Cardiac responses to stimulation of thoracic afferents in the primate and canine

1976 ◽  
Vol 231 (4) ◽  
pp. 1279-1284 ◽  
Author(s):  
DR Kostreva ◽  
GL Hess ◽  
EJ Zuperku ◽  
J Neumark ◽  
RL Coon ◽  
...  

Excitatory cardiovascular responses to electrically stimulated upper thoracic sympathetic afferent nerves were observed in halothane-anesthetized mongrel dogs and monkeys. The central end of the transected ventral limb of the left ansa subclavia was stimulated before and after several types of denervation. Significant increases in right and left ventricular maximum systolic pressures, systolic and diastolic systemic blood pressures, and aortic flow were observed. The carotid sinuses were denervated bilaterally and stimulation of the ansa was repeated. The cardiovascular responses to stimulation of the ventral ansa after carotid sinus denervation were greater in magnitude than those observed prior to denervation. This carotid sinus modulation of cardiovascular responses was observed in dogs and monkeys. Cardiovascular responses to stimulation of the ventral ansa after bilateral vagotomy were significantly less than the responses observed after carotid sinus denervation prior to vagotomy. However, the responses after vagotomy were statistically identical to responses obtained while stimulating the ventral ansa when the carotid sinuses and vagi remained intact.

1983 ◽  
Vol 245 (6) ◽  
pp. R820-R826 ◽  
Author(s):  
G. A. Ordway ◽  
J. C. Longhurst ◽  
J. H. Mitchell

Chemical stimulation of afferents from the stomach and gallbladder has been shown reflexly to activate the cardiovascular system. It is not known, however, whether stimulating afferents from the pancreas evoke similar reflex activity. Therefore we recorded the cardiovascular responses in cats anesthetized with methoxyflurane, while we applied capsaicin (200 micrograms/ml) and bradykinin (0.001-1,000 micrograms/ml) to the surface of the pancreas. Topically applying these algesic substances evoked cardiovascular responses that included increases in systemic arterial pressure, heart rate, left ventricular dP/dt at 40-mmHg developed pressure and systemic vascular resistance. Bilateral vagotomy at the level of the diaphragm did not diminish the cardiovascular responses evoked by capsaicin or bradykinin. In contrast, removal of the celiac and superior mesenteric ganglia abolished the cardiovascular responses demonstrated previously when capsaicin or bradykinin was applied to the pancreas. We conclude that afferent endings in the pancreas can be stimulated reflexly to increase cardiovascular function in cats. This reflex activation represents a potential mechanism for eliciting the cardiovascular changes observed during acute pancreatitis, particularly the marked vasoconstriction that may lead to renal failure.


1979 ◽  
Vol 236 (5) ◽  
pp. H769-H774
Author(s):  
H. O. Stinnett ◽  
D. F. Peterson ◽  
V. S. Bishop

In pentobarbital-anesthetized rabbits with aortic nerves cut, reflex heart rate and mean arterial pressure (MAP) changes were quantified in response to maximal central stimulation of the left aortic nerve (LANS) before and during steady-state changes in isolated carotid intrasinus pressure (ISP). To distinguish possible vagally mediated cardiopulmonary influences, responses were measured before and after vagotomy. Changes in MAP observed by altering ISP within +/- 15 mmHg of the equilibrium pressure (EP) were linear and inversely correlated to changes in ISP, with a slope of approximately 3 both before and after vagotomy (r greater than or equal to 0.929, P less than 0.05). The peak fall in MAP during LANS was dependent upon ISP. The change in the MAP responses to LANS for each mmHg change in ISP ranged from 1.7 with vagi intact to 1.3 after vagotomy. Heart rate was unaltered by isolation of the carotid sinus and was independent of the small changes in ISP between +/- 15 mmHg of EP. These results indicate that blood pressure changes elicited by the aortic baroreflex are extremely sensitive to the degree of carotid sinus compensation. Thus, to assess the sensitivity of any arterial reflex area, the existing level of compensation by other barosensitive areas must be known.


1986 ◽  
Vol 251 (4) ◽  
pp. H748-H755 ◽  
Author(s):  
P. M. Gootman ◽  
B. J. Buckley ◽  
S. M. DiRusso ◽  
N. Gootman ◽  
A. C. Yao ◽  
...  

Cardiovascular responses to stimulation of cardiopulmonary receptors were evaluated in standard breed developing swine (1-2 days, 1-2 wk, and 2 mo of age) and sexually mature miniswine anesthetized with 0.25-0.50% halothane in O2. Cryptenamine, a mixture of veratrum viride alkaloids (VVA), was administered as right atrial or left ventricular bolus injections in doses of 5-20 micrograms/kg. In developing swine, mean aortic pressure (AoP) decreased after 10-20 micrograms/kg VVA in 1- to 2-wk olds and after 5-20 micrograms/kg VVA in 2-mo olds. Bradycardia was always elicited. Renal (Ren) and femoral (Fem) vasodilation occurred in the 1- to 2-wk-old and 2-mo-old groups after 5-20 micrograms/kg VVA. Mesenteric (Mes) vasodilation was elicited with 10-20 micrograms/kg VVA in the 1- to 2-wk-old group and with 5-20 micrograms/kg VVA in 2-mo olds. In the 1- to 2-day-old group, VVA did not significantly alter Ren, Fem, and Mes vascular resistance. In mature miniswine, 20 micrograms/kg VVA elicited decreases in AoP and heart rate that were similar in magnitude to responses obtained with only 5 micrograms/kg VVA in dogs. Cardiovascular responses to VVA were abolished after bilateral vagotomy but were not altered after denervation of the carotid sinuses. The results indicate postnatal maturation of the Bezold-Jarisch reflex in swine.


1985 ◽  
Vol 63 (9) ◽  
pp. 1122-1132 ◽  
Author(s):  
J. A. Armour ◽  
W. C. Randall

Electrical stimulation of a canine vagosympathetic complex or a cardiopulmonary nerve can elicit a variety of negative chronotropic and inotropic cardiac responses, with or without alterations in systemic arterial pressure. In the period immediately following cessation of such a stimulation "rebound" tachycardia, increased inotropism above control values in one or more regions of the heart, and (or) elevation in systemic arterial pressure can occur. These "rebound" phenomena are abolished by propranolol or ipsilateral chronic sympathectomy. It is proposed that "vagal" poststimulation "rebound" of the canine cardiovascular system is primarily the result of activation of sympathetic neural elements present in the vagosympathetic complexes or cardiopulmonary nerves.


1995 ◽  
Vol 268 (2) ◽  
pp. H526-H534 ◽  
Author(s):  
H. L. Pan ◽  
A. C. Bonham ◽  
J. C. Longhurst

The present study examined the role of substance P (SP) as a sensory neurotransmitter in cardiovascular responses to bradykinin applied on the gallbladder. Experiments were performed in anesthetized cats in which sympathetic chains were transected at the T5-T6 level, and the tip of the intrathecal catheter was positioned at T6-T7 to limit the injectate between T6 and L2. Bradykinin (10 micrograms/ml) was applied onto the gallbladder before and after intrathecal injection of [D-Pro2,D-Phe7,D-Trp9]SP (100–200 micrograms, NK1/NK2-receptor antagonist), CP-99,994 (50–100 micrograms, selective NK1 antagonist), MEN-10,376 (100–500 micrograms, selective NK2 antagonist), or vehicle. Intrathecal injection of NK1 but not NK2 antagonist significantly reduced increases in mean arterial pressure, heart rate, and maximal rate of left ventricular pressure change by 28 +/- 2 mmHg (33 +/- 4%), 4 +/- 1 beats/min (42 +/- 5%), and 497 +/- 46 mmHg/s (36 +/- 4%), respectively. Intrathecal injection of NK1 or NK1/NK2 antagonist had no effect on cardiovascular responses evoked by electrical stimulation in the rostral ventral lateral medulla. These data suggest that endogenous SP, acting as a sensory neurotransmitter, is involved in the excitatory cardiovascular reflex caused by chemical stimulation of the gallbladder through its action on NK1 receptors in the spinal cord.


1984 ◽  
Vol 247 (3) ◽  
pp. H459-H466 ◽  
Author(s):  
J. C. Longhurst ◽  
C. L. Stebbins ◽  
G. A. Ordway

We examined the potential for cardiovascular reflexes caused by the application of either bradykinin or capsaicin to the serosal or mucosal surface of the stomach. After application to the serosa, bradykinin (10 micrograms/ml) evoked increases in mean arterial pressure of 12 +/- 2 mmHg, heart rate of 5 +/- 1 beats/min, left ventricular dP/dt (at 40 mmHg developed pressure) of 305 +/- 54 mmHg/s and systemic vascular resistance of 0.04 +/- 0.01 PRU. Capsaicin (200 microgram/ml) caused similar cardiovascular responses. There were no cardiovascular responses when either substance was applied to the gastric mucosa. The responses to both chemicals were abolished by celiac ganglionectomy but not by bilateral vagotomy. To determine whether the cardiovascular responses evoked by bradykinin were caused by smooth muscle contraction, we compared the increases in gastric smooth muscle tension and blood pressure elicited by bradykinin, bethanechol, or acetylcholine. Bethanechol and acetylcholine caused greater increases in tension than bradykinin, whereas bradykinin evoked greater increases in blood pressure than either bethanechol or acetylcholine. We conclude that stimulation of gastric afferents by capsaicin or bradykinin causes cardiovascular reflexes, primarily through activation of chemosensitive receptors.


1985 ◽  
Vol 249 (4) ◽  
pp. F542-F545 ◽  
Author(s):  
R. Vandongen ◽  
H. McGowan ◽  
H. Anderson ◽  
A. Barden

The contribution of the renal nerves in maintaining blood pressure and modulating renal prostanoid synthesis was examined in established (less than 8 wk in duration) one-kidney, one-clip (1K,1C) hypertension in the rat. Systolic blood pressure was measured for 7 days after renal denervation, at which time the renal artery clip was removed. Twenty-four-hour urinary excretion of PGE2 and 6-keto-PGF1 alpha (stable degradation product of PGI2) was determined before and after denervation and unclipping. Compared with sham-denervated rats, denervation (n = 15) resulted in a small but significant fall in blood pressure (from 216 +/- 4 to 182 +/- 4 mmHg after 48 h) and an increase in urinary 6-keto-PGF1 alpha (from 31 +/- 4 to 43 +/- 5 ng/24 h after 24 h). There was no change in PGE2 excretion. Seven days after surgery, blood pressures were similar in denervated (202 +/- 4 mmHg) and sham-denervated (211 +/- 5 mmHg) rats and fell to a similar extent 24 h after unclipping (142 +/- 3 and 147 +/- 4 mmHg, respectively). Urinary 6-keto-PGF1 alpha increased from 25 +/- 5 to 74 +/- 11 in denervated and 21 +/- 2 to 72 +/- 9 ng/24 h in sham-denervated rats in the 24 h after unclipping. PGE2 excretion increased approximately twofold over this period. These findings indicate that the renal nerves have only a minor role in established hypertension in the 1K,1C rat and that the reversal of hypertension and stimulation of renal prostanoid synthesis following unclipping is not dependent on neural mechanisms.


1991 ◽  
Vol 260 (6) ◽  
pp. R1089-R1094 ◽  
Author(s):  
R. Ermirio ◽  
P. Ruggeri ◽  
C. E. Cogo ◽  
C. Molinari ◽  
F. R. Calaresu

Effects of microinjection of atrial natriuretic factor (ANF) into cardioinhibitory sites in the nucleus ambiguous (NA) or on single vagal cardioinhibitory neurons (VCN) were investigated in urethan-anesthetized rats. Sites containing cardioinhibitory neurons were identified by observing a marked and reproducible bradycardia in response to microiontophoretically applied (20-40 nA) or microinjected (20 nl) 0.1 M L-glutamate. In 35 of the 40 (87.5%) cardioinhibitory sites identified by microinjection of glutamate, ANF (20 nl of 10(-7) M) decreased heart rate (HR; -47.1 +/- 2.5 beats/min). No responses were elicited in the other five sites. In animals paralyzed and artificially ventilated, the HR effects of ANF were not significantly different before and after muscle paralysis. Microinjections of 10 nl of 10(-7) M ANF caused excitation of 19 of 21 VCN (90%), which was followed by a decrease in HR (-20.8 +/- 2.3 beats/min); no neuronal or cardiovascular responses were elicited by ANF in the remaining two VCN. Bilateral vagotomy or atropine sulfate (1 mg/kg iv) abolished cardiac slowing without affecting neuronal activation, whereas propranolol (2 mg/kg iv) did not affect either response to ANF. These results suggest that ANF is a neuromediator involved in the excitation of cardioinhibitory neurons in the NA.


1961 ◽  
Vol 201 (1) ◽  
pp. 134-138 ◽  
Author(s):  
Richard H. Ulmer ◽  
Walter C. Randall

Pressures were recorded simultaneously from the four cardiac chambers in anesthetized, open-chest dogs during electrical stimulation of the stellate ganglion before and after bilateral vagotomy. Augmentation of atrial contraction was shown to accompany that in the ventricles by increased atrial pressures, as well as by the direct recording of atrial force. Fast-speed records revealed the augmentation was primarily in the a-wave. In some experiments mean atrial pressures increased slightly, in others they remained essentially unchanged, and, in still others, declined during stimulation. The particular response in any given animal was not predictable. There was no consistent relationship between the change in right and left mean atrial pressures, although they showed simultaneous augmentation in amplitude of the a-wave. The augmented a-wave resulted in a significant increment in the atrioventricular pressure gradient during late diastole, and thus contributed to increased ventricular filling. Mean pressures consistently increased in both right and left ventricles during stellate stimulation.


1960 ◽  
Vol 198 (6) ◽  
pp. 1139-1142 ◽  
Author(s):  
Orville A. Smith ◽  
Robert F. Rushmer ◽  
Earl P. Lasher

Devices to measure left ventricular pressure, diameter and heart rate in animals with closed chests were placed on the hearts of dogs. After recovery from this operation the dogs were trained to exercise on a treadmill and the cardiovascular responses to this exercise were recorded. Stimulating electrodes were then stereotaxically placed in the diencephalon. In some dogs the electrodes were chronically implanted, and the stimulation was carried out after recovery from this second operation. In other animals stimulation was carried out immediately while they were under chloralose anesthesia. Stimulation of the H1 and H2 fields of Forel and the periventricular gray of the third ventricle resulted in cardiovascular responses similar to those which result from exercise.


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