Coronary chemoreflex evoked by intrapericardial nicotine has a somatic component

1997 ◽  
Vol 272 (2) ◽  
pp. H827-H834 ◽  
Author(s):  
J. G. Pickar
Keyword(s):  
Blood Pressure ◽  
Vasovagal Syncope ◽  
The Other ◽  
Vagus Nerves ◽  
Knee Jerk ◽  
Autonomic Responses ◽  
Depressor Reflex ◽  
Cardiac Receptors ◽  
Muscle Reflexes ◽  
Stimulation Of

Stimulation of vagally innervated cardiac or pulmonary receptors reflexly evokes depressor responses called the coronary chemoreflex and pulmonary depressor reflex, respectively. The efferent arm of the pulmonary depressor reflex contains a somatic component wherein monosynaptic and polysynaptic muscle reflexes are attenuated. The purpose of the present investigation was to determine whether the efferent arm of the coronary chemoreflex also attenuates the monosynaptic knee-jerk reflex. Cardiac receptors were stimulated by injection of nicotine and bradykinin into the pericardial sac of 15 chloralose-anesthetized (50 mg/kg) cats. The knee-jerk reflex was elicited by tapping the patellar tendon intermittently. Intrapericardial nicotine attenuated the knee-jerk reflex by -26.2 +/- 6.5%. The attenuation was mediated by the vagus nerves, because vagotomy abolished the nicotine-induced attenuation. Stimulation of cardiac receptors evoked the attenuation, because blockade using intrapericardial procaine abolished the nicotine-induced attenuation. On the other hand, intrapericardial bradykinin augmented the knee-jerk reflex by 17.5 +/- 3.3%. The effect was not mediated by the vagus nerves; vagotomy did not abolish the bradykinin-induced augmentation. Changes in the knee-jerk reflex were not correlated with changes in blood pressure or heart rate evoked by intrapericardial nicotine or bradykinin. These findings demonstrate that reflex somatomotor responses accompany the reflex autonomic responses elicited by cardiac receptors. The somatic component of the vagally mediated coronary chemoreflex could contribute to the fainting reaction associated with exertional syncope of aortic stenosis and vasovagal syncope.

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.

Mechanisms of action of sodium cromoglycate

1985 ◽  
Vol 63 (6) ◽  
pp. 760-765 ◽  
Author(s):  
D. F. Biggs ◽  
V. Goel
Keyword(s):  
Blood Pressure ◽  
Sodium Cromoglycate ◽  
Arterial Blood Pressure ◽  
Vagal Stimulation ◽  
Cardiovascular Responses ◽  
Bilateral Stimulation ◽  
Vagus Nerves ◽  
Arterial Blood ◽  
Efferent Pathways ◽  
Stimulation Of

The effects of sodium cromoglycate (SCG) on cardiovascular and pulmonary responses to phenylbiguanide, capsaicin, and vagal stimulation were studied in anesthetized guinea pigs. Phenylbiguanide had no bronchospastic activity but induced reflex changes in arterial blood pressure which were reduced or abolished by SCG. Capsaicin induced nonreflex bronchospasm, and decreases in arterial blood pressure that were unaffected by SCG. Sodium cromoglycate, given before or after atropine, had no effect on the bronchospasm and cardiovascular responses to unilateral or bilateral stimulation of the vagus nerves. We conclude that SCG may influence both the afferent and efferent pathways of responses to drugs.

Predominance of vagal bradycardia mechanism in the brain stem of turtles

1988 ◽  
Vol 140 (1) ◽  
pp. 405-420 ◽  
Author(s):  
J. H. Hsieh ◽  
C. M. Pan ◽  
J. S. Kuo ◽  
C. Y. Chai
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Pressor Response ◽  
Inhibitory Response ◽  
Cardiac Contraction ◽  
Vagus Nerves ◽  
Arterial Blood ◽  
Vagal Bradycardia ◽  
The Brain ◽  
Stimulation Of

Cardiovascular parameters of spontaneously breathing pond turtles (Cyclemys flavomarginata) anaesthetized with chloralose (4 mg 100 g-1) and urethane (40 mg 100 g-1), were examined during exploratory electrical stimulation of the brain stem. Turtles exhibited a low mean systemic arterial blood pressure (MSAP, average 25 mmHg) and slow heart rate (average 24 beats min-1). Upon stimulation, pressor (sympathetic), depressor (sympathetic inhibition), bradycardia and hypotensive (vagal) responses were elicited from regions of the brain stem extending from the hypothalamus to the medulla, principally in the medial region. The pressor response appeared after a longer latency than did the bradycardia and hypotensive responses. It developed rather slowly, and rarely attained a magnitude double its resting value. In contrast, stimulation of many points in the brain stem produced marked slowing or even cessation of the heart beat, and thus resulted in an immediate fall of the blood pressure even to zero. This cardio-inhibitory response depended on the integrity of the vagus nerves and was particularly marked upon stimulation in the caudal medulla, the areas of the ambiguus, solitary and dorsomotor nuclei of the vagus and the midline structures. When such an area was stimulated continuously the heart stopped beating throughout the stimulation. The longest period of cardiac arrest before the appearance of escape was 35 min. With continuous stimulation of the peripheral end of the cut vagus, the earliest escape beat occurred even later (65 min). Epinephrine given intravenously produced an increase of MSAP and force of cardiac contraction, although the slope of pressor rise was shallow. Reflex bradycardia, however, was not observed. These experiments show that a very prominent vagal bradycardia can be evoked from the turtle brain stem, which may contribute to its well-known capacity for tolerating anoxia.

scholarly journals Blood Pressure and Autonomic Responses to Electrical Stimulation of the Renal Arterial Nerves Before and After Ablation of the Renal Artery

Hypertension ◽  
2013 ◽  
Vol 61 (2) ◽  
pp. 450-456 ◽  
Author(s):  
Masaomi Chinushi ◽  
Daisuke Izumi ◽  
Kenichi Iijima ◽  
Katsuya Suzuki ◽  
Hiroshi Furushima ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Renal Artery ◽  
Autonomic Responses ◽  
Before And After ◽  
Stimulation Of

Motor control of pulmonary airways studied by nerve stimulation

1965 ◽  
Vol 20 (2) ◽  
pp. 202-208 ◽  
Author(s):  
C. R. Olsen ◽  
H. J. H. Colebatch ◽  
P. E. Mebel ◽  
J. A. Nadel ◽  
N. C. Staub
Keyword(s):  
Motor Control ◽  
Vagus Nerve ◽  
Vagal Stimulation ◽  
Full Range ◽  
The Other ◽  
Vagus Nerves ◽  
Pulmonary Resistance ◽  
Impulse Frequency ◽  
Pulmonary Airways ◽  
Stimulation Of

To investigate the motor control of the pulmonary airways we combined electrical stimulation of the cervical efferent vagus nerves of cats and dogs with measurement of pulmonary resistance (Rl) and anatomic dead space (Vd), and with anatomic study of rapidly frozen lungs. Stimulus frequencies between 1 and 12/sec produced almost the full range of Rl responses in eight cats. The major constrictor response to stimulation of one vagus nerve was in the lung of the same side in dogs and cats. A decrease of Vd associated with the increase of Rl in five cats during bilateral vagal stimulation suggested that the Rl change resulted from a generalized or large airway narrowing, rather than a local constriction. In seven cats whose lungs were frozen at end inspiration during unilateral vagal stimulation, the lobar bronchi on the stimulated side were smaller in diameter than comparable bronchi of the other side. In only two of seven cats was there definite constriction of the small cartilaginous and membranous airways of the stimulated side by the criterion of longitudinal mucosal ridges; in two there was slight constriction and in the other three, no change. Respiratory bronchioles and alveolar ducts of frozen sections were not constricted. pulmonary resistance; vagus nerve distribution; anatomy of pulmonary airways; vagus nerve impulse frequency; sympathetic nerve inhibition Submitted on May 1, 1964

Chemical stimulation of cardiac receptors attenuates locomotion in mesencephalic cats

1997 ◽  
Vol 83 (1) ◽  
pp. 113-119 ◽  
Author(s):  
Joel G. Pickar
Keyword(s):  
Tibialis Anterior ◽  
Chemical Stimulation ◽  
Neural Pathway ◽  
Nerve Activity ◽  
Lateral Gastrocnemius ◽  
Decerebrate Cat ◽  
Mesencephalic Locomotor Region ◽  
Depressor Reflex ◽  
Cardiac Receptors ◽  
Stimulation Of

Pickar, Joel G. Chemical stimulation of cardiac receptors attenuates locomotion in mesencephalic cats. J. Appl. Physiol. 83(1): 113–119, 1997.—The purpose of the present investigation was to determine whether chemical stimulation of cardiac receptors is sufficient to inhibit locomotion. Decerebrate, unanesthetized cats were induced to walk on a treadmill by electrically stimulating the mesencephalic locomotor region (MLR). Cardiac receptors were stimulated by injecting nicotine (62.3 ± 8.6 μg/kg, mean ± SE) into the pericardial sac. Cardiac nerve activity was reversibly blocked by injecting procaine (2%) into the pericardial sac. Locomotion was monitored by using bipolar needle electrodes inserted into the lateral gastrocnemius (LG) and tibialis anterior (TA) muscles. Integrated electromyographic (iEMG) activity from each muscle was quantified on a step-by-step basis. Intrapericardial (ipc) nicotine inhibited locomotion and evoked the coronary chemoreflex. Blood pressure and heart rate decreased significantly by 45.6 ± 7.1 mmHg and 59.3 ± 12.3 beats/min, respectively. Nicotine ipc significantly reduced iEMG activity by 24–28% in the LG muscles. The TA muscles were not affected consistently by ipc nicotine. The locomotor inhibition and the depressor reflex paralleled each other and occurred within 5 s of nicotine injection. Procaine ipc blocked the nicotine-induced locomotor inhibition and depressor reflex. The effects of procaine were largely reversible, because ipc nicotine reduced iEMG activity in the LG (25–46%) but not in the TA muscles after washing procaine from the pericardial sac. These results demonstrate that cardiac receptors sensitive to nicotine inhibit MLR-induced locomotion in the decerebrate cat. These findings indicate the presence of a neural pathway from the heart whereby endogenous stimuli could reflexly alter motor control.

Reflux mechanisms involved in cardiac arrhythmias induced by hypothalamic stimulation

1978 ◽  
Vol 234 (2) ◽  
pp. H199-H209
Author(s):  
D. E. Evans ◽  
R. A. Gillis
Keyword(s):  
Blood Pressure ◽  
Cardiac Arrhythmias ◽  
Carotid Sinus ◽  
Vagal Afferents ◽  
Vagal Activity ◽  
Vagus Nerves ◽  
Stretch Receptors ◽  
Vagal Nerve Activity ◽  
Afferent Vagal ◽  
Stimulation Of

Electrical stimulation of widespread areas in the CNS has been shown to cause cardiac arrhythmias, which occur most frequently after cessation of stimulation. To determine the reflex and autonomic mechanism responsible for the poststimulation arrhythmias, we anesthetized cats with chloralose, and recorded arterial pressure, ECG, and cardiac vagal nerve activity. Stimulation of the hypothalamus consistently caused increases in blood pressure and heart rate during stimulation and caused arrhythmias, accompanied by vagal hyperactivity, immediately following stimulation. The arrhythmias were mediated solely by the vagus nerves because vagotomy or propantheline administration prevented them, whereas propranolol did not. Administration of either phentolamine or spinal cord transection prevented both the rise in blood pressure during stimulation and the poststimulation arrhythmias, but sectioning the carotid sinus and aortic depressor nerves had no preventative effect. However, when this denervation was combined with sectioning of vagal afferents, bursts of vagal activity (used as an index of cardiac rhythm disturbances) were prevented in three of six animals. Subsequent administration of phentolamine prevented the bursts in the remaining animals. It is concluded that poststimulation arrhythmias are elicited by the rise in blood pressure occurring during stimulation causing a sudden surge in parasympathetic outflow to the heart. The reflexogenic areas involved appear to be stretch receptors innervated by afferent vagal fibers.

Augmented pressor response to vasopressin in awake dogs after cardiac denervation

1987 ◽  
Vol 252 (1) ◽  
pp. R145-R152
Author(s):  
B. C. Wang ◽  
G. F. Ginter ◽  
K. L. Goetz
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Intravenous Infusion ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
The Other ◽  
Cardiac Denervation ◽  
Arterial Blood ◽  
Cardiac Receptors

Hemodynamic responses to varying intravenous infusion rates of vasopressin were studied in two groups of dogs; one group was cardiac denervated and the other sham operated. Vasopressin given at 200, 1,000, and 5,000 fmol X kg-1 X min-1 produced increases in aortic pressure that were significantly greater in cardiac-denervated dogs than in sham-operated dogs. The augmented pressor response in cardiac-denervated dogs was associated with greater increases in total peripheral resistance in this group; decreases in cardiac output were similar in the two groups of dogs. Vasopressin decreased heart rate significantly in each group, but the magnitude of the decrease was significantly smaller in cardiac-denervated dogs. In contrast to these results, the intravenous infusion of phenylephrine or angiotensin II in other experiments on the same dogs produced comparable increases in aortic pressure in each group. These results are consistent with earlier evidence indicating that vasopressin elicits more effective reflex mechanisms to attenuate the increases in blood pressure caused by its direct vasoconstrictor action than do other vasoconstrictor agents, such as angiotensin II and phenylephrine. Since the infusion of vasopressin produced a greater increase in arterial blood pressure in cardiac-denervated dogs than it did in sham-operated control dogs, it appears that at least part of the unique action of vasopressin may be mediated by the potentiation of a peripheral vasodepressor reflex arising from cardiac receptors.

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.

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