Modulation of bradykinin-induced gastric-cardiovascular reflexes by histamine

1992 ◽  
Vol 262 (1) ◽  
pp. R112-R119 ◽  
Author(s):  
C. L. Stebbins ◽  
G. L. Stahl ◽  
S. J. Theodossy ◽  
J. C. Longhurst
Keyword(s):  
Cardiovascular Response ◽  
Pressor Response ◽  
Left Ventricular Pressure ◽  
Inhibitory Effect ◽  
Left Ventricular ◽  
Reflex Response ◽  
Cardiovascular Reflexes ◽  
H1 Receptor ◽  
C Fibers ◽  
Before And After

Both histamine and bradykinin induce gastric-cardiovascular reflexes and are released during several pathophysiological conditions. This study examined the possibility that histamine modulates the magnitude of the reflex response to stimulation by bradykinin. Thus in chloralose anesthetized cats, the cardiovascular response to stimulation of the gastric serosa with 1 microgram/ml bradykinin was monitored before and after topical application of 100 micrograms/ml histamine (n = 6) or 1 mg/ml diphenhydramine (H1-receptor antagonist) and histamine (n = 5). After application of histamine, bradykinin-induced increases in mean arterial pressure and left ventricular pressure were attenuated by 23 and 27%, respectively. Conversely, when the H1-receptors on the serosal surface of the stomach were blocked (n = 5) before application of histamine, the pressor response to bradykinin was augmented by 26%. To determine the afferents that might contribute to the attenuating effect of histamine, we recorded single unit activity in 14 A delta and 21 C visceral afferent fibers in response to bradykinin stimulation before and after histamine stimulation. We observed that the impulse activity of 10 of the A delta and 14 of the C fibers to bradykinin stimulation was reduced after treatment with histamine. These results suggest that histamine induces an inhibitory effect on the nerve endings of visceral A delta and C fibers to the action of bradykinin through an H1-receptor mechanism. This inhibitory effect attenuates the magnitude of the consequent cardiovascular reflex response.

Cardiovascular reflexes elicited by passive gastric distension in anesthetized cats

1981 ◽  
Vol 240 (4) ◽  
pp. H539-H545 ◽  
Author(s):  
J. C. Longhurst ◽  
H. L. Spilker ◽  
G. A. Ordway
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Diastolic Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Reflex Response ◽  
Gastric Distension ◽  
Cardiovascular Reflexes ◽  
Myocardial Oxygen Demand ◽  
Before And After

Hemodynamic responses to passive gastric distension were examined in alpha-chloralose anesthetized cats. Gastric balloons were distended with 37 degrees C fluid at slow (50 ml/min) and rapid (250 ml/min) infusion rates before and after laparotomy. Passive gastric distension at the slow infusion rate significantly (P less than 0.05) increased mean arterial pressure (MAP) by 28%, dP/dt at 40 mmHg developed pressure by 29%, and systemic vascular resistance (SVR) by 35%. Likewise, the rapid distension rate significantly (P less than 0.05) increased MAP (20%), dP/dt (16%), and SVR (23%). Heart rate, aortic flow, and left ventricular end-diastolic pressure remained unchanged at both distension rates. Cardiovascular responses to passive gastric distension were similar before and after laparotomy. Section of the vagus nerve at the diaphragm did not alter the responses, whereas abdominal splanchnic nerve section significantly (P less than 0.05) reduced the changes in mean arterial pressure and dP/dt. These results indicate that passive gastric distension in the cat elicits cardiovascular reflexes sufficient to increase myocardial oxygen demand. Such a reflex response could potentially contribute to postprandial angina in humans.

Cardiovascular reflexes evoked by histamine stimulation of the stomach

1991 ◽  
Vol 260 (4) ◽  
pp. H1098-H1105 ◽  
Author(s):  
C. L. Stebbins ◽  
S. J. Theodossy ◽  
J. C. Longhurst
Keyword(s):  
Cardiovascular Response ◽  
Pressor Response ◽  
Gastric Wall ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Cardiovascular Reflexes ◽  
Histamine Stimulation ◽  
Serosal Surface ◽  
H2 Antagonist ◽  
Stimulation Of

This study examined the potential for histamine to cause cardiovascular reflexes when applied to the serosal or mucosal surface of the stomach. Thus, in chloralose-anesthetized cats, histamine was applied to the serosal surface of the stomach in concentrations ranging from 0.5 to 1,000 micrograms/ml. This resulted in graded increases in mean arterial pressure (MAP), maximal left ventricular pressure over time (dP/dt), and heart rate ranging from 9 +/- 4 to 30 +/- 3 mmHg, 450 +/- 103 to 1,710 +/- 610 mmHg/s, and 2 +/- 1 to 13 +/- 4 beats/min, respectively. Histamine stimulation of the gastric serosa evoked a greater pressor response than that observed when the same concentration of histamine (100 micrograms/ml) was applied to the gastric mucosa (43 +/- 7 vs. 13 +/- 3 mmHg, respectively). In six cats, celiac ganglionectomy abolished the previously observed cardiovascular response to histamine stimulation of the serosal surface of the stomach. When the gastric serosa was treated with the H1-receptor antagonist diphenhydramine (1 mg/ml) (n = 5), the cardiovascular response to histamine was abolished. In five other cats, administration of the H2-antagonist ranitidine (1 mg/ml) had no effect on the histamine-induced responses. When indomethacin (2-5 mg/ml), was applied to the serosal surface of the stomach (n = 6), histamine-induced increases in MAP and dP/dt were attenuated. However, application of PGE2 (1 microgram/ml) restored these two responses. These results suggest that histamine stimulates H1-receptors in the gastric wall to cause reflex cardiovascular responses that are dependent, in part, on the local production of prostaglandins.

Nociceptin in rVLM mediates electroacupuncture inhibition of cardiovascular reflex excitatory response in rats

2005 ◽  
Vol 98 (6) ◽  
pp. 2056-2063 ◽  
Author(s):  
Melissa M. Crisostomo ◽  
Peng Li ◽  
Stephanie C. Tjen-A-Looi ◽  
John C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Pressor Response ◽  
Inhibitory Effect ◽  
Reflex Response ◽  
Ventrolateral Medulla ◽  
Gastric Distension ◽  
Sprague Dawley ◽  
Nociceptin Receptor

Electroacupuncture (EA) at Neiguan-Jianshi acupoints through an opioid mechanism inhibits the cardiovascular pressor response induced by mechanical stimulation of the stomach. Because nociceptin also may regulate cardiovascular activity through its action in the brain stem, we hypothesized that this neuromodulator serves a role in the EA-related inhibitory effect. Blood pressure in ventilated male Sprague-Dawley rats (400–600 g) anesthetized by ketamine and α-chloralose was measured during balloon inflation of the stomach. Gastric distension with 6–8 ml of air induced consistent pressor reflexes of 26 ± 1 mmHg that could be repeated every 10 min for 100 min. When nociceptin (10 nM) was microinjected into the rostral ventrolateral medulla (rVLM), the pressor response induced by gastric distension was inhibited by 68 ± 6%. Thirty minutes of EA also decreased the reflex response by 75 ± 11%; microinjection of saline into the rVLM did not alter the inhibitory effect of EA. In contrast, microinjection of a nociceptin receptor antagonist into the rVLM promptly reversed the EA response. Pretreatment with the opioid receptor antagonist naloxone did not influence the EA-like inhibitory effect of nociceptin on the distension-induced pressor reflex (22 ± 1 to 8 ± 2 mmHg). Furthermore, a μ-opioid receptor agonist microinjected into the rVLM after microinjection of a nociceptin receptor antagonist during EA promptly reversed the nociceptin receptor antagonist-related inhibition of the EA effect. Thus, in addition to the classical opioid system, nociceptin, through opioid receptor-like-1 receptor stimulation in the rVLM, participates in the modulatory influence of EA on reflex-induced increases in blood pressure.

Influence of CO2 on cardiovascular response to hypoxia in conscious dogs

1980 ◽  
Vol 239 (4) ◽  
pp. H545-H545 ◽  
Author(s):  
Raymond C. Koehler ◽  
Brian W. McDonald ◽  
John A. Krasney
Keyword(s):  
Cardiovascular Response ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Coronary Vasodilation ◽  
Circulatory Response ◽  
Wide Range ◽  
Before And After ◽  
Tension Time ◽  
Arterial Chemoreceptor

The modulating effect of CO2 on the circulatory response to hypoxia in chronically instrumented conscious dogs was examined over a wide range of arterial partial pressure of O2 [PaO2 (from 80 to 25 Torr)] during a 41-min rebreathing period at three CO2 levels: hypocapnia (from PaCO2 of 32 to 18 Torr), eucapnia (32 Torr), and mild hypercapnia (40 Torr). Eucapnic and hypercapnic hypoxic responses were also measured after sinoaortic denervation (SAD) to assess the arterial chemoreceptor and baroreceptor reflex contributions. Elevating PaCO2 attenuated the tachycardia during hypoxia and produced progressively greater systemic, renal, and splanchnic vasoconstriction before but not after SAD. Vagal block converted the rises in renal and splanchnic flows observed during hypocapnic hypoxia to declines. The increase in left ventricular dP/d tmax was not affected by varying PaCO2 either before or after SAD. Coronary flow increased an additional onefold during hypoxia when PaCO2 was elevated both before and after SAD, but the tension-time indices did not differ significantly. These results indicate that: a) cardiopulmonary vagal afferents effectively counteract chemoreflex-induced vasoconstriction during hypocapnic hypoxia; b) chemoreflex vasoconstriction predominates in the renal and splanchnic beds when PaCO2 is elevated; c) the sinoaortic reflexes restrain the heart rate, but not the contractility response to hypoxia when PaCO2 is increased; and d) the augmented coronary vasodilation produced by CO2 is probably mediated by local CO2-hypoxic interactions.

Reflex pressor response to arterial phenylbiguanide: role of abdominal sympathetic visceral afferents

1998 ◽  
Vol 275 (6) ◽  
pp. H2025-H2035 ◽  
Author(s):  
Liang-Wu Fu ◽  
John C. Longhurst
Keyword(s):  
Serotonin Receptor ◽  
Pressor Response ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Visceral Afferents ◽  
Reflex Response ◽  
Selective Agonist ◽  
Cervical Vagotomy ◽  
Increased Activity

Phenylbiguanide (PBG), a 5-HT3 (serotonin) receptor agonist, has been used in many studies as a “selective” agonist to elicit reflex bradycardia and hypotension through activation of cardiac and pulmonary vagal afferents. Because we have shown that endogenous 5-HT stimulates ischemically sensitive abdominal sympathetic afferents through 5-HT3 receptors, we investigated the possibility that left ventricular (LV) and intra-arterial administration of PBG may evoke a competing reflex response by increasing the activity of sympathetic visceral afferents in anesthetized cats. Mean arterial pressure (MAP) and heart rate (HR) were monitored. When both vagal and sympathetic afferents were intact, PBG (40 μg/kg, injected into the LV) significantly decreased MAP and HR in 8 of 10 cats but increased MAP in the remaining 2 cats. After bilateral cervical vagotomy, LV PBG significantly increased MAP. PBG (40 μg/kg ia) significantly increased MAP and HR, whereas intravenous PBG significantly decreased MAP and HR ( n = 10 cats). Furthermore, the pressor response to PBG (40 μg /kg ia) was reduced by 68% ( P < 0.05; n = 4 cats) by celiac and mesenteric ganglionectomies. In studies of single-unit abdominal sympathetic afferents, intra-arterial but not intravenous PBG (40 μg/kg) significantly increased activity of 10 ischemically sensitive afferents but not ischemically insensitive afferents. Blockade of 5-HT3 receptors with tropisetron (200 μg/kg iv) eliminated the response of the afferents and the pressor response to PBG. These data indicate that PBG administered into the LV usually, but not always, evokes a depressor response that is converted to a pressor response following cervical vagotomy. Also, intra-arterial PBG induces a pressor response by stimulating 5-HT3receptors largely associated with ischemically sensitive abdominal sympathetic afferents.

Myoglobin function in the isolated fluorocarbon-perfused dog heart

1978 ◽  
Vol 234 (5) ◽  
pp. H567-H572 ◽  
Author(s):  
R. P. Cole ◽  
B. A. Wittenberg ◽  
P. R. Caldwell
Keyword(s):  
Oxygen Consumption ◽  
Left Ventricle ◽  
Mechanical Performance ◽  
Left Ventricular Pressure ◽  
Dry Weight ◽  
Left Ventricular ◽  
Facilitated Diffusion ◽  
Dog Heart ◽  
Before And After ◽  
Ringer’S Lactate

An isolated dog heart preparation perfused with hemoglobin-free fluorocarbon suspension has been developed to study the role of myoglobin in myocardial function. The coronary vasculature was perfused at constant flow, with oxygen consumption determined from arteriovenous PO2 differences. Muscle function was assessed by measurement of pressures generated in a latex balloon placed in the left ventricle. The perfusate consisted of 20% perfluorotributylamine and 80% Ringer's lactate with 16 mM glucose. Steady-state oxygen consumption decreased from 0.30 to 0.11 ml/min per gram dry weight left ventricle, as perfusate PO2 decreased from 690 to 150 mmHg. Left ventricular pressure generation and oxygen consumption were determined before and after addition of 8 mM sodium nitrite, which changed functional ferrous myoglobin to high-spin ferric myoglobin. Over the range of perfusate PO2 studied, nitrite addition did not alter mechanical performance or myocardial oxygen consumption. These data suggest that those conditions necessary for substantial myoglobin-facilitated diffusion of oxygen in the myocardium are not present in the isolated fluorocarbon-perfused dog heart.

Cardiovascular response to experimental spinal cord compression

1973 ◽  
Vol 38 (3) ◽  
pp. 326-331 ◽  
Author(s):  
Eduardo E. Eidelberg
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Compression ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Blocking Agent ◽  
Cord Compression ◽  
Left Ventricular ◽  
Cervical Cord ◽  
Content Type ◽  
Ectopic Beats

✓ Anesthetized, and unanesthetized decerebrate, cats were used to study the arterial pressor response to spinal cord compression. To produce a cervical compression it was necessary that the cervical cord be functionally connected to the thoracic cord, pressor response by the reverse was not true. A pressor response above 200 mm Hg systolic was associated with electrocardiographic (EKG) signs of left ventricular overload and ventricular ectopic beats. These changes were not prevented by atropine, hexamethonium, or propanolol. Both the pressor response and the EKG abnormalities were prevented by an alpha-adrenergic blocking agent. The authors conclude that alpha-adrenergically mediated arterial vasoconstriction is the effector mechanism in the pressor response to increased intracranial pressure or cord compression.

Detection of Cardiac Variability in the Isolated Rat Heart

2006 ◽  
Vol 8 (1) ◽  
pp. 55-66 ◽  
Author(s):  
Autumn M. Schumacher ◽  
Joseph P. Zbilut ◽  
Charles L. Webber ◽  
Dorie W. Schwertz ◽  
Mariann R. Piano
Keyword(s):  
Rat Heart ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Isolated Rat Heart ◽  
Rat Hearts ◽  
Before And After ◽  
Quantification Analysis ◽  
Physical Attributes ◽  
Cardiac Variability ◽  
Isolated Rat

Cardiac variability can be assessed from two perspectives: beat-to-beat performance and continuous performance during the cardiac cycle. Linear analysis techniques assess cardiac variability by measuring the physical attributes of a signal, whereas nonlinear techniques evaluate signal dynamics. This study sought to determine if recurrence quantification analysis (RQA), a nonlinear technique, could detect pharmacologically induced autonomic changes in the continuous left ventricular pressure (LVP) and electrographic (EC) signals from an isolated rat heart—a model that theoretically contains no inherent variability. LVP and EC signal data were acquired simultaneously during Langendorff perfusion of isolated rat hearts before and after the addition of acetylcholine (n = 11), norepinephrine (n = 12), or no drug (n = 12). Two-minute segments of the continuous LVP and EC signal data were analyzed by RQA. Findings showed that%recurrence,%determinism, entropy, maxline, and trend from the continuous LVP signal significantly increased in the presence of both acetylcholine and norepinephrine, although systolic LVP significantly increased only with norepinephrine. In the continuous EC signal, the RQA trend variable significantly increased in the presence of norepinephrine. These results suggest that when either the sympathetic or parasympathetic division of the autonomic nervous system overwhelms the other, the dynamics underlying cardiac variability become stationary. This study also shows that information concerning inherent variability in the isolated rat heart can be gained via RQA of the continuous cardiac signal. Although speculative, RQA may be a tool for detecting alterations in cardiac variability and evaluating signal dynamics as a nonlinear indicator of cardiac pathology.

Nitric oxide modulates sympathoexcitatory cardiac-cardiovascular reflexes elicited by bradykinin

2001 ◽  
Vol 281 (5) ◽  
pp. H2010-H2017 ◽  
Author(s):  
S. C. Tjen-A-Looi ◽  
N. T. Phan ◽  
J. C. Longhurst
Keyword(s):  
Nitric Oxide ◽  
Pressor Response ◽  
Reflex Response ◽  
Cardiovascular Reflexes ◽  
Control Group ◽  
Neural Modulation ◽  
Arterial Blood ◽  
Nos Inhibitor ◽  
Pressor Reflex ◽  
Cardiac Afferents

A number of studies have demonstrated an important role for nitric oxide (NO) in central and peripheral neural modulation of sympathetic activity. To assess the interaction and integrative effects of NO release and sympathetic reflex actions, we investigated the influence of inhibition of NO on cardiac-cardiovascular reflexes. In anesthetized, sinoaortic-denervated and vagotomized cats, transient reflex increases in arterial blood pressure (BP) were induced by application of bradykinin (BK, 0.1–10 μg/ml) to the epicardial surface of the heart. The nonspecific NO synthase (NOS) inhibitor N G-monomethyl-l-arginine (l-NMMA, 10 mg/kg iv) was then administered and stimulation was repeated. l-NMMA increased baseline mean arterial pressure (MAP) from 129 ± 8 to 152 ± 9 mmHg and enhanced the change in MAP in response to BK from 32 ± 3 to 39 ± 5 mmHg ( n = 9, P < 0.05). Pulse pressure was significantly enhanced during the reflex response from 6 ± 4 to 27 ± 6 mmHg after l-NMMA injection due to relatively greater potentiation of the rise in systolic BP. Both the increase in baseline BP and the enhanced pressor reflex were reversed by l-arginine (30 mg/kg iv). Because l-NMMA can inhibit both brain and endothelial NOS, the effects of 7-nitroindazole (7-NI, 25 mg/kg ip), a selective brain NOS inhibitor, on the BK-induced cardiac-cardiovascular pressor reflex also were examined. In contrast to l-NMMA, we observed significant reduction of the pressor response to BK from 37 ± 5 to 18 ± 3 mmHg 30 min after the administration of 7-NI ( n = 9, P < 0.05), an effect that was reversed by l-arginine (300 mg/kg iv, n = 7). In a vehicle control group for 7-NI (10 ml of peanut oil ip), the pressor response to BK remained unchanged ( n = 6, P > 0.05). In conclusion, neuronal NOS facilitates, whereas endothelial NOS modulates, the excitatory cardiovascular reflex elicited by chemical stimulation of sympathetic cardiac afferents.

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