Respiratory Reflexes Research Articles

Effect of esmolol infusion on myocardial oxygen consumption during extubation and quality of recovery in elderly patients undergoing general anesthesia: randomized, double blinded, clinical trial

BackgroundUpon recovery from anesthesia and during extubation, there will be mechanical stimulation of receptors in the respiratory tract that results in both respiratory and cardiovascular reflex responses. Heart rate plays a major determinant of myocardial oxygen consumption and cardiac workload, so decreasing the heart rate will increase the ischemic threshold and improve the cardiac performance.ObjectiveTo evaluate the effect of esmolol infusion on myocardial oxygen consumption during extubation and quality of recovery in elderly patients undergoing general anesthesia.MethodsHundred adult patients ASA I & II scheduled for elective open unilateral inguinal hernia were randomized, double-blindly into one of two parallel groups, esmolol group (E) (n = 50) and control group (C) (n = 50). In the esmolol group, 1 mg/kg esmolol was given as bolus over 30 s then followed by a continuous esmolol infusion of 100 μg/kg/min starting 10 min before end of surgery till 5 min after extubation. While patients in group C received normal saline bolus of the same volume followed by a continuous normal saline infusion of the same volume per hour as group E. Mean heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean blood pressure (MBP), rate pressure product (RPP), anesthesia time, recovery time, postoperative nausea & vomiting, number of doses of antiemetic agent and quality of extubation were recorded.ResultsThe results showed that patients in the esmolol group had lower values of (RPP) after esmolol infusion with statistically significant difference when compared with patients in the control group using unpaired t-test (P < 0.05), this will decrease oxygen consumption in esmolol group. Also, there was statistically significant difference between both groups regarding values of HR (beat/min), SBP (mmHg), DBP (mmHg) and MBP (mmHg) starting 2 min after esmolol infusion and continued till 10 min after extubation using unpaired t-test (p < 0.05). As regards PONV, there was lower incidence in esmolol group when compared to control group using unpaired t-test with statistically significant difference (P < 0.05).ConclusionsEsmolol is a safe, effective and well-tolerated drug that can be used in elderly patients undergoing general anesthesia to reduce the myocardial oxygen consumption and improve the quality of recovery.

Acid aspiration evoked respiratory reflexes persist in TRPV1 and TRPA1 knockout mice

Acid aspiration evoked respiratory reflexes persist in TRPV1 and TRPA1 knockout mice

Chronic intermittent hypoxia orchestrates cardiorespiratory cacophony--adapting melody to malady.

Chronic intermittent hypoxia orchestrates cardiorespiratory cacophony--adapting melody to malady.

Comparison of the Full Outline of UnResponsiveness score and the Glasgow Coma Scale in predicting mortality in critically ill patients*.

Impaired consciousness has been incorporated in prediction models that are used in the ICU. The Glasgow Coma Scale has value but is incomplete and cannot be assessed in intubated patients accurately. The Full Outline of UnResponsiveness score may be a better predictor of mortality in critically ill patients. Thirteen ICUs at five U.S. hospitals. One thousand six hundred ninety-five consecutive unselected ICU admissions during a six-month period in 2012. Glasgow Coma Scale and Full Outline of UnResponsiveness score were recorded within 1 hour of admission. Baseline characteristics and physiologic components of the Acute Physiology and Chronic Health Evaluation system, as well as mortality were linked to Glasgow Coma Scale/Full Outline of UnResponsiveness score information. None. We recruited 1,695 critically ill patients, of which 1,645 with complete data could be linked to data in the Acute Physiology and Chronic Health Evaluation system. The area under the receiver operating characteristic curve of predicting ICU mortality using the Glasgow Coma Scale was 0.715 (95% CI, 0.663-0.768) and using the Full Outline of UnResponsiveness score was 0.742 (95% CI, 0.694-0.790), statistically different (p = 0.001). A similar but nonsignificant difference was found for predicting hospital mortality (p = 0.078). The respiratory and brainstem reflex components of the Full Outline of UnResponsiveness score showed a much wider range of mortality than the verbal component of Glasgow Coma Scale. In multivariable models, the Full Outline of UnResponsiveness score was more useful than the Glasgow Coma Scale for predicting mortality. The Full Outline of UnResponsiveness score might be a better prognostic tool of ICU mortality than the Glasgow Coma Scale in critically ill patients, most likely a result of incorporating brainstem reflexes and respiration into the Full Outline of UnResponsiveness score.

Detection and identification of oral anaerobes in intraoperative bronchial fluids of patients with pulmonary carcinoma.

Postoperative pneumonia may occur when upper respiratory tract protective reflexes such as cough and/or swallowing reflexes are impaired; thus, silent aspiration of oral bacteria may be a causative factor in postoperative pneumonia. This study aimed to quantify and identify bacteria in intraoperative bronchial fluids and to evaluate the relationship between impairment of cough/swallowing reflexes and silent aspiration of oral bacteria in elderly patients. After obtaining informed consent, cough and swallowing reflexes were assessed using an ultrasonic nebulizer and a nasal catheter, respectively. Using a micro-sampling probe, intraoperative bronchial fluids were collected from nine subjects with pulmonary carcinoma and cultured anaerobically on blood agar plates. After 7 days, CFUs were counted and isolated bacteria were identified by 16S rRNA gene sequencing. Four subjects (aged 71.0 ± 8.4 years) had impaired swallowing reflexes with normal cough reflexes, whereas five subjects (73.6 ± 6.5 years) had normal cough and swallowing reflexes. The bacterial counts (mean CFU ± SD) tended to be higher in intraoperative bronchial fluids of subjects with impaired swallowing reflexes ([5.1 ± 7.7] × 10(5)) than in those of subjects with normal reflexes ([1.2 ± 1.9] × 10(5)); however, this difference was not statistically significant. Predominant isolates from intraoperative bronchial fluids were Streptococcus (41.8%), Veillonella (11.4%), Gemella (8.9%), Porphyromonas (7.6%), Olsenella (6.3%) and Eikenella (6.3%). These findings indicate that intraoperative bronchial fluids contain bacteria, probably derived from the oral microbiota, and suggest that silent aspiration of oral bacteria occurs in elderly patients irrespective of impairment of swallowing reflex.

The nucleus of the solitary tract and the coordination of respiratory and sympathetic activities.

It is well known that breathing introduces rhythmical oscillations in the heart rate and arterial pressure levels. Sympathetic oscillations coupled to the respiratory activity have been suggested as an important homeostatic mechanism optimizing tissue perfusion and blood gas uptake/delivery. This respiratory-sympathetic coupling is strengthened in conditions of blood gas challenges (hypoxia and hypercapnia) as a result of the synchronized activation of brainstem respiratory and sympathetic neurons, culminating with the emergence of entrained cardiovascular and respiratory reflex responses. Studies have proposed that the ventrolateral region of the medulla oblongata is a major site of synaptic interaction between respiratory and sympathetic neurons. However, other brainstem regions also play a relevant role in the patterning of respiratory and sympathetic motor outputs. Recent findings suggest that the neurons of the nucleus of the solitary tract (NTS), in the dorsal medulla, are essential for the processing and coordination of respiratory and sympathetic responses to hypoxia. The NTS is the first synaptic station of the cardiorespiratory afferent inputs, including peripheral chemoreceptors, baroreceptors and pulmonary stretch receptors. The synaptic profile of the NTS neurons receiving the excitatory drive from afferent inputs is complex and involves distinct neurotransmitters, including glutamate, ATP and acetylcholine. In the present review we discuss the role of the NTS circuitry in coordinating sympathetic and respiratory reflex responses. We also analyze the neuroplasticity of NTS neurons and their contribution for the development of cardiorespiratory dysfunctions, as observed in neurogenic hypertension, obstructive sleep apnea and metabolic disorders.

Synaptic and paracrine mechanisms at carotid body arterial chemoreceptors

Mammalian carotid bodies are the main peripheral arterial chemoreceptors, strategically located at the bifurcation of the common carotid artery. When stimulated these receptors initiate compensatory respiratory and cardiovascular reflexes to maintain homeostasis. Thus, in response to low oxygen (hypoxia) or increased CO2/H(+) (acid hypercapnia), chemoreceptor type I cells depolarize and release excitatory neurotransmitters, such as ATP, which stimulate postsynaptic P2X2/3 receptors on afferent nerve terminals. The afferent discharge is shaped by autocrine and paracrine mechanisms involving both excitatory and inhibitory neuromodulators such as adenosine, serotonin (5-HT), GABA and dopamine. Recent evidence suggests that paracrine activation of P2Y2 receptors on adjacent glia-like type II cells may help boost the ATP signal via the opening of pannexin-1 channels. The presence of an inhibitory efferent innervation, mediated by release of nitric oxide, provides additional control of the afferent discharge. The broad array of neuromodulators and their receptors appears to endow the carotid body with a remarkable plasticity, most apparent during natural and pathophysiological conditions associated with chronic sustained and intermittent hypoxia.

Sensory Nerve Terminal Mitochondrial Dysfunction Induces Hyperexcitability in Airway Nociceptors via Protein Kinase C

Airway sensory nerve excitability is a key determinant of respiratory disease-associated reflexes and sensations such as cough and dyspnea. Inflammatory signaling modulates mitochondrial function and produces reactive oxygen species (ROS). Peripheral terminals of sensory nerves are densely packed with mitochondria; thus, we hypothesized that mitochondrial modulation would alter neuronal excitability. We recorded action potential firing from the terminals of individual bronchopulmonary C-fibers using a mouse ex vivo lung-vagal ganglia preparation. C-fibers were characterized as nociceptors or non-nociceptors based upon conduction velocity and response to transient receptor potential (TRP) channel agonists. Antimycin A (mitochondrial complex III Qi site inhibitor) had no effect on the excitability of non-nociceptors. However, antimycin A increased excitability in nociceptive C-fibers, decreasing the mechanical threshold by 50% and increasing the action potential firing elicited by a P2X2/3 agonist to 270% of control. Antimycin A-induced nociceptor hyperexcitability was independent of TRP ankyrin 1 or TRP vanilloid 1 channels. Blocking mitochondrial ATP production with oligomycin or myxothiazol had no effect on excitability. Antimycin A-induced hyperexcitability was dependent on mitochondrial ROS and was blocked by intracellular antioxidants. ROS are known to activate protein kinase C (PKC). Antimycin A-induced hyperexcitability was inhibited by the PKC inhibitor bisindolylmaleimide (BIM) I, but not by its inactive analog BIM V. In dissociated vagal neurons, antimycin A caused ROS-dependent PKC translocation to the membrane. Finally, H2O2 also induced PKC-dependent nociceptive C-fiber hyperexcitability and PKC translocation. In conclusion, ROS evoked by mitochondrial dysfunction caused nociceptor hyperexcitability via the translocation and activation of PKC.

The role of vagal nerve root injury on respiration disturbances in subarachnoid hemorrhage.

We examined whether there is a relationship between vagal nerve root injury and the severity of respiration disorders associated with subarachnoid hemorrhage (SAH). This study was conducted on 20 rabbits. Experimental SAH was induced by injecting homologous blood into the cisterna magna. During the experiment, electrocardiography and respiratory rhythms were measured daily. After the experiment, any axonal injury or changes to the arterial nervorums of the vagal nerves were examined. All respiratory irregularities and vagal nerve degenerations were statistically analyzed. Normal respiration rate, as measured in the control group, was 30 ± 6 bpm. In the SAH-induced group, respiration rates were initially 20 ± 4 bpm, increasing to 40 ± 9/min approximately ten hours later, with severe tachypneic and apneic variation. In histopathological examinations, axon density of vagal nerves was 28,500 ± 5,500 in both control and sham animals, whereas axon density was 22,250 ± 3,500 in survivors and 16,450 ± 2,750 in dead SAH animals. The severity of axonal degeneration of vagal nerves was greater in the six dead animals than in the survivors. If vagal nerves are lesioned, the muscles of respiration are paralyzed and respiratory reflexes are disrupted. That the ischemic and mechanical factors created by SAH cause vagal nerve root injury and respiration disorders may be inevitable and fatal.

Chapter 7 - The physiological significance of postinspiration in respiratory control

The term postinspiration is commonly used in the scientific literature concerned with neural generation and the control of breathing movements. Because postinspiration belongs functionally to the mechanical act of expiration, the physiological significance of postinspiration as a distinct phase of the breathing cycle is often underappreciated. The present review will give an overview of the physiological significance of postinspiratory motor activity in laryngeal adductor (constrictor) muscles and the crural diaphragm. The functional importance of postinspiratory motor activity is discussed for the eupneic respiratory cycle, and for various protective respiratory reflex mediations (e.g., sneeze, cough, and breath-hold). Also, the implications of recruited postinspiratory activity during nonventilatory behaviors such as vocalization, swallowing, or vomiting are underpinned. Finally, we describe the impact of absence or malfunction of postinspiratory motor function in neurological diseases.

Effects of a Single Bout of Interval Hypoxia on Cardiorespiratory Control in Patients With Type 1 Diabetes

Hypoxemia is common in diabetes, and reflex responses to hypoxia are blunted. These abnormalities could lead to cardiovascular/renal complications. Interval hypoxia (IH) (5–6 short periods of hypoxia each day over 1–3 weeks) was successfully used to improve the adaptation to hypoxia in patients with chronic obstructive pulmonary disease. We tested whether IH over 1 day could initiate a long-lasting response potentially leading to better adaptation to hypoxia. In 15 patients with type 1 diabetes, we measured hypoxic and hypercapnic ventilatory responses (HCVRs), ventilatory recruitment threshold (VRT-CO2), baroreflex sensitivity (BRS), blood pressure, and blood lactate before and after 0, 3, and 6 h of a 1-h single bout of IH. All measurements were repeated on a placebo day (single-blind protocol, randomized sequence). After IH (immediately and after 3 h), hypoxic and HCVR increased, whereas the VRT-CO2 dropped. No such changes were observed on the placebo day. Systolic and diastolic blood pressure increased, whereas blood lactate decreased after IH. Despite exposure to hypoxia, BRS remained unchanged. Repeated exposures to hypoxia over 1 day induced an initial adaptation to hypoxia, with improvement in respiratory reflexes. Prolonging the exposure to IH (>2 weeks) in type 1 diabetic patients will be a matter for further studies.

Rhinovirus upregulates transient receptor potential channels in a human neuronal cell line: implications for respiratory virus-induced cough reflex sensitivity

BackgroundThe mechanism underlying respiratory virus-induced cough hypersensitivity is unknown. Upregulation of airway neuronal receptors responsible for sensing physical and chemical stimuli is one possibility, and the transient receptor potential (TRP)...

The Death Rattle and the Old Man's Friend

To the Editor: Sir William Osler first referred to pneumonia as “the old man's friend”—identifying it as a common cause of relatively peaceful death in the late 1800s.1 Pneumonia remains among the most common primary or proximate causes of death in 2012.2 Most pneumonias share the common feature of defeating the normally robust mechanical, cellular, and immune mechanisms to prevent infection of the lower respiratory tract. Denudation of the trachea or bronchi due to viral (e.g., influenza) infections or toxic inhalants (e.g., smoking-related injury) predisposes to bacterial superinfection and subsequent pneumonia.3 Dysphagia is also a well-studied risk for aspiration of upper aerodigestive secretions causing pneumonia,3 but little has been written about another antecedent, encountered by clinicians regularly and recognized since the time of Laennac. This is upper airway incompetence marked by the sound of air gurgling through secretions above the glottis, heard with or without the stethoscope, when individuals speak or breathe—gargouillement.4 Laennac may also have been first to connote gurgling breath sounds with death—“the death rattle.”5 There is no published research that ties the “death rattle” or gargouillement to pneumonia, even though early clinicians acknowledged this association.4, 5 One study demonstrated gurgling in 20 individuals admitted during a 5-month period to a 24-bed hospital ward; 11 developed pneumonia, and the odds of pneumonia in gurglers were 130 times those of nongurglers.6 The epidemiology of inappropriate pooling of supraglottic secretions and gurgling, rates of subglottic aspiration in such individuals, and subsequent rates of pneumonia of those who aspirate are all unknown. There are some data that describe the relationship between advancing age and disease and aspiration. For example, of 127 home-based elderly adults (mean age 84), 44% had “laryngeal penetrations” seen on nasopharyngeal endoscopy. Medications (neuroleptics), stroke, and other neurological disorders were risks, and odds of aspiration were 12 times as great in those with abnormal water swallowing tests.7 In another study, subglottic aspiration was noted in 62% of hospitalized elderly adults and 6% of ambulatory normal elderly adults. Pooled secretions in the larynx were associated with aspiration, but age was not.8 “Wet phonation” is highly associated with subglottic penetration of secretions,9 and another study showed that “none of the patients coughed or cleared their throats after penetrating/aspirating.”10 Risk factors for pathological pooling of secretions and gurgling include neurological disorders,7 dementia,6 acute nonneurological illness in elderly adults,6, 10 and sedating medications.6 There are no data to support that risk of gurgling increases with age, except insofar as diseases and medications that predispose to gurgling accumulate with age. There is abundant evidence that antipsychotics increase the risk of pneumonia, presumably by causing occult micro-aspiration.7 There is a subset of such individuals with extreme medication-induced blunting of upper respiratory reflexes unto gurgling.6 If it is accepted that gurgling breath sounds promote pneumonia and that pneumonia is a common cause of death in elderly adults, a number of research questions arise that may be of interest to those—geriatricians, internists, intensivists, palliative care clinicians—who provide care at the end of life. What are the epidemiology, risks, and reversible causes of gurgling? For reversible causes, what are countermeasures (e.g., levels of care and monitoring, medications, positions, frequent oropharyngeal suctioning) that can be taken to mitigate risk until gurgling is corrected by treating underlying causes? For irreversible causes of gurgling, is pneumonia inevitable? If so, is there any long-term benefit to treating the pneumonia with antibiotics or endotracheal intubation if it will only recur, or do such treatments simply prolong dying—inevitably of pneumonia or its complications? All who gurgle are not certain to develop pneumonia and die.6 Gargouillement may be a rattle, but not necessarily a death rattle. Perhaps a more-accurate description in 2013 is that gurgling is a “risk-of-death rattle,” and greater understanding of gurgling sounds may permit clinicians to more-deliberately identify and treat reversible causes. To the extent that gurgling may signal extreme risk,6 this clinical sign, easily recognized by simple physical examination, might also be a useful additional trigger for rapid response, assessment, and treatment for as-yet-to-be-determined reversible causes or to allow those whose gurgling portends recurrent pneumonia to die peacefully—as Osler described—without multiple endotracheal intubations and trials of death-prolonging critical care. Conflict of Interest: Dr. Manthous has no financial conflicts of interest relevant to this manuscript. Author Contributions: Dr. Manthous is responsible for the entire content of this paper. Sponsor's Role: None.

The effect of tracheal occlusion on the load compensation response and the changes in inhibitory neurotransmitter in the brainstem of conscious rats

Respiratory load compensation in conscious animals is mediated by cortical, subcortical modulation and brainstem mediated reflexes. We hypothesized that consciousness behavior would reconfigure the brainstem mediated respiratory load compensation reflex in respond to tracheal occlusion (TO). We also hypothesized that glycinergic neurons in the NTS would not be activated in conscious rats as we found in anesthetized rats in a previous study. A tracheal occluder and diaphragm electrodes were implanted in six experimental (E) and six sham (S) rats for the measurement of respiratory parameters. Seven days after recovery, the E rats had 2–3 seconds TOs separated by 10–15 unloaded breaths for 10 minutes. Ninety minutes after TO, the rats were anesthetized, brainstem were perfused and harvested for the double immnofluorescence staining of c‐Fos and glycine transporter 2. The results showed that conscious rats prolonged expiratory time (Te) in respond to TO but inspiratory time (Te) was unaffected by the load. The glycinergic neurons in the NTS were activated in conscious rats. In conclusion, conscious rat load compensation responses are characterized by maintaining normal Ti and modulating Te which differs from anesthetized rats, but glycinergic neurons in the NTS were activated which are similar to anesthetized rats.

Dissecting the role of TRPV1 in detecting multiple trigeminal irritants in three behavioral assays for sensory irritation

Polymodal neurons of the trigeminal nerve innervate the nasal cavity, nasopharynx, oral cavity and cornea. Trigeminal nociceptive fibers express a diverse collection of receptors and are stimulated by a wide variety of chemicals. However, the mechanism of stimulation is known only for relatively few of these compounds. Capsaicin, for example, activates transient receptor potential vanilloid 1 (TRPV1) channels. In the present study, wildtype (C57Bl/6J) and TRPV1 knockout mice were tested in three behavioral assays for irritation to determine if TRPV1 is necessary to detect trigeminal irritants in addition to capsaicin. In one assay mice were presented with a chemical via a cotton swab and their response scored on a 5 level scale. In another assay, a modified two bottle preference test, which avoids the confound of mixing irritants with the animal’s drinking water, was used to assess aversion. In the final assay, an air dilution olfactometer was used to administer volatile compounds to mice restrained in a double-chambered plethysmograph where respiratory reflexes were monitored. TRPV1 knockouts showed deficiencies in the detection of benzaldehyde, cyclohexanone and eugenol in at least one assay. However, cyclohexanone was the only substance tested that appears to act solely through TRPV1.

Three-Dimensional Computer Model of Brainstem Respiratory Neuronal Circuits - Application for Research in Respirology

Abstract Methods that had been applied to study central neuronal circuits regulating cough and respiratory reflexes so far rely on recording performed in vivo, ex vivo, micro injecting and lesion methods. Based on the available data it is clear that this network is complicated, multilevel, holarchical, undergoing reconfiguration under afferent inputs. For many students and researchers it is complicated to get a virtual spatial image of these cooperating neuronal populations. The project was aimed to create graphical three-dimensional computer model of the brainstem using environment MATLAB and the matrix algebra to visualize neuron localization within the brainstem. Relevant data for the model had been taken from recent and also former research papers published in particular areas. This model may help scientists to visualize groups of neurons, help them to find targets for microinjecting or lesion studies together with stereotaxic positioning. The model is upgradeable and highly flexible for future use, research and teaching applications in MATLAB environment. MATLAB is a high-level language and interactive environment that enables you to perform computationally intensive tasks faster than with traditional programming languages

Expanding role of ATP as a versatile messenger at carotid and aortic body chemoreceptors

In mammals, peripheral arterial chemoreceptors monitor blood chemicals (e.g. O(2), CO(2), H(+), glucose) and maintain homeostasis via initiation of respiratory and cardiovascular reflexes. Whereas chemoreceptors in the carotid bodies (CBs), located bilaterally at the carotid bifurcation, control primarily respiratory functions, those in the more diffusely distributed aortic bodies (ABs) are thought to regulate mainly cardiovascular functions. Functionally, CBs sense partial pressure of O(2) ( ), whereas ABs are considered sensors of O(2) content. How these organs, with essentially a similar complement of chemoreceptor cells, differentially process these two different types of signals remains enigmatic. Here, we review evidence that implicates ATP as a central mediator during information processing in the CB. Recent data allow an integrative view concerning its interactions at purinergic P2X and P2Y receptors within the chemosensory complex that contains elements of a 'quadripartite synapse'. We also discuss recent studies on the cellular physiology of ABs located near the aortic arch, as well as immunohistochemical evidence suggesting the presence of pathways for P2X receptor signalling. Finally, we present a hypothetical 'quadripartite model' to explain how ATP, released from red blood cells during hypoxia, could contribute to the ability of ABs to sense O(2) content.

Persistent hiccups after acute supratentorial stroke: Report of seven cases and review of literature

Persistent hiccups are hiccups that last for at least 48 h, and may occur following a legion of causes including strokes. They have been described following infarctive and hemorrhagic strokes. Hiccup is a respiratory reflex action that occurs following the sudden contraction of the diaphragmatic and intercostals muscles with closure of the glottis; and putatively believed to be a form of myoclonus (very brief repeated contractions of striated muscles) that occurs from irritation of the medullary mediated reflex arc that has supratentorial inputs. This underpins the association of hiccups with suprabulbar lesions like strokes, apparently following repeated excitatory inputs from the higher centers. Hiccups are ordinarily self-limiting, but persistent hiccups are advisedly treated with pharmacologic agents, of which baclofen, a GABA B agonist muscle relaxant has proven to be remarkably efficient. It is believed that the action of baclofen interrupts the hiccup reflex arc. Nonpharmacologic remedies like vagus nerve stimulation have also been found to be effective and may be complementary. This case series highlights the use of baclofen in persistent hiccups following supratentorial infarcts.

CONVENTIONAL RESPIRATORY REFLEX TO INCREASED RESPIRATORY RESISTANCE AS AN EXPERIMENTAL MODEL OF ADAPTIVE ACTIVITY

State Budget Educational Institution of Higher Professional Education “Ryazan State Medical University named after academician I.P. Pavlov” of the Ministry of Public Health and Social Development of the Russian Federation, Ryazan In the article it’s verified that conventional respiratory reflex to resistive load is the organism’s multicomponent reaction which can be used adequately as a model of adaptive human activity due to some methodical advantages: rapid reflex formation, relative strength, distinct quantitative evaluation criteria of components, relative simplicity of fulfillment of the methods. A step-like change in reinforcement of congenital respiratory reflex essentially rebuilts spatiotemporal structure of adaptive activity as well as its physiological cost.

Modulation of Sensory Irritation Responsiveness by Adenosine and Malodorants

Respiratory tract reflex responses are an important defense mechanism against noxious airborne materials. This study was aimed at defining the effects of adenosine on sensory irritation responsiveness and its role in odorant-irritant interactions. These experiments were aimed at testing the hypothesis that adenosine, through the A2 receptor, enhances trigeminal nerve responses to multiple irritants and that odorants enhance responsiveness to irritants through A2 pathways in the female C57Bl/6 mouse. The adenosine precursor, AMP, immediately and markedly increased the sensory irritation response to capsaicin, cyclohexanone, and styrene, irritants that activate chemosensory nerves through differing receptor pathways. The neuromodulatory effect was blocked by the general adenosine receptor antagonist theophylline and by the A2 receptor-specific antagonist DMPX. Multiple odorants were examined, including R-carvone (spearmint), linalool (lavender), trimethylamine (rotting fish), mercaptoethanol, and ethyl sulfide (stench and rotten eggs). Of these, only mercaptoethanol and ethyl sulfide exhibited neuromodulatory effects, enhancing the sensory irritation response to styrene or cyclohexanone. This effect was blocked by theophylline and DMPX indicating the importance of adenosine A2 receptor pathways in this effect. These results highlight that trigeminal chemosensory responsiveness is not static, but can be quickly modulated by adenosine and select odors resulting in hyperresponsive states.