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.

Vagal stimulation-induced gastric damage in rats

1991 ◽  
Vol 261 (1) ◽  
pp. G104-G110
Author(s):  
L. E. Hierlihy ◽  
J. L. Wallace ◽  
A. V. Ferguson
Keyword(s):  
Vagal Stimulation ◽  
Mucosal Damage ◽  
Vagal Afferents ◽  
Gastric Damage ◽  
Gastric Mucosal Damage ◽  
Sprague Dawley ◽  
Vagus Nerves ◽  
Sprague Dawley Rats ◽  
Series Of Experiments ◽  
Stimulation Of

The role of the vagus nerve in the development of gastric mucosal damage was examined in urethan-anesthetized male Sprague-Dawley rats. Electrical stimulation was applied to the vagus nerves for a period of 60 min, after which macroscopic gastric damage was scored and samples of the stomach were fixed for later histological assessment. Damage scores were assigned blindly based on a 0 (normal) to 3 (severe) scale. Stimulation of vagal afferents or efferents in isolation did not result in significant damage to the gastric mucosa (P greater than 0.1). In contrast, stimulation of both intact vagus nerves resulted in significant gastric mucosal damage (mean damage score, 2.0 +/- 0.33, P less than 0.01). A second series of experiments demonstrated this gastric damage to be induced within 30-60 min; extending the stimulation period to 120 min did not worsen the gastric damage scores significantly (P greater than 0.1). In a third study, stimulation of both intact vagus nerves after paraventricular nucleus (PVN) lesion resulted in damage scores (0.33 +/- 0.17) that were significantly reduced compared with intact PVN and non-PVN-lesioned animals (P less than 0.01). These results indicate that the development of vagal stimulation-induced gastric damage requires the activation of both afferent and efferent vagal components and suggest further that such damage is dependent upon an intact PVN.

Effect of baroreceptor denervation on stimulation of drinking by angiotensin II in conscious dogs

1991 ◽  
Vol 260 (3) ◽  
pp. E333-E337 ◽  
Author(s):  
C. K. Klingbeil ◽  
V. L. Brooks ◽  
E. W. Quillen ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Plasma Osmolality ◽  
Plasma Angiotensin ◽  
High Doses ◽  
Stimulation Of

Angiotensin II causes marked stimulation of drinking when it is injected centrally but is a relatively weak dipsogen when administered intravenously. However, it has been proposed that the dipsogenic action of systemically administered angiotensin II may be counteracted by the pressor action of the peptide. To test this hypothesis, the dipsogenic action of angiotensin II was investigated in dogs, in which low and high baroreceptor influences had been eliminated by denervation of the carotid sinus, aortic arch, and heart. In five sham-operated dogs, infusion of angiotensin II at 10 and 20 ng.kg-1.min-1 increased plasma angiotensin II concentration to 109.2 +/- 6.9 and 219.2 +/- 38.5 pg/ml and mean arterial pressure by 20 and 29 mmHg, respectively, but did not induce drinking. In four baroreceptor-denervated dogs, the angiotensin II infusions produced similar increases in plasma angiotensin II concentration and mean arterial pressure but, in contrast to the results in the sham-operated dogs, produced a dose-related stimulation of drinking. Water intake with the low and high doses of angiotensin II was 111 +/- 44 and 255 +/- 36 ml, respectively. The drinking responses to an increase in plasma osmolality produced by infusion of hypertonic sodium chloride were not different in the sham-operated and baroreceptor-denervated dogs. These results demonstrate that baroreceptor denervation increases the dipsogenic potency of intravenous angiotensin II and provides further support for the hypothesis that the dipsogenic action of intravenous angiotensin II is counteracted by the rise in blood pressure.

Role of vagal afferents in the control of abdominal expiratory muscle activity in the dog

1991 ◽  
Vol 71 (5) ◽  
pp. 1795-1800 ◽  
Author(s):  
S. B. Hollstien ◽  
M. L. Carl ◽  
E. S. Schelegle ◽  
J. F. Green
Keyword(s):  
Muscle Activity ◽  
Vagal Afferents ◽  
Oblique Muscle ◽  
Vagus Nerves ◽  
Expiratory Muscle ◽  
C Fibers ◽  
C Fiber ◽  
Before And After ◽  
Afferent Vagal ◽  
Alpha Chloralose

We examined the contribution of afferent vagal A- and C-fibers on abdominal expiratory muscle activity (EMA). In seven spontaneously breathing supine dogs anesthetized with alpha-chloralose we recorded the electromyogram of the external oblique muscle at various vagal temperatures before and after the induction of a pneumothorax. When myelinated fibers were blocked selectively by cooling the vagus nerves to 7 degrees C, EMA decreased to 40% of control (EMA at 39 degrees C). With further cooling to 0 degrees C, removing afferent vagal C-fiber activity, EMA returned to 72% of control. On rewarming the vagus nerves to 39 degrees C, we then induced a pneumothorax (27 ml/kg) that eliminated the EMA in all the dogs studied. Cooling the vagus nerves to 7 degrees C, during the pneumothorax, produced a slight though not significant increase in EMA. However, further cooling of the vagus nerves to 0 degrees C caused the EMA to return vigorously to 116% of control. In three dogs, intravenous infusion of a constant incrementally increasing dose of capsaicin, a C-fiber stimulant, decreased EMA in proportion to the dose delivered. These results suggest that EMA is modulated by a balance between excitatory vagal A-fiber activity, most likely from slowly adapting pulmonary stretch receptors, and inhibitory C-fiber activity, most likely from lung C-fibers.

THE EFFECT OF VAGOTOMY AND DENERVATION OF THE CAROTID SINUS ON DIURESIS FOLLOWING PLASMA VOLUME EXPANSION

1959 ◽  
Vol 37 (1) ◽  
pp. 81-90 ◽  
Author(s):  
J. W. Pearce
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Carotid Sinus ◽  
Urine Flow ◽  
Flow Section ◽  
Plasma Volume Expansion ◽  
Reflex Mechanism ◽  
Albumin Infusion ◽  
Stretch Receptors ◽  
Afferent Vagal

The hypothesis exists that afferent vagal fibers, arising in cardiac atrial stretch receptors, serve as the sensory limb of a reflex mechanism sensitive to variations in blood volume and producing corresponding changes in urine flow. Section of the vagi did not, however, prevent the diuretic and chloruretic response to expansion of the plasma volume with isotonic infusions. Carotid sinus denervation alone or combined with vagotomy also failed to prevent the diuresis and chloruresis following infusion in most experiments, although in a few cases the response was absent or diminished after the combined procedure. Reasons are given for believing that the bovine albumin infusion used did not act directly on the kidney to increase urine output, but rather through a reflex mechanism which could not have depended on the integrity of the vagi. It is concluded that receptors additional to those in the cardiac atria and the carotid sinus must contribute to the sensory component of a reflex mechanism regulating plasma volume.

Vasomotor inhibition in rabbits by vagal nonmedullated fibers from cardiopulmonary area

1975 ◽  
Vol 229 (5) ◽  
pp. 1410-1413 ◽  
Author(s):  
PN Thoren ◽  
G Mancia ◽  
JT Shepherd
Keyword(s):  
Blood Pressure ◽  
Vagal Afferents ◽  
Total Contribution ◽  
C Fibers ◽  
Aortic Blood ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Vagal Nerves ◽  
Aortic Blood Pressure ◽  
Aortic Baroreceptors

In anesthetized rabbits with sinus and aortic nerve cut, when the cervical vagal nerves were cooled to 12, 8, 6, and 0degreeC, there were progressive increases in aortic blood pressure of 7 +/- 1, 15 +/- 2, 25 +/- 1, and 41 +/- 2 mmHg (SE), respectively. For comparison, during cooling of the aortic and vagal nerves, at 12degreesC there was a decrease in firing in the afferent fibers from aortic baroreceptors (48 +/- 4%) and pulmonary stretch receptors (57 +/- 5%), and at 6degreesC all activity was abolished. Thus, at 6degreesC the activity in medullated fibers from the aortic baroreceptors and pulmonary stretch receptors is blocked, but the increase in aortic blood pressure with vagal cooling is only 60% of that with cooling to 0degreeC. This demonstrates that cardiopulmonary receptors with nonmedullated vagal afferents (C fibers) contribute to the tonic inhibition of the vasomotor center. Because of overlap in sensitivity of different vagal fibers to cooling, the total contribution of these C fibers cannot be evaluated.

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.

Acute Device-Based Blood Pressure Reduction: Electrical Activation of the Carotid Baroreflex in Patients Undergoing Elective Carotid Surgery

Vascular ◽  
2007 ◽  
Vol 15 (2) ◽  
pp. 63-69 ◽  
Author(s):  
Jürg Schmidli ◽  
Hannu Savolainen ◽  
Friedrich Eckstein ◽  
Eric Irwin ◽  
Tim K. Peters ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Carotid Sinus ◽  
Blood Pressure Reduction ◽  
Acute Effect ◽  
Carotid Surgery ◽  
Proof Of Concept ◽  
Sinus Wall ◽  
Carotid Baroreflex ◽  
Voltage Dependent ◽  
Stimulation Of

Carotid sinus baroreceptors are involved in controlling blood pressure (BP) by providing input to the cardiovascular regulatory centers of the medulla. The acute effect of temporarily placing an electrode on the carotid sinus wall to electrically activate the baroreflex was investigated. We studied 11 patients undergoing elective carotid surgery. Baseline BP was 146+30/66±17 mm Hg and heart rate (HR) 72±7 bpm (mean ± standard deviation). An electrode was placed upon the carotid sinus and after obtaining a steady state baseline of BP and HR, an electric current was applied and increased in 1-volt increments. A voltage dependent and highly significant reduction in BP was observed which averaged 18±26* and 8.0±12 mm Hg for systolic BP and diastolic BP, respectively. Maximal reductions occurred at 4.4±1.2 V: 23±24 mm Hg*, 16±10 mm Hg* and 7±12 bpm* for systolic BP, diastolic BP and HR, respectively (= p <.05). Thus, electrical stimulation of the carotid sinus activates the carotid baroreflex resulting in a reduction in BP and HR. This presents a proof of concept for device based baroreflex modulation in acute BP regulation and adds to the available data which provide a rationale for evaluating this system in the context of chronic BP reduction in hypertensive patients.

scholarly journals Modulation of cardiopulmonary depressor reflex in nucleus ambiguus by electroacupuncture: roles of opioids and γ-aminobutyric acid

2012 ◽  
Vol 302 (7) ◽  
pp. R833-R844 ◽  
Author(s):  
Stephanie C. Tjen-A-Looi ◽  
Peng Li ◽  
Min Li ◽  
John C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Low Frequency ◽  
Vagal Afferents ◽  
Nucleus Ambiguus ◽  
Aminobutyric Acid ◽  
Vagal Activity ◽  
Induced Hypotension ◽  
Cardiopulmonary Receptors ◽  
Depressor Reflex

Stimulation of cardiopulmonary receptors with phenylbiguanide (PBG) elicits depressor cardiovascular reflex responses, including decreases in blood pressure and heart rate mediated in part by the brain stem parasympathetic cardiac neurons in the nucleus ambiguus (NAmb). The present study examined NAmb neurotransmitter mechanisms underlying the influence of electroacupuncture (EA) on the PBG-induced hypotension and bradycardia. We hypothesized that somatic stimulation during EA modulates PBG responses through opioid and γ-aminobutyric acid (GABA) modulation in the NAmb. Anesthetized and ventilated cats were studied during repeated stimulation with PBG or cardiac vagal afferents while low-frequency EA (2 Hz) was applied at P5–6 acupoints overlying the median nerve for 30 min and NAmb neuronal activity, heart rate, and blood pressure were recorded. Microinjection of kainic acid into the NAmb attenuated the PBG-induced bradycardia from −60 ± 11 to −36 ± 11 beats/min. Likewise, EA reduced the PBG-induced depressor and bradycardia reflex by 52 and 61%, respectively. Cardiac vagal afferent evoked preganglionic cellular activity in the NAmb was reduced by EA for about 60 min. Blockade of opioid or GABAA receptors using naloxone and gabazine reversed the EA-related modulation of the evoked cardiac vagal activity by 73 and 53%, respectively. Similarly, naloxone and gabazine reversed EA modulation of the negative chronotropic responses from −11 ± 5 to −23 ± 6 and −13 ± 4 to −24 ± 3 beats/min, respectively. Thus EA at P5–6 decreases PBG evoked hypotension and bradycardia as well as the NAmb PBG-sensitive preganglionic cardiac vagal outflow through opioid and GABA neurotransmitter systems.

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.

Effect of blood pressure on medial medulla-induced muscle atonia

1987 ◽  
Vol 252 (6) ◽  
pp. H1249-H1257 ◽  
Author(s):  
Y. Y. Lai ◽  
J. M. Siegel ◽  
W. J. Wilson
Keyword(s):  
Blood Pressure ◽  
Carotid Sinus ◽  
Muscle Tone ◽  
Blood Pressure Reduction ◽  
Base Line ◽  
Cervicothoracic Junction ◽  
Medullary Reticular Formation ◽  
Muscle Atonia ◽  
6 Hydroxydopamine ◽  
Stimulation Of

Stimulation of the medial medullary reticular formation (MMRF) has long been reported to produce generalized inhibition of skeletal muscle activity. However, several studies have reported that in most cases MMRF stimulation produces only increases in muscle tone. In the present investigation we have found that blood pressure is a critical variable, determining whether MMRF stimulation will produce muscle excitation or inhibition. When mean arterial pressure (MAP) was greater than 80 mmHg but less than 148 mmHg, MMRF stimulation produced muscle antonia. Reductions of blood pressure by pharmacological or mechanical techniques induced a reversal of response to MMRF stimulation; stimulation that produced inhibition in base-line conditions produced excitation after MAP reduction. MAP reductions of as little as 10% could cause the reversal response. In contrast, the EMG reduction to MMRF stimulation was not changed or was augmented when MAP was raised. MMRF induced atonia, and its reversal by blood pressure reduction persisted after bilateral isolation of the carotid sinus combined with vagotomy, and in the 6-hydroxydopamine-treated cat. Spinal transection at the cervicothoracic junction did not block atonia or the reversal response. It is suggested that the reversal is mediated centrally.

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