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Biomedical subjects

M J Joyner

Publications and source records attributed to M J Joyner.

At least 73 records · Page 4Linked to original sources
PubMed1996

Cardiovascular and peak VO2 responses to supine exercise: effects of age and training status.

Although stroke volume during exercise is affected by aging and posture, few studies have carefully examined the heart rate, blood pressure, and peak oxygen uptake (VO2) responses of older subjects to supine exercise. The present study examined these responses during graded supine cycling in younger (21-30 yr) and older (51-62 yr) untrained (Treadmill VO2max = 47.0 vs 32.3 ml.kg-1.min-1) and endurance-trained (66.3 vs 52.7 ml.kg-1.min-1) men (N = 6/group). All subjects had lower (P < 0.05) peak VO2 (ml.min-1) and peak heart rate responses during supine cycling compared with treadmill exercise. Additionally, the age-related reduction in peak VO2 (approximately 20-30%) was similar for supine compared with treadmill testing, even when normalized to fat-free leg volume and fat-free mass, respectively. However, at given absolute intensities (VO2) of supine exercise, heart rates were 10-15 beats.min-1 less (P < 0.05) in both older groups. Across relative supine work intensities (% of peak), systolic pressure increased most rapidly in the younger trained and older untrained groups. These findings suggest that the effects of aging on peak VO2 are similar during treadmill and supine exercise in both endurance-trained and untrained men. These data also indicate that the heart rate response to supine exercise is attenuated in healthy older men and contributes to their reduced peak VO2.

Adult↗
PubMed1996

Autonomic control of colonic tone and the cold pressore test.

BACKGROUND: Cardiovascular responses to cold stimulation are well characterised. It is unclear, however, whether cold pain stimulates responses in colonic tone in the transverse and sigmoid regions. AIMS: To assess the effects of cold stimulation on tone nd motility in the transverse and sigmoid colon and on cardiovascular autonomic activity. METHODS: Phasic and tonic motility of the transverse and sigmoid colon, pulse rate, and beat to beat pulse variability (which are measures of centrally mediated changes in autonomic function) were measured before, during, and after a standard cold pressor test in 22 healthy volunteers. RESULTS: Cold pain induced a significant increase in colonic tone but not phasic contractility in the transverse and sigmoid regions. Simultaneously, cold pain increased pulse interval variability. CONCLUSION: The findings are consistent with the hypotheses that cold pain produces coactivation of both the sympathetic and parasympathetic limbs of the autonomic nervous system and that cold induced changes in colonic tone are temporally associated with alterations in central autonomic nervous activity.

Adult↗
PubMed1996

Local cholinergic mechanisms mediate nitric oxide-dependent flow-induced vasorelaxation in vitro.

To determine whether local cholinergic mechanisms evoke nitric oxide (NO)-mediated flow-induced vasorelaxation, canine coronary artery rings without endothelium were suspended beneath an organ chamber that contained a stainless steel tube and a femoral artery segment with endothelium. The rings were superfused at a basal rate of 1 ml/min with physiological salt solution that was bubbled with 95% O2-5% CO2 and maintained at 37 degrees C. They were stretched to optimal length and contracted with prostaglandin F 2 alpha (2 x 10(-6) M). When flow through the stainless steel tube (direct superfusion) was increased from the basal rate of 1 to 4 ml/min, coronary force did not change. Superfusion of the rings (n = 8) with effluent from the femoral segment (endothelial superfusion) at 4 ml/min to study flow-induced vasodilation caused a 67.3 +/- 10.8% relaxation. Treatment of the segment with the NO synthase blocker NG-monomethyl-L-arginine (10(-4) M) eliminated the relaxation seen during endothelial superfusion (P < 0.05 vs. control). Application of atropine (10(-6) M) to additional femoral segments (n = 8) abolished the coronary relaxation observed during endothelial superfusion at 1 ml/ min, and the flow-induced relaxation observed at 4 ml/min was reduced from 64 +/- 8.3 to 27 +/- 5.6% (P < 0.05 vs. control). In studies on additional segments and rings (n = 6), the flow-induced relaxations at 4 ml/min of endothelial superfusion were blunted from 86 +/- 10 to 28 +/- 13% after the segments were treated with acetylcholinesterase (0.00028 U/min for 20 min). These data indicate that basal- and flow-induced release of NO from the vascular endothelium can be mediated by local cholinergic mechanisms. It is possible that flow causes acetylcholine release from certain endothelial cells, which stimulates NO release from these cells or from neighboring endothelial cells.

Acetylcholine↗
PubMed1996

Peak calf blood flow estimates are higher with Dohn than with Whitney plethysmograph.

Estimates of calf blood flow with venous occlusion plethysmography vary widely between studies, perhaps due to the use of different plethysmographs. Consequently, we compared calf blood flow estimates at rest and during reactive hyperemia in eight healthy subjects (four men and four women) with two commonly used plethysmographs: the mercury-in-silastic (Whitney) strain gauge and Dohn air-filled cuff. To minimize technical variability, flow estimates were compared with a Whitney gauge and a Dohn cuff on opposite calves before and after 10 min of bilateral femoral arterial occlusion. To account for any differences between limbs, a second trial was conducted in which the plethysmographs were switched. Resting flows did not differ between the plethysmographs (P = 0.096), but a trend toward lower values with the Whitney was apparent. Peak flows averaged 37% lower with the Whitney (27.8 +/- 2.8 ml.dl-1.min-1) than with the Dohn plethysmograph (44.4 +/- 2.8 ml.dl-1.min-1; P < 0.05). Peak flow expressed as a multiple above baseline was also lower with the Whitney (10-fold) than with the Dohn plethysmograph (14.5-fold; P = 0.02). Across all flows at rest and during reactive hyperemia, estimates were highly correlated between the plethysmographs in all subjects (r2 = 0.96-0.99). However, the mean slope for the Whitney-Dohn relationship was only 60 +/- 2%, indicating that over a wide range of flows the Whitney gauge estimate was 40% lower than that for the Dohn cuff. These results demonstrate that the same qualitative results can be obtained with either plethysmograph but that absolute flow values will generally be lower with Whitney gauges.

Adult↗
PubMed1996

Contribution of nitric oxide and prostaglandins to reactive hyperemia in human forearm.

We investigated the separate and combined contributions of nitric oxide (NO) and vasodilating prostaglandins as mediators of reactive hyperemia in the human forearm. Forearm blood flow (FBF) was measured with venous occlusion plethysmography after 5 min of ischemia. In one protocol (n = 12), measurements were made before and after intra-arterial administration of the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) to one forearm. In a separate protocol (n = 7), measurements were made before and after systemic administration of the cyclooxygenase inhibitor ibuprofen and again after L-NMMA. L-NMMA reduced baseline FBF at rest (2.7 +/- 0.4 to 1.6 +/- 0.2 ml.100 ml-1.min-1; P < 0.05) and had a modest effect on peak forearm vascular conductance and flow (forearm vascular conductance = 31.1 +/- 3.1 vs. 25.7 +/- 2.5 ml.min-1.100 ml forearm-1.100 mmHg of perfusion pressure-1.min-1, P < 0.05; FBF = 26.6 +/- 2.9 vs. 22.8 +/- 2.6 ml.100 ml-1.min-1, P = 0.055). Total excess flow above baseline during reactive hyperemia was unaffected by L-NMMA (14.3 +/- 3.0 vs. 13.1 +/- 2.4 ml/100 ml; P < 0.05). Ibuprofen did not change FBF at rest, reduced peak FBF from 27.6 +/- 1.9 to 20.3 +/- 2.7 ml.100 ml-1.min-1 (P < 0.05), but had no effect on total excess flow above baseline, Infusion of L-NMMA after ibuprofen reduced FBF at rest by 40%, had no effect on peak flow, but reduced total excess flow above baseline from 12.0 +/- 2.5 to 7.6 +/- 1.3 ml/100 ml (P < 0.05). These date demonstrate that NO synthase inhibition has a modest effect on peak vasodilation during reactive hyperemia but plays a minimal role later. Prostaglandins appear to be important determinants of peak flow. The effects of NO synthase inhibition during reactive hyperemia may also be potentiated by concurrent cyclooxygenase inhibition.

Adolescent↗
PubMed1996

American College of Sports Medicine position stand. The use of blood doping as an ergogenic aid.

Blood doping has been achieved by either infusing red blood cells or by administering the drug erythropoietin to artificially increase red blood cell mass. Blood doping can improve an athlete's ability to perform submaximal and maximal endurance exercise. In addition, blood doping can help reduce physiologic strain during exercise in the heat and perhaps at altitude. Conversely, blood doping is associated with risks that can be serious and impair athletic performance. These known risks are amplified by improper medical controls, as well as the interaction between dehydration with exercise and environmental stress. Finally, the medical risks associated with blood doping have been estimated from carefully controlled research studies, and the medically unsupervised use of blood doping will increase these risks. It is the position of the American College of Sports Medicine that any blood doping procedure used in an attempt to improve athletic performance is unethical, unfair, and exposes the athlete to unwarranted and potentially serious health risks.

Altitude↗
PubMed1995

Role of nitric oxide in exercise hyperaemia during prolonged rhythmic handgripping in humans.

1. We sought to determine whether the vasodilating molecule nitric oxide (NO) contributes to the forearm hyperaemia observed during prolonged rhythmic handgripping in humans. 2. Two bouts of exercise were performed during experimental protocols conducted on separate days. During each protocol the subject performed a 10 min and a 20 min bout of rhythmic (30 min-1) handgripping at 15% of maximum. Two exercise bouts were required to facilitate pharmacological interventions during the second protocol. Blood flow in the exercising forearm was measured every minute with plethysmography during brief pauses in the contractions. During both exercise bouts in the first protocol, forearm blood flow increased 2- to 3-fold above rest after 1 min of handgripping and remained constant at that level throughout the exercise. 3. During the 10 min bout of exercise in the second protocol, acetylcholine was given via a brachial artery catheter at 16 micrograms min-1 for 3 min to evoke NO release from the vascular endothelium. This caused forearm blood flow to increase above the values observed during exercise alone. 4. During the 20 min trial of handgripping in the second protocol, the NO synthase blocker NG-monomethyl-L-arginine (L-NMMA) was infused in the exercising forearm via the brachial catheter after 5 min of handgripping. The L-NMMA was infused at 4 mg min-1 for 10 min. 5. L-NMMA during exercise caused forearm blood flow to fall to values approximately 20-30% lower than those observed during exercise alone. When ACh was given during exercise after L-NMMA administration the rise in blood flow was also blunted, indicating blockade of NO synthase. These data suggest NO plays a role in exercise hyperaemia in humans.

Acetylcholine↗
PubMed1995

Chest wall responses to rebreathing in halothane-anesthetized dogs.

BACKGROUND: The pattern of respiratory muscle use during halothane-induced anesthesia differs markedly among species breathing quietly. In humans, halothane accentuates phasic activity in rib cage and abdominal expiratory muscles, whereas activity in the parasternal intercostal muscles is abolished. In contrast, halothane abolishes phasic expiratory muscle activity during quiet breathing in dogs, but parasternal muscle activity is maintained. Respiratory muscle responses to CO2 rebreathing were measured in halothane-anesthetized dogs to determine if species differences present during quiet breathing persist over a wide range of central respiratory drive. METHODS: Chronic electromyogram electrodes were implanted in three expiratory agonists (the triangularis sterni, transversus abdominis, and external oblique muscles) and three inspiratory agonists (the parasternal intercostal muscle, costal and crural diaphragm) of six mongrel dogs. After a 1-month recovery period, the dogs were anesthetized in the supine position with halothane. The rebreathing response was determined by Read's method during anesthesia with stable 1 and 2 minimum alveolar end-tidal concentrations of halothane. CO2 concentrations were measured in the rebreathing bag using an infrared analyzer. Chest wall motion was measured by fast three-dimensional computed tomographic scanning. RESULTS: Halothane concentration did not significantly affect the slope of the relationship between minute ventilation (VE) and PCO2 (0.34 +/- 0.04 [M +/- SE] and 0.28 +/- 0.05 l.min-1.mmHg-1 during 1 and 2 minimum alveolar concentration anesthesia, respectively). However, 2 minimum alveolar concentration anesthesia did significantly decrease the calculated VE at a PCO2 of 60 mmHg (from 7.4 +/- 1.2 to 4.0 +/- 0.6 l.min-1), indicating a rightward shift in the response relationship. No electromyographic activity was observed in any expiratory muscle before rebreathing. Rebreathing produced electromyographic activity in at least one expiratory muscle in only two dogs. Rebreathing significantly increased electromyographic activity in all inspiratory agonists. Rebreathing significantly increased inspiratory thoracic volume change (delta Vth), with percentage of delta Vth attributed to outward rib cage displacement increasing over the course of rebreathing during 1 minimum alveolar concentration anesthesia (from 33 +/- 6% to 48 +/- 2% of delta Vth). CONCLUSIONS: Rebreathing did not produce expiratory muscle activation in most dogs, demonstrating that the suppression of expiratory muscle activity observed at rest persists at high levels of ventilatory drive. Other features of the rebreathing response also differed significantly from previous reports in halothane-anesthetized humans, including (1) an increase in the rib cage contribution to tidal volume during the course of rebreathing, (2) recruitment of parasternal intercostal activity by rebreathing, (3) differences in the response of ventilatory timing, and (4) the lack of effect of anesthetic depth on the slope of the ventilatory response. These marked species differences are further evidence that the dog is not a suitable model to study anesthetic effects on the activation of human respiratory muscles.

Anesthetics, Inhalation↗
PubMed1995

Hyperventilation, central autonomic control, and colonic tone in humans.

Symptoms attributable to hyperventilation are common among patients with the irritable bowel syndrome (IBS); indeed, some have suggested that hyperventilation may exacerbate the alimentary symptoms of IBS. Hyperventilation changes haemodynamic function through central and peripheral mechanisms; its effects on colonic motor function, however, are unknown. The aim of this study, therefore, was to assess the effects of hyperventilation on colonic tone and motility and on cardiovascular autonomic activity, and to discover if hypocapnia was critical to elicit the response. Phasic and tonic motility of the transverse and sigmoid colon, end tidal PCO2, pulse rate, and beat to beat pulse variability were assessed before, during, and after a five minute period of hypocapnic hyperventilation in 15 healthy volunteers; in seven other subjects, effects of both eucapnic and hypocapnic hyperventilation were evaluated. Hypocapnic but not eucapnic hyperventilation produced an increase in colonic tone and phasic contractility in the transverse and sigmoid regions and an increase in pulse rate and pulse interval variability. The findings are consistent with inhibition of sympathetic innervation to the colon or direct effects of hypocapnia on colonic smooth muscle, or both. These physiological gut responses suggest that some of the changes in colonic function are caused by altered brain or autonomic control mechanisms.

Adult↗
PubMed1994

Nitric oxide contributes to the rise in forearm blood flow during mental stress in humans.

1. Our aim was to determine whether the vasodilating substance nitric oxide (NO) contributes to the rise in forearm blood flow observed during mental stress in humans. We also determined whether the NO might be released as a result of cholinergic stimulation of the vascular endothelium. 2. Blood flow was measured in both forearms using plethysmography during several 3-5 min bouts of a colour word test. In one forearm the nitric oxide synthase blocker NG-monomethyl-L-arginine (L-NMMA) and other drugs were infused via a brachial artery catheter. The contralateral forearm served as a control. 3. When L-NMMA was given prior to mental stress it blunted the rise in blood flow in the treated forearm almost completely. The normal blood flow response returned during a second bout of stress conducted after a wash-out period. During a third bout of mental stress, administration of more L-NMMA again blunted the blood flow responses to mental stress. 4. When atropine was given prior to mental stress, the increases in blood flow were reduced in the treated forearm. Subsequent administration of both atropine and L-NMMA caused a somewhat greater reduction in the blood flow responses than those observed with atropine alone. 5. These data demonstrate that NO plays a role in forearm vasodilatation during mental stress in humans. It is likely that most of the NO is released by cholinergic stimulation of the vascular endothelium.

Adolescent↗
PubMed1994

Is nitric oxide involved in cutaneous vasodilation during body heating in humans?

The neurotransmitter responsible for neurogenic vasodilation in human skin during body heating is unknown. We sought to determine whether the vasodilating substance nitric oxide (NO) is involved in this phenomenon. Six subjects were heated for 50 min by use of a water-perfused suit while forearm blood flow (FBF) was measured with plethysmography and skin blood flow (SkBF) was measured by the laser-Doppler method in both arms. In one forearm, NG-monomethyl-L-arginine (L-NMMA), an NO synthase blocker, was infused into the brachial artery. Bolus doses of L-NMMA (< or = 4 mg/min) for 5 min were given to blunt NO-mediated vasodilator responses to acetylcholine (ACh, 64 micrograms/min). A continuous infusion of L-NMMA (< or = 1.0 mg/min) was used during body heating to maintain NO synthase blockade. In the forearm receiving L-NMMA, FBF was 1.8 +/- 0.3 ml.100 ml-1.min-1 before drug infusion and rose to 9.5 +/- 1.3 ml.100 ml-1.min-1 with ACh. After L-NMMA infusion, FBF was 1.3 +/- 0.2 ml.100 ml-1.min-1 and rose to 2.6 +/- 0.4 ml.100 ml-1.min-1 with ACh (both P < 0.05 vs. pre-L-NMMA). Similar changes in SkBF were seen with ACh and L-NMMA, confirming that the drugs reached cutaneous vessels. With body heating, oral temperature increased by 1.2 degrees C, heart rate increased by 34 beats/min, and mean arterial pressure remained constant at approximately 75 mmHg. FBF in the treated forearm rose to 11.5 +/- 2.1 vs. 12.6 +/- 1.7 ml.100 ml-1.min-1 in the control forearm (P > 0.05, control vs. treated response).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1994

Anesthesia and chest wall function in dogs.

Three anesthetics (pentobarbital, halothane, and isoflurane) were studied in six mongrel dogs to systematically compare their effects on chest wall function during spontaneous breathing. Each dog received each anesthetic on separate occasions. Electrical activities of several respiratory muscles were measured with chronically implanted electrodes, and chest wall motion was assessed by high-speed three-dimensional computed tomography scanning. Phasic expiratory muscle activity was markedly depressed by volatile anesthetics halothane and isoflurane compared with pentobarbital. In contrast, inspiratory activity in parasternal intercostal muscles was relatively well preserved during anesthesia with these volatile agents. The contribution of expiratory muscles to tidal volume was diminished during halothane and isoflurane compared with pentobarbital anesthesia. As anesthesia was deepened, expiratory muscle activity was unchanged during pentobarbital anesthesia, enhanced in some dogs during isoflurane anesthesia, and remained absent during halothane anesthesia. Activity in parasternal intercostal muscle was depressed as inspired concentration of halothane or isoflurane was increased, whereas diaphragmatic activity was unchanged. Depression of expiratory muscle activity by halothane persisted when breathing was stimulated by positive end-expiratory pressure, with significant mechanical consequences for chest wall configuration. Many of these findings are in contrast with previous observations in humans and suggest that the dog is not a suitable model for the study of the effects of anesthetic drugs on the pattern of human respiratory muscle activity.

Abdominal Muscles↗
PubMed1994

Haemoglobin-based blood substitutes: what's on the horizon?

Military and civilian medical organisations have long recognised that an oxygen-carrying volume expander which is easy to store, transport and administer could be life-saving for trauma victims. Concern over fatal blood-borne pathogens including hepatitis and human immunodeficiency virus (HIV), as well as a shrinking donor pool further highlight the need for such a product. A variety of substances that transport oxygen and augment intravascular volume in the absence of red cells are emerging as possible "blood substitutes" for use in humans. These include haemoglobin solutions, liposome encapsulated haemoglobin (LEH) and perfluorocarbons. The purpose of this review is to discuss issues related to the various oxygen-carrying volume-expanding solutions by addressing the following questions: 1) What are the ideal properties of an oxygen-carrying volume expander? 2) What types of oxygen-carrying solutions are under development? 3) How does the efficacy of these compounds compare to their limitations and side effects? and 4) What are the potential clinical applications of these products?

Blood Substitutes↗
PubMed1993

Increased muscle perfusion reduces muscle sympathetic nerve activity during handgripping.

This study sought to determine whether increasing blood flow to active muscles can blunt the normal rise in muscle sympathetic nerve activity (MSNA) during heavy rhythmic forearm exercise in humans. Subjects performed 5- to 6-min exercise bouts of handgripping (30/min) at 40-50% of maximum voluntary contraction (MVC). Blood flow was increased by application of suction (50 mmHg) around the forearm. Suction increased deep venous oxygen saturation in blood draining the forearm from 34 +/- 4 to 45 +/- 4%, indicating that muscle blood flow had risen by approximately 20%. Suction had no impact on the heart rate, perceived exertion, or electromyographic responses to the handgripping. During 6 min of exercise at 50% of MVC, MSNA rose from 376 +/- 67 to 970 +/- 125 units during the control trial vs. 396 +/- 69 to 729 +/- 94 units during the suction trial, and the difference was maintained during 2 min of postexercise ischemia (P < 0.05; suction < control). Mean arterial pressure (MAP) rose from 99 +/- 4 to 129 +/- 6 mmHg during control vs. 99 +/- 4 to 126 +/- 6 mmHg during the suction trial, and these responses were only different (P < 0.05; suction < control) during the final minute of the exercise bouts. During postexercise ichemia, MAP was 122 +/- 6 mmHg after the control trial but was only 112 +/- 4 mmHg after the suction trial. These results indicate that forearm suction augmented muscle blood flow, limited the activation of chemosensitive muscle afferents, and blunted the rise in MSNA during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Respiratory modulation of muscle sympathetic nerve activity in intact and lung denervated humans.

We determined the influences of breathing-induced changes in intrathoracic and intravascular pressures, central respiratory drive, and pulmonary vagal feedback on the within-breath variation in skeletal muscle sympathetic nerve activity (MSNA) in humans. MSNA (peroneal microneurography), arterial blood pressure (Finapres finger monitor), and tidal volume (VT) were recorded continuously in six normal subjects and four heart-lung transplant patients during: 1) spontaneous air breathing; 2) increased FICO2; 3) voluntary augmentation of VT with and without inspiratory resistance; and 4) positive pressure, passive mechanical ventilation. During conditions 3 and 4, which were performed under isocapnic conditions with a high MSNA background (either high resting activity or nonhypotensive lower body suction), subjects breathed at control or elevated VT with normal or prolonged inspiratory time (TI); breathing frequency was 12 breaths per minute. During control breathing in normal subjects there was a distinct within-breath pattern of MSNA, with approximately 70% of the activity occurring during low lung volumes (initial half of inspiration and latter half of expiration). This within-breath variation of MSNA was potentiated with increased VT breathing (> 85% of activity occurring during low lung volumes; p < 0.05 versus control breathing) and was similar during the voluntary and CO2-induced hyperpneas. MSNA decreased progressively and markedly from onset to late inspiration; fell slightly further, reaching its nadir at end-inspiration/onset-expiration; and rose sharply during mid-late expiration. Only the nadir of MSNA was associated with any change in arterial pressure. Resistive breathing, especially at elevated VT, caused a fall in arterial pressure and increased respiratory drive during inspiration, yet MSNA still declined as lung volume increased. Normal within-breath modulation of MSNA also was observed during control and elevated VT induced via positive pressure with passive ventilation, which reversed lung inflation/deflation-induced intrathoracic pressure changes and reduced or removed respiratory motor output. During control breathing in transplant patients the specific within-breath pattern of MSNA was somewhat different than that of the normal subjects, but on average, the overall low lung volume to high lung volume MSNA ratio was similar to normal subjects. In contrast to the normal subjects, however, there was no potentiation of the within-breath variation of MSNA with elevated tidal breathing. These findings indicate that during normal levels of tidal breathing most of the respiratory phase influence on muscle sympathetic outflow observed in normal conscious humans is independent of baroreceptor-sensed fluctuations in intrathoracic or intravascular pressures and of lung inflation-stimulated vagal afferent activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1992

Muscle chemoreflexes and exercise in humans.

This review focuses on the role afferent nerves from the contracting muscles play in linking muscle metabolism to the cardiovascular adjustments during exercise by means of a 'muscle chemoreflex'. In the 1930s Alam and Smirk provided the first clear evidence that human (and animal) skeletal muscles are innervated by chemosensitive afferents that can evoke increases in arterial blood pressure. They proposed that the purpose of the increase in pressure was to improve blood flow to the active muscles. Subsequent studies have identified the slowly conducting group IV afferents as the major class of fibres participating in the sensory arm of this reflex. Most of these fibres travel via the dorsal roots to the ipsilateral spinal cord where they synapse in the substantia gelatinosa and release substance P or other peptide transmitters. The second order (or higher) neurons cross to the contralateral side of the spinal cord and travel rostrally to stimulate brainstem cardiovascular centres and increase arterial pressure. Current evidence favours the concept that substances associated with muscle acidosis provide the stimulus to the afferents. In humans, chemosensitive afferent activation causes a marked increase in vasoconstrictor efferent muscle sympathetic nerve activity. It is unclear if the muscle chemoreflex improves blood flow to 'underperfused' active muscles by augmenting arterial pressure, or if the increase in sympathetic outflow restrains metabolic vasodilatation to regulate arterial blood pressure during activities like running or cycling.

Afferent Pathways↗
PubMed1992

Halothane changes the relationships between lung resistances and lung volume.

The authors hypothesized that relaxation of airway smooth muscle by halothane lessens the dependence of airway resistance on lung volume, and that halothane alters the relationship between pulmonary resistance and lung volume by changing both the airway and tissue components of pulmonary resistance. The relationship among airway resistance, tissue resistance, and lung volume was examined in mongrel dogs before and during the administration of halothane, both in airways with reduced smooth muscle tone (after vagotomy) and during moderate increases in smooth muscle tone caused by vagus nerve stimulation (VNS). Resistance were measured at several levels of positive end-expiratory pressure (PEEP, 4-15 cmH2O) using an alveolar capsule technique. Before halothane administration, airway resistance increased at low PEEP; VNS accentuated this increase. Tissue resistance increased at low PEEP only during VNS. Halothane had no significant effect on any resistance before VNS. During VNS, halothane markedly blunted increases in airway resistance and tissue resistance as PEEP decreased. The authors conclude that during stimulation of airway smooth muscle in dogs, halothane attenuates increases in airway resistance and tissue resistance with reductions in lung volume in dogs. Thus, moderate changes in lung volume have little effect on these resistances during halothane anesthesia under these conditions.

Airway Resistance↗