory "gate" through which afferent stimuli pass on their way to the nucleus ambiguus, and which can be operated by the hypothalamic defence and depressor areas, is postulated and discussed.

Rate of release of hepatic triacylglycerol into serum in the starved rat.

After an intravenous injection of a pulse of [U-14C]palmitate to starved rats, the time-dependent radioactivity profiles were determined in the triacylglycerol (triglyceride) of hepatic microsomal fractions, floating fat, mitochondria and nuclei. The profile of activity in serum gave a value of 0.08 mg/min per 100 g body wt. for the irreversible disposal rate of triacylglycerol from serum. This value, combined with the previously estimated rate of movement of triacylglycerol from serum to liver, and the reported rate from intestine to serum, gave a calculated value of 0.35 mg/min per 100 g body wt. for release rate of triacylglycerol from liver to serum. The rate of release of hepatic triacylglycerol into serum was also measured by the widely used Triton WR-1339 method. The rate obtained with this technique (0.15 mg of triacylglycerol/min per 100 g body wt.) was identical with that reported previously. During the interval from 45 min to 3h after ethanol administration this rate increased to 0.18 mg/min per 100 g body wt. It was concluded that the use of Triton underestimates the true rate of movement of triacylglyerol from liver to serum.

Electrical activity in sympathetic fibres to hind limb muscles of the cat produced by hypothalamic stimulation.

Electrical stimulation of the "Defence Area" of the hypothalamus in anaesthetized cats was accomplished by stereotaxic placement of bipolar stainless steel electrodes; the spinal cord was sectioned at L4. The muscle blood flow in one hind limb was recorded with an electromagnetic flowmeter. Increases of between 100% and 300% were observed during hypothalamic stimulation. Electroneurographic recordings from small nerve filaments supplying tibialis anterior muscle revealed two populations of neurones whose activity was abolished by lumbar sympathectomy. It appears that the increased blood flow in skeletal muscle during stimulation of the hypothalamic "Defence Area" is brought about by a simultaneous inhibition of vasoconstrictor activity and increase in cholinergic vasodilator discharge.