Stimulation Of Sensory Nerve Endings Research Articles

Clinical Aspects and Cellular Mechanisms of Fascia, their Interactions, and Importance in Medicine

The fascial system is a 3D continuum of soft, collagen‐containing, loose and dense fibrous connective tissues, widely including adipose tissue, adventitiae and neurovascular sheaths, aponeuroses, deep and superficial fasciae, epineurium, membranes, joint capsules, ligaments, meninges, myofascial expansions, periostea, retinaculae, septa, tendons, visceral fasciae, and all the intramuscular and intermuscular connective tissues including endo‐/peri‐/epimysium. These muscle layers may seem distinct in 2D sections, but the borders are somewhat arbitrary when viewed as an extensive 3 D network, with connective tissue fibers extending both along and across muscle fibers. The fascial system interpenetrates and surrounds all organs, muscles, bones and nerve fibers, endowing the body with a functional structure, and providing an environment that enables all body systems to operate in an integrated manner. Fascia is traditionally named according to the discrete anatomic structure that it surrounds which obscures its continuity and distinct layers.Fascial tissue provides a structural framework, continuously adapting and transmitting mechanical and chemical signals to differentiate tissue. The continuum of fascia throughout the body allows it to serve as a body‐wide mechanosensitive signaling system. The extracellular matrix plays an essential role in the development of skeletal musculature in the embryo. Fascia is a composite material of collagen fibers and matrix. In outer layers of the extremities and neck, fibers are found in parallel directions oriented at 55 degrees to the layer underneath, similar to a garden hose, which resists pressure and remains flexible. In other layers, collagen fibers are less regular and may have a wavy or helical structure. Fascia may also vary in proportions of collagen type I, III, IV and V and in rate of turnover. Fascial structure has functional implications. For example, when one muscle contracts against a thick, resistant fascia layer, the compartment pressure increases, and this pumps blood and lymphatic fluid against gravity and raises the contractile efficiency of other muscles in the same compartment. A fiber connects a muscle to the nitric oxide receptor of its arteriole, which is pulled open during contraction to increase blood flow. Thoracolumbar fascia balances abdominal and spinal muscle tension.Fascia is gaining interest from researchers, physicians and many types of therapists. Manual therapy techniques treat the fascial layers by altering density, tonus, viscosity, and the arrangement of fascia. Manual stimulation of sensory nerve endings may lead to tonus changes in muscle. The fascial system is now being recognized in the etiology of pain and proprioception. Fascia research can help understand aspects of musculoskeletal problems such as myofascial trigger points, low back pain, and fibromyalgia. Connective tissue influences the normal or pathological processes in a wide variety of organ systems e.g. intramuscular connective tissue architecture changes after immobilization of an extremity.The mechanical interactions among muscle, tendon and fascia in humans developed over many thousands of years and allow us to adapt to a wide range of activities. We are just beginning to understand these enough to develop specific fascial exercises and activities.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Local Effect of Neurotrophin-3 in Neuronal Inflammation of Allergic Rhinitis: Preliminary Repor

Allergic rhinitis is a common inflammatory nasal mucosal disease characterized by sneezing, watery nasal discharge, nasal obstruction and itching. Although allergen-specific antibodies play a main role in the allergic airway inflammation, neuronal inflammation may also contribute to the symptoms of allergic rhinitis. Neuronal inflammation is primarily caused by the stimulation of sensory nerve endings with histamine. It has been shown that neurotrophins may also have a role in allergic reactions and neuronal inflammation. Nerve growth factor, neurotrophin 3 (NT-3), neurotrophin 4/5 and brain-derived neurotrophic factor are members of the neurotrophin family. Although nerve growth factor and brain-derived neurotrophic factor are well studied in allergic rhinitis patients, the exact role of Neurotrophin-3 is not known. To investigate the possible roles of neurotrophin-3 in allergic rhinitis patients. Case-control study. Neurotrophin-3 levels were studied in the inferior turbinate and serum samples of 20 allergic rhinitis and 13 control patients. Neurotrophin-3 staining of nasal tissues was evaluated by immunohistochemistry and ELISA was used for the determination of serum Neurotrophin-3 levels. Neurotrophin-3 staining scores were statistically higher in the study group than in the control patients (p=0.001). Regarding serum Neurotrophin-3 levels, no statistically significant difference could be determined between allergic rhinitis and control patients (p=0.156). When comparing the serum NT-3 levels with tissue staining scores, there were no statistically significant differences in the allergic rhinitis and control groups (p=0.254 for allergic rhinitis and p=0.624 for control groups). We suggest that Neurotrophin-3 might affect the nasal mucosa locally without being released into the systemic circulation in allergic rhinitis patients.

Action of rare earth metal complexes on neurogenic as well as on bradykinin-induced inflammation.

Abstract Both neurogenically evoked inflammation and that induced by bradykinin are not satisfactorily inhibited by the usual anti-inflammatory agents. It has been found that anticoagulant rare earth metal compounds inhibit these types of inflammation. In rats, neurogenic inflammation induced either by antidromic electrical stimulation of the saphenous nerve, or by orthodromic stimulation of sensory nerve endings with capsaicin could almost totally be prevented by a neodymium complex of pyrocatechol sodium disulphonate. In rats and rabbits a dose-dependent inhibition of the permeability increase was observed at the site of the injection of bradykinin, kallikrein or bothrops venom. Similarly, there was marked inhibition of “thermic oedema.” The results are in accord with the hypothesis that the blood clotting system plays an important role in the mechanism of inflammation.

Correlation between CGRP and Migraine Attacks

Any hypothesis regarding pain in primary headache disorders rests on the classic observations which describe painful sensations as a result of mechanical or electrical stimulation of large cerebral arteries, venous sinuses, and dural arteries, by Ray and Wolff (1). These pain-sensitive supratentorial structures are supplied by nerve fibres that arise in the trigeminal ganglion. The fibres and the cell bodies contain a number of messengers but calcitonin gene-related peptide (CGRP) is the one most frequently expressed (2). A role of the trigemino-cerebrovascular system in the transmission of nociceptive information to the central nervous system is thus a viable proposition. Antidromic or local mechanical stimulation of sensory nerve endings results in vasodilation via the release of vasoactive materials such as CGRP. The cell bodies are located in the trigeminal ganglion, they send sensory fibres to various cranial structures, and connect to the CNS via the trigeminal nerve. In primary headaches, there is a clear association between the headache and the release of CGRP, but not with any of the other neuronal messengers. The background and current status have recently been reviewed in the journal (3). Several primary headaches, such as migraine, cluster and chronic paroxysmal hemicrania, are associated with increased levels of CGRP in the jugular vein during pain (3). Furthermore, CGRP in the antecubital vein increases by 25–30% during nitroglycerin-induced migraine attacks and the increase in CGRP correlates markedly with the headache intensity (4). In the present issue of the journal Juhasz and colleagues (5) demonstrate that sumatriptan decreases the plasma CGRP concentration in the antecubital vein during migraine attacks elicited by nitroglycerin administration. This decrease was present only in those patients whose headache showed parallel clinical improvement. In those patients whose headache did not improve, the CGRP concentrations failed to show a decrease after the administration of nasal sumatriptan. Furthermore, plasma CGRP significantly correlated with headache scores after sumatriptan treatment. These results underline the close relationship of CGRP release and migraine headache (6).

Microarray analysis of gene expression in the subacromial bursa in patients with rotator cuff disease (SS-74)

The role of the subacromial bursa in the pathogenesis of rotator cuff disease is controversial. Initial histologic studies suggested that the bursa was a reparative tissue and was important in rotator cuff healing and repair. More recent reports have suggested that the subacromial bursa is an inflammatory membrane that can lead to shoulder pain through stimulation of afferent nerve endings and their products. The potential role of inflammatory cytokines and proteases in this process remain undefined. The present investigations were undertaken to determine the gene expression pattern of cells in the subacromial bursa in patients with rotator cuff disease. Materials and Methods: Following an IRB approved protocol, subacromial bursa biopsies were obtained intraoperatively from patients undergoing shoulder surgery and analyzed for the expression of cytokines and matrix metalloproteases (MMP). Analysis was performed for two primary rotator cuff repairs, two patients with revision rotator cuff repairs, and one patient undergoing surgery for shoulder instability was used as control. RNA was extracted from the samples using the RNeasy Fibrous Tissue Mini Kit and stored at −70°C. Complementary DNA-array hybridization was done using GE Array Q Series Kits for inflammatory cytokine/receptor genes. The arrays were hybridized with Biotin-dUTP labeled cDNA probes. Images of the bursal specimens were obtained by chemiluminescent detection on x-ray films. Data analysis and normalization was accomplished using ScanAlyze and GE ARRAY Analyzer software. Results: Matrix metalloproteinases (MMP-2, MMP-14, MMP-26, MT1-MMP) and tissue inhibitor of metalloproteinase (TIMP-1, TIMP-2, and TIMP-3) displayed increased expression in the subacromial bursa in both primary and revision rotator cuff repairs, though to a greater degree in revision repair samples. Tumor necrosis factor alpha and its receptor (TNFRSF1A) were slightly increased in subacromial bursa specimens with rotator cuff disease. While the receptors for IL-1B (IL-1R1) and IL-6 (IL-6ST) were increased in rotator cuff disease, IL-1B and IL-6 themselves were not increased. Members of the small inducible cytokine subfamily (SCYA2, SCYA5, SCYC2, SCYE1) genes were all increased in patients with rotator cuff disease. While these results represent trends in gene expression relative to controls, statistical significance could not be determined due to the small numbers of specimens. Discussion: While inflammation in the subacromial bursa has been proposed as the mechanism leading to pain in patients with rotator cuff disease, the exact roles of cytokines and other proteins during this inflammatory process are currently unknown. In these initial studies, gene expression as demonstrated by microarray analysis of cytokines (TNF, IL-1, SCY) and metalloproteases (MMP-2, TIMP) were found to be increased in patients with rotator cuff disease as compared to control. These data provide initial indication that cytokines and metalloproteases play an important role in the pathology of subacromial bursitis. Further investigation will emphasize the isolation and characterization of these genes.

Pathophysiology of nasal symptoms.

Symptoms are perceived by the patient and all nasal symptoms must eventually relate to stimulation of sensory nerves or some change in the activity of the CNS. Although it is the symptoms that are of prime importance to the patient, the role of sensory nerves and psychology in the generation and perception of symptoms has been relatively neglected compared to the large amount of research on inflammatory mediators. This paper discusses how physical and chemical changes in the nasal epithelium result in the generation of inflammatory mediators that are responsible for symptoms. Inflammatory mediators can cause symptoms in three ways. (1) By having direct action on glands and blood vessels to cause glandular secretion, vasodilation, increased vascular permeability, and transudation of a plasma exudate. (2) By stimulation of sensory nerve endings to cause reflex glandular secretion, sneezing, and sensations such as itching, irritation, pain, and pressure. (3) By effects on the central nervous system to cause, headache, fever, tiredness, and mood changes.

Changes in afferent impulse activity of small intestine mesenteric nerves in response to antigen challenge

Sprague–Dawley rats (weight 130–150 g) were sensitized by an intraperitoneal injection of 1 mg chicken egg albumin with 0.25 ml Freund's adjuvant to stimulate immunoglobulin E antibody production. Leukocyte migration inhibitory factor was used as an indicator of animal sensitization. In acute electrophysiological experiments on sensitized animals, an intra-arterial or intraluminal chicken egg albumin (100 μg) challenge evoked a 10% enhancement of the activity of mesenteric nerves of the small intestine, regardless of the injection site chosen. Afferent nerve activity in control animals was not changed during the chicken egg albumin challenge. Morphometry at the light microscope level showed activation of mast cell degranulation after the antigen challenge to presensitized rats. Intraluminal injections of a stimulator of mast cell degranulation, compound 48/80 (20–30 mg), were found to increase afferent discharges in intact rats. An antagonist of H 1 histamine receptors, clemastine, reduced the effect of compound 48/80. The results obtained provide direct evidence for the stimulation of sensory nerve endings by mast cell mediators released during mast cell degranulation.

Inhaled nicotine in humans: effect on the respiratory and cardiovascular systems

Inhalation of nicotine (0-64 mg/ml) and capsaicin (2 x 10(-6)-2.5 x 10(-4) M) in 24 healthy nonsmoking subjects produced a concentration-dependent cough response. Two subjects coughed to capsaicin but not to nicotine. The mean (95% confidence interval) nicotine concentrations causing two and five coughs were 5.5 (3.5-8.7) and 15.8 (10.0-25.1) mg/ml, respectively, and were reproducible over 3 different days. Capsaicin inhalation did not alter the response to nicotine and vice versa. Both agents increased respiratory resistance, but the response was more rapid to capsaicin. Inhalation of nicotine (0-8 mg/ml) over 5 min caused increases in heart rate and blood pressure and a decrease in skin temperature. Inhaled ipratropium bromide (0.50 mg) had an antitussive effect and also inhibited the nicotine-induced bronchoconstriction, indicating a vagally mediated effect. Sodium cromoglycate (0.20 mg) did not affect cough or airway resistance changes caused by nicotine. This study shows that inhaled nicotine produces a concentration-dependent cough and airway obstruction in healthy subjects, probably because of stimulation of afferent nerve endings in the bronchial mucosa and mediated through parasympathetic cholinergic pathways. Respiratory reflexes evoked by nicotine are similar to those produced by capsaicin, but it is unclear whether these reflexes are mediated by the same type of sensory nerves.

Role of Peptidergic Sensory Neurons in Gastric Mucosal Blood Flow and Protectiona

The present findings have revealed a new aspect of how mechanisms of gastric mucosal resistance to injury are called into effect and are coordinated by the nervous system. Capsaicin-sensitive sensory neurons in the stomach play a physiological role in monitoring acid influx into the superficial mucosa. Once activated, they strengthen gastric mucosal defense against deep injury, with a key process in this respect being an increase in blood flow through the gastric mucosa. This concept opens up completely new perspectives in the physiology and pathophysiology of the gastric mucosa if we consider that the long-term integrity of the gastric mucosa may be under the subtle control of acid-sensitive sensory neurons and that, vice versa, improper functioning of these neutral control mechanisms may predispose to gastric ulcer disease. The present observations also indicate that some of the peptides contained in gastric sensory nerve endings might fulfill a transmitter or mediator role in controlling gastric mucosal blood flow and integrity. Whereas substance P and neurokinin A are unlikely to play a role in the regulation of gastric mucosal blood flow, there is severalfold evidence that CGRP is very important in this respect. This peptide, which in the rat gastric mucosa originates exclusively from spinal sensory neurons, is released upon stimulation of sensory nerve endings and is extremely potent in facilitating gastric mucosal blood flow and in protecting the mucosa from injurious factors. Selective ablation of spinal sensory neurons containing CGRP weakens the resistance of the gastric mucosa against acid injury, which is most likely due to inhibition of protective vasodilator reflexes. We now aim at providing direct pharmacological evidence that antagonism of endogenously released CGRP results in similar pathophysiological consequences as ablation of capsaicin-sensitive sensory neurons.

Peripheral opioid receptors and the cough reflex

The cough reflex originates from stimulation of sensory nerve endings located in the upper and lower respiratory tract. Opiates are among the most potent and widely used drugs which inhibit the cough reflex, and it has been generally assumed that they act generally. However, opioid receptors have been identified on the sensory arm of the vagus nerve. Although the functional significance of these receptors is not clear, recent evidence suggests that their activation may be involved in the modulation of airway reflexes. This review briefly examines the evidence to support the hypothesis that opioid receptors on vagal sensory nerves may mediate peripheral opioid-induced antitussive activity.

Afferent nerve-mediated protection against deep mucosal damage in the rat stomach

Intragastric capsaicin protects against ethanol-induced gross mucosal lesion formation by stimulation of afferent nerve endings in the rat stomach. The aims of the present study were to examine histologically the protective effect of capsaicin and to test whether this effect is related to changes in mucosal eicosanoid formation and mucosal blood flow. Intragastric capsaicin (160 μM) significantly reduced gross mucosal lesion formation induced by 25% ethanol. Light microscopy revealed that the depth of erosions was attenuated likewise. However, capsaicin did not prevent ethanol from causing superficial damage to the mucosa as observed by light and scanning electron microscopy. The protective action of capsaicin against ethanol remained unchanged by a dose of indomethacin that reduced the ex vivo formation of prostaglandin E 2 and 6-oxo-prostaglandin F 1α in the gastric mucosa by about 90%. Capsaicin alone did not affect the ex vivo formation of these prostaglandins and of leukotriene C 4. Intragastric capsaicin (160 μM) enhanced gastric mucosal blood flow by 89% as measured by the hydrogen gas clearance technique. This effect was also observed when capsaicin was administered together with 25% ethanol. These data indicate that afferent nerve stimulation by intragastric capsaicin protects against deep mucosal damage in response to ethanol, an effect that seems related to an increase in mucosal blood flow but not to eicosanoid formation.

Intragastric capsaicin enhances rat gastric acid elimination and mucosal blood flow by afferent nerve stimulation

1. This study investigated the effects of intragastric capsaicin on acid output, clearance of aniline, potential difference, and morphology of the mucosa in the rat stomach. The experiments were carried out on rats anaesthetized with urethane in which the stomachs were continuously perfused with saline. 2. When the stomach was perfused with normal saline (pH approximately 6), intragastric capsaicin (32-640 microM) had no effect on the output of titratable acid. In contrast, when acid output was stimulated by pentagastrin or when the stomach was perfused with acid saline (pH 3), capsaicin reduced acid output. Acid loss which occurred during perfusion with saline of pH 2 was not significantly increased by capsaicin. This suggests that capsaicin does not enhance acid back-diffusion but facilitates acid elimination by other means. 3. The gastric clearance of [14C]-aniline, which is an indirect index of gastric mucosal blood flow, was estimated while the stomach was perfused with saline of pH 3. The clearance of aniline rose by 50-60% following intragastric administration of capsaicin (160 microM) whereas the mean arterial blood pressure was increased by about 2.5 mmHg only. Combined pretreatment of the rats with atropine, phentolamine, and propranolol did not alter the effect of capsaicin on the gastric clearance of aniline. 4. The gastric potential difference was not altered by capsaicin (160 microM) administered together with saline of pH 3. This and the finding that there were no signs of mucosal damage by light and scanning electron microscopy indicate that intragastric capsaicin does not irritate the gastric mucosa. 5. The effects of intragastric capsaicin on gastric acid output and aniline clearance and on blood pressure were absent in rats in which capsaicin-sensitive afferent neurones had been ablated by neonatal treatment with a neurotoxic dose of capsaicin, which indicates that they result from stimulation of afferent nerve endings in the stomach. It is concluded that facilitation of acid elimination and mucosal blood flow may contribute to the previously reported protective action of capsaicin on the gastric mucosa.

Nasal Reactions Elicited by Unilateral Allergen Challenge

Nasal reactions to unilateral allergen provocation were studied separately in both nasal cavities of 9 subjects with established seasonal allergic rhinitis. Three tests with the same allergen at the same concentration were performed in the same cavity at 48-h intervals. The parameters observed were clinical symptoms, changes in nasal airway resistance on rhinomanometry, and amount, weight and histamine content of the collected secretion. Nasal obstruction increased significantly on the provoked side but not contralaterally. Secretion increased symmetrically but the histamine content rose only on the provoked side. No priming effect was observed. The results are compatible with the view that the release of histamine has a 2-fold effect. Histamine directly caused vasodilatation of capacitance vessels and capillaries, which resulted in obstruction on the provoked side, and indirectly the histamine release led to stimulation of sensory nerve endings, which by triggering parasympathetic reflexes caused rhinorrhea in both nasal halves.

Stimulation of afferent nerve endings by intragastric capsaicin protects against ethanol-induced damage of gastric mucosa

Ablation of capsaicin-sensitive afferent neurons enhances experimentally induced ulceration in the rat gastric mucosa, which suggests that these neurons are involved in gastric mucosal protection. To provide direct evidence for such a function it was investigated whether stimulation of afferent nerve endings by the intragastric administration of capsaicin could counteract the ulcerogenic effect of 25% ethanol. Capsaicin (3.2–640μM), administered together with ethanol, inhibited the development of haemorrhagic lesions in a concentration-dependent fashion but did not alter the ethanol-induced fall in the gastric potential difference. This suggests that capsaicin does not prevent ethanol from damaging gastric epithelial cells but can counteract the vascular lesions caused by ethanol. The anti-lesion effect of intragastric capsaicin was absent in adult rats which had been treated with a high dose of systemic capsaicin as neonates in order to achieve a permanent degeneration of unmyelinated afferent neurons. It would appear, therefore, that intragastric capsaicin reduces lesion formation by an action on afferent neurons. The protective effect of intragastric capsaicin was not altered following acute subdiaphragmatic vagotomy, acute removal of the coeliac-superior mesenteric ganglion complex, acute bilateral ligation of the adrenal glands, or pretreatment of the rats with atropine or guanethidine. These findings indicate that stimulation of afferent neurons by intragastric capsaicin affords protection of the rat gastric mucosa against ethanol-induced damage. As the autonomic nervous system is not involved gastroprotection appears to represent a local effector function of sensory nerve endings in the stomach.

Neuropeptide transmitters may mediate gastric mucosal protection due to stimulation of afferent nerve endings in the stomach

Neuropeptide transmitters may mediate gastric mucosal protection due to stimulation of afferent nerve endings in the stomach

Substance P-inducing massive postmortem bronchoconstriction in guinea pig lungs

To further examine the role that substance P plays in initiating the observed massive postmortem bronchoconstriction in guinea pig lungs and to explore the role of neural reflex in this airway spasm, six groups of animals were employed: control (n = 6), morphine (n = 6), substance P (n = 5), chronic capsaicin pretreatment + substance P (n = 5), tetrodotoxin (TTX) + acute capsaicin (n = 4), and chlorisondamine + acute capsaicin (n = 5). Pressure-volume curves were performed prior to and following the initiation of artificial pulmonary perfusion with 1% bovine serum albumin and 5% dextran in Tyrode's solution. A decrease in inflation volume (the lung volume between transpulmonary pressure of 0 and 30 cmH2O during inflation) was used as an index of bronchoconstriction. In control animals, inflation volume decreased to 20-30% of the base-line value at 15-30 min of perfusion, indicating massive bronchial constriction during this time period. Morphine (an agent inhibiting substance P release) significantly attenuated the spasm, whereas the presence of substance P in the perfusate markedly enhanced the constriction. Depletion of endogenous substance P by chronic capsaicin pretreatment did not affect exogenous substance P-induced spasm. Acute capsaicin-induced bronchoconstriction was significantly attenuated by TTX but was not affected by the ganglionic blocking agent, chlorisondamine. These data suggest that substance P initiates the massive postmortem bronchoconstriction in guinea pig lungs and that substance P is released by local stimulation of sensory nerve endings via axonal reflex.

Effects of inhaled lidocaine on exercise-induced asthma.

Experiments were performed to determine if stimulation of afferent nerve endings in the respiratory mucosa plays a major role in the initiation of exercise-induced asthma. Five asthmatic subjects were studied in two sessions of 10 min treadmill exercise using an identical workload. In the control session the subjects were exercised without treatment; in the other session aerosol lidocaine (1.5 mg/kg) was inhaled from residual volume to total lung capacity before exercise was started. Pulmonary function tests were measured (1) to obtain baseline values before the aerosol inhalation or exercise was commenced, (2) 2-3 min after completion of lidocaine inhalation, and (3) 4 min after termination of exercise. In the control session the mean postexercise forced expiratory volume in 1 s (FEV1) and the mean forced expiratory flow during the middle half of forced vital capacity (FEF25-75%) were decreased to 61 and 44% of the baseline values, respectively. Similarly, with the lidocaine treatment the post-exercise FEV1 and FEF25-75% were decreased to 54 and 44% of the baseline values, respectively. These data indicate that the afferent nerves in the respiratory mucosa may not play a critical role in the development of exercise-induced asthma.

Diving reflex. Another method of treating paroxysmal supraventricular tachycardia.

Bradycardia during submersion has long been known to occur in diving animals.1,2This diving reflex is initiated through a complex cardiovascular reflex partly through cold water stimulation of afferent nerve endings on the body and partly by apnea.3,4Apnea alone causes similar but much less extreme cardiovascular response. The efferent limb of the reflex is mediated through increased sympathetic stimulation of peripheral vasculature (except in heart and brain), which causes vasoconstriction and intense vagal stimulation of the heart. This reflex mechanism prominently seen in aquatic animals allows them to slow their heart rate, decrease oxygen demand, increase oxygen extraction, redistribute blood flow, and maintain arterial pressure when submerged.5Though in a less intense form, man has retained this reflex. Bradycardia is commonly observed in human divers when they are submerged in water.6This reflex is attenuated by a reduction in water temperature7,8and can be

Mode of action of intravenous nicotine in causing a fall of blood pressure in the cat

Small amounts of nicotine (5–20 μg/kg) injected into the femoral vein or pulmonary artery of cats anaesthetized with chloralose usually caused a fall in blood pressure within a few seconds of their injection. The fall in blood pressure was usually followed by a much larger rise. When similar amounts of nicotine were injected into the left atrium there was no initial fall in blood pressure and this was also the usual result when nicotine was introduced into the lungs in tobacco smoke. Analysis of this nicotine depressor response has shown that it is due to stimulation of sensory nerve endings in the lungs, the afferent nerve of the reflex response being the vagus. Two efferent pathways are involved — the vagus and the sympathetic nerves to the blood vessels.

Stimulation of the Cough Reflex

Two research-minded students compare the effects of reflex coughing elicited by stimulation of sensory nerve endings with ice and the effects of coughing induced by deep breathing and forced expiration.