Phenyl biguanide does not inhibit locomotion in conscious rabbits

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
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
New Zealand ◽  
Saline Infusion ◽  
C Fibers ◽  
New Zealand White Rabbits ◽  
Saline Vehicle ◽  
Cardiac Receptors ◽  
Respiratory Responses ◽  
Stimulation Of

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.

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
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Striated Muscle ◽  
Adrenergic Nerve ◽  
Tissue Blood Flow ◽  
Bathing Medium ◽  
Myelinated Fibers ◽  
C Fibers ◽  
The Right ◽  
Stimulation Of

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.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Nervous control of heart rate: activity in the cardiac vagus of the dogfish

1982 ◽  
Vol 53 (6) ◽  
pp. 1330-1335 ◽  
Author(s):  
E. W. Taylor ◽  
P. J. Butler
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Action Potentials ◽  
Sympathetic Innervation ◽  
Nervous Control ◽  
Temporal Relationships ◽  
Maximum Water ◽  
External Stimuli ◽  
Neurophysiological Basis ◽  
Stimulation Of

In the absence of any sympathetic innervation to the heart, nervous control of heart rate in the dogfish is solely attributable to inhibitory parasympathetic input from the vagus nerve. Action potentials can be recorded from the cardiac vagus of the dogfish following its exposure in the anterior cardinal sinus. The rates of heartbeat and ventilation, blood pressure, hematocrit, and responses to external stimuli such as hypoxia, which include a bradycardia, remained typical of fish with their nervous and circulatory systems virtually intact. The recordings included sporadically active units that accelerated during hypoxia, possibly inducing the bradycardia, and regular bursts of action potentials synchronous with ventilatory movements that appeared to arise reflexly from stimulation of pharyngeal proprioceptors. These bursts may loosely couple the respiratory and cardiac pumps, increasing the probability of concurrence between periods of maximum water and blood flow. The preparation enables detailed study of the temporal relationships between the pumps and its neurophysiological basis.

SOME RESPIRATORY AND CARDIOVASCULAR EFFECTS OF GRADUAL SARIN POISONING IN THE RAT

1961 ◽  
Vol 39 (6) ◽  
pp. 1001-1011 ◽  
Author(s):  
W. C. Stewart ◽  
D. H. McKay
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Gastrocnemius Muscle ◽  
Artificial Ventilation ◽  
Cardiovascular Effects ◽  
Vagus Nerves ◽  
Toxic Dose ◽  
Circulatory Insufficiency ◽  
Slow Intravenous Infusion ◽  
Stimulation Of

Anesthetized rats were given sarin (isopropyl methylphosphonofluoridate) by slow intravenous infusion, while respiration, blood pressure, heart rate, and contractions of the gastrocnemius muscle in response to stimulation of the sciatic nerve were recorded.When artificial ventilation was not carried out, breathing stopped after a toxic dose of sarin had been given, even though the blood pressure was above normal and neuromuscular conduction was not impaired. On the other hand, when artificial ventilation was provided after breathing stopped, the blood pressure and heart rate fell, and death was apparently caused by circulatory insufficiency.Infusion of sarin caused slowing of the heart rate which was not prevented by previous section of the vagus nerves. Injection of atropine restored the heart rate to normal, and enabled the animals to withstand large doses of sarin as long as artificial ventilation was maintained.It was concluded that sarin caused a cholinergic circulatory collapse which was the cause of death in rats maintained with artificial ventilation. This circulatory insufficiency was alleviated by large doses of atropine. Possible causes of the depression of circulation are discussed, and reasons are given for believing it to be due mainly to cholinergic diminution of cardiac output, caused by accumulation of acetylcholine in the heart.

scholarly journals Intravenous adenosine and dyspnea in humans

2005 ◽  
Vol 98 (1) ◽  
pp. 180-185 ◽  
Author(s):  
Nausherwan K. Burki ◽  
Wheeler J. Dale ◽  
Lu-Yuan Lee
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Peripheral Chemoreceptor ◽  
C Fibers ◽  
Group Data ◽  
Lung Resistance ◽  
Time Latency ◽  
Stimulation Of

Intravenous adenosine for the treatment of supraventricular tachycardia is reported to cause bronchospasm and dyspnea and to increase ventilation in humans, but these effects have not been systematically studied. We therefore compared the effects of 10 mg of intravenous adenosine with placebo in 21 normal subjects under normoxic conditions and evaluated the temporal sequence of the effects of adenosine on ventilation, dyspnea, and heart rate. The study was repeated in 11 of these subjects during hyperoxia. In all subjects, adenosine resulted in the development of dyspnea, assessed by handgrip dynamometry, without any significant change ( P > 0.1) in lung resistance as measured by the interrupter technique. There were significant increases ( P < 0.05) in ventilation and heart rate in response to adenosine. The dyspneic response occurred slightly before the ventilatory or heart rate responses in every subject, but the timing of the dyspneic, ventilatory, and heart rate responses was not significantly different when the group data were analyzed (18.9 ± 5.8, 20.3 ± 5.5, and 19.7 ± 4.5 s, respectively). During hyperoxia, adenosine resulted in similar effects, with no significant differences in the magnitude of the ventilatory response; however, compared with the normoxic state, the intensity of the dyspneic response was significantly ( P < 0.05) reduced, whereas the heart rate response increased significantly ( P < 0.05). These data indicate that intravenous adenosine-induced dyspnea is not associated with bronchospasm in normal subjects. The time latency of the response indicates that the dyspnea is probably not a consequence of peripheral chemoreceptor or brain stem respiratory center stimulation, suggesting that it is most likely secondary to stimulation of receptors in the lungs, most likely vagal C fibers.

Sign in / Sign up

Export Citation Format

Share Document