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A lung-inflation reflex carried through vagus nerve sensory pathways that inhibits inspiration. It was described in 1868 by Ewald Hering and Josef Breuer, after the 1867 examination.

The nervous system regulates visceral movement, glandular secretion, blood flow and coordinated bodily responses, while also influencing nutrition indirectly through those functions. Organic or vegetative life here means activities maintaining the body, such as blood circulation, digestion, pulmonary ventilation, secretion and excretion. It does not designate an independent form of living substance.

One influence is directly motor. Autonomic nerves alter the rate and force of the heart, contract or relax smooth muscle in the intestine, urinary bladder, airways and blood vessels, and coordinate movement with the opening and closure of sphincters. Their effect need not be excitatory: an active vagus nerve can slow the heart, while other pathways accelerate it. In the modern account, sympathetic and parasympathetic effects depend on the target and its receptors; they are not respectively universal accelerator and brake systems. Some organs receive both divisions, while others do not have a simple balanced double supply.^[ref]

A second influence is secretomotor. Activity in appropriate nerves can increase salivary secretion, alter gastric acid secretion and promote sweating. This is distinguishable from moving a duct or changing its calibre. A convincing experiment collects a secretion from a cannulated duct while a nerve is stimulated, rather than inferring secretion from a change of colour or organ size. For example, stimulation of the chorda tympani can evoke fluid from the submandibular gland. The response depends on functioning secretory biological cells; the nerve communicates a command rather than supplying the material constituents of saliva.

A third influence is vasomotor. Changing the calibre of arterioles changes local vascular resistance and perfusion. The classic comparison of an ear before and after interruption of its cervical sympathetic supply illustrates loss of vasoconstrictor tone: the vessels dilate and the ear becomes warmer because more warm blood reaches it. Stimulation of the peripheral cut pathway can produce the converse vascular effect. Warmth therefore need not mean that the local nerves themselves generate more heat. Vascular control also changes the delivery of oxygen and nutrients to a gland or tissue, so it can modify function indirectly.

These outputs are organized by sensory feedback and reflexes. Distension of the intestine can evoke coordinated movement; changes in blood pressure or blood-gas composition influence heart rate and breathing. Local circuits in the enteric nervous system permit some digestive activity without an intact connection to the brain, while longer reflexes involve the spinal cord or brainstem. Central states also matter: the sight or expectation of food can initiate preparatory digestive responses, and fear can alter heart rate, sweating and visceral movement.^[ref]

Somatic motor activity also supports vegetative functions. Breathing uses the respiratory diaphragm and other skeletal muscles; swallowing and continence use coordinated skeletal muscle as well as smooth muscle. Thus organic function cannot be identified solely with the anatomical distribution of the sympathetic nervous system.

The historical idea of a direct trophic influence requires discrimination. A denervation region may change through loss of movement, altered perfusion, loss of protective sensation or changed secretion. Those observations alone do not establish a special nutritive fluid flowing down the nerve. Modern biology recognizes molecular signalling between nerves and their targets, as well as neuroendocrine signalling pathways: the hypothalamus can influence hormone release, and sympathetic input can evoke adrenal medulla secretion. These are mechanisms added to, rather than evidence for an undefined historical nutritive force. A useful experimental design measures the motor, vascular and secretory consequences separately before assigning a residual effect to direct trophic action.

Ordinary cantharides blisters owe their activity to cantharidin; other blistering methods act through different chemical irritants or through physical injury. There is no single substance common to every way of raising a blister.

In the standard historical preparations, the dried blister beetle supplies cantharidin. A plaster, blistering paper, blistering liquid, or cantharides vinegar is a different vehicle for delivering the same vesicant to the skin. Extracting the beetle into a liquid does not make the solvent the specific active principle. The 1867 British Pharmacopoeia includes Emplastrum cantharidis, Charta epispastica, Liquor epispasticus and Acetum cantharidis.^[ref]

Other historical means need separate explanations. Moist mustard develops an irritant volatile product, principally allyl isothiocyanate from black mustard; its usual intended effect is reddening, with prolonged exposure capable of more destructive injury. This differs from the fixed mustard seed oil: the irritant volatile product develops after moistening the powdered seeds.^[ref] Strong Ammonia acts as an alkaline irritant. Croton oil can produce an inflammatory and pustular eruption, which is not the same lesion as a clean cantharides blister. A sufficiently hot object or hot liquid raises a blister through thermal damage, without a medicinal active molecule. These differences matter because erythema, a fluid-filled blister, a pustule, and tissue destruction are not interchangeable endpoints.

For cantharidin, the modern tissue explanation involves loss of adhesion between epidermal cells, including disruption of desmosomes, with separation within the epidermis and accumulation of fluid. The blister is therefore a local lesion of cell adhesion accompanied by inflammation, rather than a pocket containing disease drawn from a remote organ. The FDA review describes this acantholysis and distinguishes it from the incompletely understood mechanism of clinical benefit in a particular modern indication.^[ref]

A nineteenth-century answer would usually describe two supposed routes to benefit:

Thus the demonstrable processes are local injury, inflammation, fluid exudation, and sensory stimulation; the broad historical claims of remote benefit require separate evidence. Current approved topical cantharidin use for molluscum contagiosum does not validate nineteenth-century blistering for diseases of internal organs. The modern label explicitly states that the mechanism of action in molluscum contagiosum is unknown and documents local skin reactions.^[ref]

The assertion is too absolute: a remedy can cause a distant response through a reflex or another intervening physiological change without first being absorbed into the blood. It is substantially right for the direct action of a circulating drug on a distant target, but does not describe every remote effect of treatment.

Three mechanisms should be distinguished:

The distinction is between transport of the medicinal substance and transmission of its consequences. A reflex transmits activity in neurons; a locally acting intestinal agent changes a physical condition; a circulating drug delivers molecules to its distant target. The same remedy may combine these routes, and an apparently rapid effect does not by itself settle which route caused it.

A useful experimental design would therefore compare remote responses with measurements of the agent in blood, and would test the proposed neural pathway separately. In an appropriate physiological preparation, recording the response while interrupting a relevant afferent pathway can test whether that pathway is necessary; preserving the circulation while interrupting nerve conduction distinguishes neural transmission from vascular transport. Conversely, a remote effect after vascular transfer supports a circulating agent, provided contamination and other transferred mediators are controlled. Failure to detect a drug is only as strong as the analytical detection limit.

Absorption is one route to remote action, not a universal prerequisite for every distant physiological consequence. The historical language “animal economy” means the functioning organism; it should not conceal the distinction between a direct pharmacological effect and a secondary physiological response.

A functional change in an organism following a stimulus. The response can occur remotely through reflexes without transport of the original stimulus to the responding tissue.