Microvascular dilation evoked by chemical stimulation of C-fibers in rats

2015 ◽  
Vol 118 (1) ◽  
pp. 55-60 ◽  
Author(s):  
Andrew M. Roberts ◽  
Jerry Yu ◽  
Irving G. Joshua

Activation of pulmonary C-fibers can reflexively decrease heart rate, blood pressure, and peripheral vascular resistance. However, the effects of these afferents on microvascular tone remain incompletely understood. In this study, we examined the effects of these afferents on microvascular tone in a striated muscle vascular bed. The right cremaster muscle in pentobarbital-anesthetized rats with intact circulation and innervation was suspended in a tissue bath, and diameters of small arterioles were measured by intravital video microscopy. Stimulation of pulmonary C-fibers by injecting capsaicin (5 μg/kg) or phenylbiguanide (20 μg/kg) into the right atrium dilated small arterioles and decreased blood pressure and heart rate. The effects persisted when the cervical vagus nerves were cooled to 5 to 7°C (blocking myelinated fibers), but were prevented by cooling to 0°C (blocking C-fibers and myelinated fibers), by cutting the genital femoral nerve (GFN) supplying the cremaster to block the nerve supply to the muscle, or by adding 6-hydroxydopamine to the bathing medium to selectively block sympathetic effects by depleting norepinephrine from adrenergic nerve terminals. Our results show that stimulation of pulmonary C-fibers reflexively dilates small arterioles in striated muscle by a mechanism that could involve withdrawal of sympathetic adrenergic tone. In conclusion, pulmonary C-fibers can exert an inhibitory influence on neural tone of the microcirculation at an important site where microvascular resistance and tissue blood flow are regulated.

1995 ◽  
Vol 79 (4) ◽  
pp. 1346-1350 ◽  
Author(s):  
K. P. O'Hagan ◽  
R. S. Anderson ◽  
L. B. Bell ◽  
S. W. Mittelstadt ◽  
P. S. Clifford

Stimulation of cardiopulmonary vagal C fibers with phenyl biguanide (PBG) reflexly inhibits locomotion in addition to causing depression of blood pressure (BP), heart rate (HR), and respiration in cats and rats. We investigated whether PBG caused somatomotor inhibition during exercise in the rabbit, a species in which it is known that the hemodynamic and respiratory responses to PBG are mediated by cardiac rather than by pulmonary receptors. In eight New Zealand White rabbits, BP, HR, and hindlimb electromyographic (EMG) responses to 60 and 120 micrograms/kg PBG and saline vehicle were evaluated during two separate 3-min exercise bouts at 10 m/min at 0% grade. During exercise, 60 micrograms/kg PBG decreased BP (-27 +/- 4 mmHg) and HR (-95 +/- 16 beats/min) but did not inhibit locomotion as suggested by the EMG response (+112 +/- 8% of preinfusion EMG). Hemodynamic and EMG responses to 120 micrograms/kg PBG were similar to 60 micrograms/kg PBG. Saline infusion during exercise had no effect on HR, BP, or locomotion (+114 +/- 8% of preinfusion EMG). Locomotion is not inhibited by PBG in rabbits, which suggests that PBG-induced reflex somatomotor inhibition observed in other species is primarily mediated by pulmonary rather than by cardiac receptors.


PEDIATRICS ◽  
1989 ◽  
Vol 83 (2) ◽  
pp. 240-243
Author(s):  
Myung K. Park ◽  
Da-Hae Lee

Indirect BP measurement was obtained in the right upper arm in 219 healthy newborn infants with the Dinamap monitor and was compared with values obtained from the calf to establish normative BP values and to help establish a diagnosis of hypertension and coarctation of the aorta in the newborn. There were 174 Mexican-Americans (79.5%), 33 whites (15.0%), and 12 blacks (5.5%). The width of the BP cuff was selected to be 0.4 to 0.5 times the circumference of the extremities. Three supine position readings of BPs and heart rate were obtained from each site and were averaged for statistical analyses. Mean arm BP values (±SD) of the neonate less than 36 hours of age were 62.6±6.9/38.9± 5.7 mm Hg (48.0±6.2 mm Hg). Neonates older than 36 hours had slightly but significantly (P<.05) greater values (4 to 6 mm Hg) than did infants younger than 36 hours of age. Active neonates had values 6 to 10 mm Hg greater than quiet neonates (P<.05). BP values in the calf obtained with the same-sized cuff were almost identical with those obtained from the arm. Differences in consecutively obtained arm and calf BPs (arm values minus calf values) were 1.1±7.7 mm Hg systolic, -0.01 ± 6.2 mm Hg diastolic, and 0.9 ±6.9 mm Hg mean pressures. Mean heart rate (±SD) of neonates less than 36 hours of age was 129.4± 13.2 beats per minute and that of neonates older than 36 hours of age was 139.4± 14.1 beats per minute. These results show the following: (1) arm BPs and calf BPs using the same-sized cuff are almost identical with mean values of approximately 65/ 41 mm Hg (50 mm Hg) in neonates one to three days of age, (2) arm BP of 75/49 mm Hg (59 mm Hg) or greater is in the hypertensive range, and (3) calf BPs that are less than arm BPs by mean + 1 SD (6 to 9 mm Hg) necessitate a thorough investigation for coarctation of the aorta.


1993 ◽  
Vol 75 (2) ◽  
pp. 663-667 ◽  
Author(s):  
M. Saito ◽  
A. Tsukanaka ◽  
D. Yanagihara ◽  
T. Mano

The aim of this study was to clarify the relationship between sympathetic outflow to skeletal muscle and oxygen uptake during dynamic exercise. Muscle sympathetic nerve activity (MSNA) was recorded from the right median nerve microneurographically in eight healthy volunteers during leg cycling at four different intensities in a seated position for a 16-min bout. Work loads selected were 20, 40, 60, and 75% of maximal oxygen uptake (VO2max). Heart rate and blood pressure were measured during each exercise test. MSNA burst frequency was suppressed by 28% during cycling at 20% VO2max (23 vs. 33 bursts/min for control). Thereafter, it increased in a linear fashion with increasing work rate, with a significantly higher burst frequency during 60% VO2max than the control value. Both heart rate and mean blood pressure rose significantly during 20% VO2max from the control value and increased linearly with increased exercise intensity. During light exercise, MSNA was suppressed by arterial and cardiopulmonary baroreceptors as a result of the hemodynamic changes associated with leg muscle pumping. The baroreflex inhibition may overcome the muscle metaboreflex excitation to induce MSNA suppression during light exercise. These results suggest that during light exercise MSNA is inhibited, perhaps due to loading of the cardiopulmonary and arterial baroreflexes, and that during heavier exercise the increase in MSNA occurs as muscle metaboreflexes are activated.


1992 ◽  
Vol 72 (3) ◽  
pp. 1039-1043 ◽  
Author(s):  
V. K. Somers ◽  
K. C. Leo ◽  
R. Shields ◽  
M. Clary ◽  
A. L. Mark

Recent evidence indicates that muscle ischemia and activation of the muscle chemoreflex are the principal stimuli to sympathetic nerve activity (SNA) during isometric exercise. We postulated that physical training would decrease muscle chemoreflex stimulation during isometric exercise and thereby attenuate the SNA response to exercise. We investigated the effects of 6 wk of unilateral handgrip endurance training on the responses to isometric handgrip (IHG: 33% of maximal voluntary contraction maintained for 2 min). In eight normal subjects the right arm underwent exercise training and the left arm sham training. We measured muscle SNA (peroneal nerve), heart rate, and blood pressure during IHG before vs. after endurance training (right arm) and sham training (left arm). Maximum work to fatigue (an index of training efficacy) was increased by 1,146% in the endurance-trained arm and by only 40% in the sham-trained arm. During isometric exercise of the right arm, SNA increased by 111 +/- 27% (SE) before training and by only 38 +/- 9% after training (P less than 0.05). Endurance training did not significantly affect the heart rate and blood pressure responses to IHG. We also measured the SNA response to 2 min of forearm ischemia after IHG in five subjects. Endurance training also attenuated the SNA response to postexercise forearm ischemia (P = 0.057). Sham training did not significantly affect the SNA responses to IHG or forearm ischemia. We conclude that endurance training decreases muscle chemoreflex stimulation during isometric exercise and thereby attenuates the sympathetic nerve response to IHG.


1945 ◽  
Vol 22 (1-2) ◽  
pp. 63-74
Author(s):  
JOSEPH BARCROFT ◽  
D. H. BARRON

1. A method (the needle method) is described for the measurement of the pressure in the stream going through a vessel. 2. In the foetal sheep the needle method applied to the umbilical artery gives substantially the same results as the mercurial manometer applied to the carotid, until about half-way through the gestation period. 3. As gestation proceeds the needle method applied at the first moment at which it can be applied to the umbilical artery (or a branch) gives readings substantially lower, and increasingly lower as gestation proceeds, than does the mercurial manometer read at the first moment at which it can be read. 4. The discrepancy is due to the sum of a number of causes which are discussed, but of these the most important is an actual rise of pressure between the time of delivery and the completion of the dissections contingent on the use of the mercurial manometer. 5. The cause of this is not at present demonstrated, but either or both of two factors may be concerned: (a) a dulling of the central nervous system which weakens the depressor reflex; (b) the establishment of a greater degree of vasomotor tone consequent on the bombardment of the central nervous system with sensory stimuli. 6. The pulse rates in utero and just after delivery of the foetus into a saline bath at 39-40°C. (the umbilical circulation being unimpaired) are not significantly different. 7. The pulse rate quickens up to the 70th-80th day, after which it becomes slower as gestation proceeds. 8. If both vagi be severed, the pulse rate te to quicken throughout gestation. The pulse, therefore, comes increasingly under vagus inhibition from the 80th-90th day onwards. 9. Even after the vagi have been cut after the 120th day (it has not been tried before) adrenalin in sufficient quantity will cause a further quickening of the pulse. 10. The earliest date at which stimulation of the peripheral end of the right vagus was observed to slow the heart was the 77th day. On the 85th day peripheral stimulation of the left vagus also failed, but succeeded on the 101st day. 11. Central stimulation of the left vagus, with the right vagus intact, produced slowing on the 77th day. 12. Slowing of the heart synchronous with rise of arterial pressure has been observed on the 111th day. 13. Slowing of the heart which bears evidence of being reflex has been obtained by raising the blood pressure (clamping the cord) on the 121st day and by injection of adrenalin on the 118th day. 14. Approaching term both the carotid sinus and cardiac depressor mechanisms are functional. 15. Lowering of the blood pressure as the result of stimulation of the central end of the vagus and with both vagi severed can be demonstrated late in gestation.


1994 ◽  
Vol 267 (6) ◽  
pp. H2398-H2406 ◽  
Author(s):  
H. L. Pan ◽  
G. L. Stahl ◽  
S. V. Rendig ◽  
O. A. Carretero ◽  
J. C. Longhurst

Abdominal ischemia and reperfusion reflexly activate the cardiovascular system. In the present study, we evaluated the role of endogenously produced bradykinin (BK) in the stimulation of ischemically sensitive visceral afferents. Single-unit activity of abdominal visceral C fiber afferents was recorded from the right thoracic sympathetic chain of anesthetized cats during 5 min of abdominal ischemia. Abdominal ischemia increased the portal venous plasma BK level from 49 +/- 10 to 188 +/- 66 pg/ml (P < 0.05). Injection of BK (1 microgram/kg ia) into the descending aorta significantly increased impulse activity (0.88 +/- 0.16 impulses/s) of 10 C fibers, whereas a kinin B1-receptor agonist, des-Arg9-BK (1 microgram/kg), did not alter the discharge rate. Inhibition of kininase II activity with captopril (4 mg/kg i.v.) potentiated impulse activity of 14 ischemically sensitive C fibers (0.44 +/- 0.09 vs. precaptopril, 0.33 +/- 0.08 impulses/s; P < 0.05). In addition, a kinin B2-receptor antagonist (NPC-17731; 40 micrograms/kg i.v.) attenuated activity of afferents during ischemia (0.39 +/- 0.08 vs. pre-NPC-17731, 0.72 +/- 0.13 impulses/s; P < 0.05) and eliminated the response of 10 C fibers to BK. Another kinin B2-receptor antagonist, Hoe-140 (30 micrograms/kg iv), had similar inhibitory effects on six other ischemically sensitive C fibers. In 15 separate cats treated with aspirin (50 mg/kg i.v.), Hoe-140 (30 micrograms/kg i.v.) attenuated impulse activity of only 3 of 16 ischemically sensitive C fibers. These data suggest that BK produced during abdominal ischemia contributes to the stimulation of ischemically sensitive visceral C fiber afferents through kinin B2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)


1965 ◽  
Vol 209 (4) ◽  
pp. 751-756 ◽  
Author(s):  
Vincent V. Glaviano ◽  
Mary Ann Klouda

Cardiac responses to electrical stimulation of the right or left stellate ganglion were recorded from 16 open-chest anesthetized dogs in hemorrhagic shock. Shock was induced by bleeding the animals to a mean blood pressure of 40 mm Hg. This level of pressure was maintained for 4 hr, during which time blood pressure, heart rate, force of myocardial contraction, and intraventricular pressures were recorded. Stimulation of the stellate ganglion for 15–40 sec every 30 min after hemorrhage showed a gradual decrease in these parameters to levels below control. The reinfusion of blood and the infusion of exogenous l-norepinephrine did not restore an increase in force of cardiac contraction to stellate stimulation. Myocardial epinephrine and norepinephrine levels in shock were found not to differ from those in 14 normal dog hearts. In contrast to almost complete myocardial refractoriness to stellate stimulation in hemorrhagic shock, stimulation of the vagus nerve elicited bradycardia and eventual cardiac arrest. The decrease observed in force of cardiac contraction to stimulation of the stellate ganglion in hemorrhagic shock may be due to depletion of norepinephrine stores in the heart.


1985 ◽  
Vol 58 (3) ◽  
pp. 907-910 ◽  
Author(s):  
H. D. Schultz ◽  
A. M. Roberts ◽  
C. Bratcher ◽  
H. M. Coleridge ◽  
J. C. Coleridge ◽  
...  

Stimulation of bronchial C-fibers evokes a reflex increase in secretion by tracheal submucosal glands, but the influence of pulmonary C-fibers on tracheal gland secretion is uncertain. In anesthetized dogs with open chests, we sprayed powdered tantalum on the exposed mucosa of a segment of the upper trachea to measure the rate of secretion by submucosal glands. Secretions from the gland ducts caused elevations (hillocks) in the tantalum layer. We counted hillocks at 10-s intervals for 60 s before and 60 s after we injected capsaicin (10–20 micrograms/kg) into the right atrium to stimulate pulmonary C-fiber endings. Right atrial injection of capsaicin increased the rate of hillock formation fourfold, but left atrial injection had no significant effect. The response was abolished by cutting the vagus nerves or cooling them to 0 degree C. We conclude that the reflex increase in tracheal submucosal gland secretion evoked by right atrial injection of capsaicin was initiated as capsaicin passed through the pulmonary vascular bed, and hence that pulmonary C-fibers, like bronchial C-fibers, reflexly increase airway secretion.


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