Mechanical distension appears to be one of the most powerful of all stimuli to excite rrrythmical contraction in involuntary muscular fibre.

Luchsinger observed distinct pulsation in the veins of a bat's wing twenty hours after the death of the animal, if artificial circulation was kept up. This appears to show that the power of rhythmical contraction resides in the muscular fibres of the veins, as it does in the nerveless apex of the frog's heart, and the contractile tissue of the medusa; but here also an external stimulus appears to be required to induce contraction. When the pressure by which artificial circulation was maintained fell to zero, the pulsation stopped, but if it were raised to forty or fifty centimetres of water, so as to distend the vascular wall, rhythmical pulsation again commenced. It appears possible, however, that when involuntary muscular fibre is perfectly healthy and possesses the highest degree of irritability, it may contract rhythmically without any extra stimulus. Thus Engelmann2 observed that the ureter, in which he could find no nerves at all, contracted rhythmically when freshly exposed, although it was not distended or subjected to any mechanical irritation; but if artificial respiration has been long kept up, and the animal is exhausted, so that the excitability of the ureter is diminished, then the effect of minimum distension in increasing its rhythm becomes very evident.

Cold causes the isolated non-striated muscles of animals to relax. Heat causes them to contract.3

The influence of heat and cold, however, does not seem to be constant, and in the non-striated muscle of frogs they have an opposite connection to that just described. It is probable that the different results may depend to a great extent upon the amount of heat or cold applied, and its relation to the condition of the tissues at the time of application; for mechanical stimulation has also an opposite effect, according to its amount; and while gentle stimulation of involuntary muscular fibre, such as that of the small blood-vessels, causes dilatation, more powerful irritation produces contraction.1

1 Langendorff, Archiv f. Anat. u. Phys. Physiolog., Abtg. 1886, p. 267.

2 Pfliiger's Archiv, 1869, Bd. 11, p. 251.

3 Luchsinger and Sokoloff, Pflilger's Archiv, Bd. 26, p. 465.

The influence of various drugs upon involuntary muscular fibre, as seen in the contraction of the blood-vessels, will be described when considering the circulation.

The Relation of the Contractile Tissue to the Nerves is different in voluntary and involuntary muscular fibre. In the latter there are no end plates, but the terminal twigs form a plexus around the fibres. The motor nerves of involuntary muscular fibre appear to be affected by atropine and its congeners in a similar way to those of voluntary muscle by curare. There appears also to be a certain relationship between the atropine and curare group. Small doses of atropine paralyse the motor nerves of involuntary muscle, while very large doses of curare are required. The converse is the case with voluntary muscle. These effects are usually supposed to be due to a definite paralysing action on the nerves themselves. There are difficulties, however, in the way of this hypothesis, and a more probable one, perhaps, is that these drugs disturb the relations between the nerves and the muscular fibres which they excite. On the idea of a specific action it seems hard to explain the results obtained by Szpilman and Luchsinger,2 who found that atropine produces paralysis of the motor fibres of the vagi supplying the oesophagus, only in those parts of it where involuntary muscular fibre is present. Thus the oesophagus of the frog and the crop of birds consist of involuntary muscular fibre, and atropine destroys the motor power of the vagus over them. The oesophagus of the dog and rabbit contains striated muscular fibre, and atropine does not paralyse the motor nerves. The oesophagus of the cat contains striated muscular fibres in its upper three-fourths, and non-striated in its lower fourth; atropine destroys the motor action of the vagus upon the lower fourth, but not upon the upper part.3