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 during abdominal ischemia in cats

1994 ◽  
Vol 267 (1) ◽  
pp. R97-R106 ◽  
Author(s):  
H. S. Huang ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Vena Cava ◽  
Left Ventricular ◽  
Mesenteric Arteries ◽  
Cardiovascular Reflexes ◽  
Group 3

The cardiovascular effects of regional abdominal ischemia and reperfusion were studied in cats anesthetized with alpha-chloralose. In group 1 (n = 9), central venous pressure was kept constant by a servo-controller while the celiac and superior mesenteric arteries were occluded by loop snares for 10 min. In group 2 (n = 9), a constant-perfusion circuit to the celiac and superior mesenteric arteries that could divert flow to the femoral vein was used to induce abdominal ischemia. In group 3 (n = 7), venous return from the inferior vena cava was controlled, and a constant-perfusion circuit was used to induce abdominal ischemia. Abdominal ischemia significantly (P < 0.05) increased portal venous blood lactate from 4.3 +/- 0.6 to 6.0 +/- 0.6 mM in group 3. The early increases in blood pressure caused by passive volume shifts in groups 1 and 2 were abolished in group 3. The late, i.e., 10 min, response to abdominal ischemia consisted of significant (P < 0.05) increases in mean arterial pressure (29 +/- 7, 24 +/- 7, and 33 +/- 8 mmHg in groups 1, 2, and 3, respectively). Abdominal ischemia also significantly (P < 0.05) increased the first derivative of left ventricular pressure at 40 mmHg developed pressure from 4,355 +/- 377 to 4,839 +/- 407 mmHg/s in group 3. Celiac and superior mesenteric ganglionectomy abolished the late but not the early hemodynamic changes. Ganglionectomy also significantly (P < 0.05) enhanced the decrease in mean arterial pressure during reperfusion in all groups. We conclude that the pressor and contractile responses during 10 min of abdominal ischemia and the relative maintenance of blood pressure during reperfusion after ischemia are reflex in nature.

Hemodynamic effects of periodic obstructive apneas in sedated pigs with congestive heart failure

2000 ◽  
Vol 88 (3) ◽  
pp. 1051-1060 ◽  
Author(s):  
Ling Chen ◽  
Quihu Shi ◽  
Steven M. Scharf
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Air Breathing ◽  
Obstructive Sleep

Because of similar physiological changes such as increased left ventricular (LV) afterload and sympathetic tone, an exaggerated depression in cardiac output (CO) could be expected in patients with coexisting obstructive sleep apnea and congestive heart failure (CHF). To determine cardiovascular effects and mechanisms of periodic obstructive apnea in the presence of CHF, 11 sedated and chronically instrumented pigs with CHF (rapid pacing) were tested with upper airway occlusion under room air breathing (RA), O2 breathing (O2), and room air breathing after hexamethonium (Hex). All conditions led to large negative swings in intrathoracic pressure (−30 to −39 Torr) and hypercapnia ([Formula: see text] ∼60 Torr), and RA and Hex also caused hypoxia (to ∼42 Torr). Relative to baseline, RA increased mean arterial pressure (from 97.5 ± 5.0 to 107.3 ± 5.7 Torr, P < 0.01), systemic vascular resistance, LV end-diastolic pressure, and LV end-systolic length while it decreased CO (from 2.17 ± 0.27 to 1.52 ± 0.31 l/min, P < 0.01), stroke volume (SV; from 23.5 ± 2.4 to 16.0 ± 4.0 ml, P < 0.01), and LV end-diastolic length (LVEDL). O2 and Hex decreased mean arterial pressure [from 102.3 ± 4.1 to 16.0 ± 4.0 Torr ( P < 0.01) with O2 and from 86.0 ± 8.5 to 78.1 ± 8.7 Torr ( P < 0.05) with Hex] and blunted the reduction in CO [from 2.09 ± 0.15 to 1.78 ± 0.18 l/ml for O2 and from 2.91 ± 0.43 to 2.50 ± 0.35 l/ml for Hex (both P< 0.05)] and SV. However, the reduction in LVEDL and LV end-diastolic pressure was the same as with RA. There was no change in systemic vascular resistance and LVEDL during O2 and Hex relative to baseline. In the CHF pigs during apnea, there was an exaggerated reduction in CO and SV relative to our previously published data from normal sedated pigs under similar conditions. The primary difference between CHF (present study) and the normal animals is that, in addition to increased LV afterload, there was a decrease in LV preload in CHF contributing to SV depression not seen in normal animals. The decrease in LV preload during apneas in CHF may be related to effects of ventricular interdependence.

Sympathoexcitatory neurotransmission of the chemoreflex in the NTS of awake rats

1999 ◽  
Vol 276 (1) ◽  
pp. R69-R80 ◽  
Author(s):  
Andréa S. Haibara ◽  
Leni G. H. Bonagamba ◽  
Benedito H. Machado
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Kynurenic Acid ◽  
Pressor Response ◽  
Potassium Cyanide ◽  
Cardiovascular Responses ◽  
Metabotropic Receptors ◽  
Metabotropic Receptor ◽  
Before And After ◽  
Awake Rats

Cardiovascular responses to chemoreflex activation by potassium cyanide (KCN, 20 μg/rat iv) were analyzed before and after the blockade of ionotropic or metabotropic receptors into the nucleus of the solitary tract (NTS) of awake rats. Microinjection of ionotropic antagonists [6,7-dinitroquinoxaline-2,3-dione or kynurenic acid (Kyn)] into the lateral commissural NTS (NTSlat), the midline commissural NTS (NTSmid), or into both (NTSlat+mid), produced a significant increase in basal mean arterial pressure, and the pressor response to chemoreflex activation was only partially reduced, whereas microinjection of Kyn into the NTSmid produced no changes in the pressor response to the chemoreflex. The bradycardic response to chemoreflex activation was abolished by microinjection of Kyn into the NTSlat or into NTSlat+mid but not by Kyn microinjection into the NTSmid. Microinjection of α-methyl-4-carboxyphenylglycine, a metabotropic receptor antagonist, into the NTSlat or NTSmid produced no changes in baseline mean arterial pressure or heart rate or in the chemoreflex responses. These results indicate that 1) the processing of the parasympathetic component (bradycardia) of the chemoreflex seems to be restricted to the NTSlat and was blocked by ionotropic antagonists and 2) the pressor response of the chemoreflex was only partially reduced by microinjection of ionotropic antagonists and not affected by injection of metabotropic antagonists into the NTSlat or NTSmid or into NTSlat+mid in awake rats.

Bradykinin-induced chemoreflexes from skeletal muscle: implications for the exercise reflex

1985 ◽  
Vol 59 (1) ◽  
pp. 56-63 ◽  
Author(s):  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Skeletal Muscle ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Diastolic Pressure ◽  
Cardiovascular Response ◽  
Muscle Afferents ◽  
Left Ventricular ◽  
Gracilis Muscle ◽  
Initial Increase

We examined the cardiovascular response to bradykinin stimulation of skeletal muscle afferents and the effect of prostaglandins on this response. Intra-arterial injection of 1 microgram bradykinin into the gracilis muscle of cats reflexly increased mean arterial pressure by 16 +/- 2 mmHg, left ventricular end-diastolic pressure by 1.6 +/- 0.6 mmHg, maximal dP/dt by 785 +/- 136 mmHg/s, heart rate by 11 +/- 2 beats/min, and mean aortic flow by 22 +/- 3 ml/min. The hemodynamic responses were abolished following denervation of the gracilis muscle. The increases in mean arterial pressure and maximal dP/dt were reduced by 68 and 45%, respectively, following inhibition of prostaglandin synthesis with indomethacin (2–8 mg/kg iv). Treatment with prostaglandin E2 (PGE2, 15–25 micrograms ia) restored the initial increase in mean arterial pressure, but not dP/dt, caused by bradykinin stimulation. Injection of PGE2 (15–30 micrograms ia) into the gracilis, without prior treatment with indomethacin, augmented the bradykinin-induced increases in mean arterial pressure and dP/dt. We conclude that small doses of bradykinin injected into skeletal muscle are capable of reflexly activating the cardiovascular system and that prostaglandins are necessary for the full manifestation of the corresponding hemodynamic response. The pattern of hemodynamic adjustment following bradykinin injection into skeletal muscle is very similar to that induced by static exercise. Therefore, it is possible that intense exercise provides a stimulus for this bradykinin-induced reflex in vivo.

Impairment of cardiopulmonary baroreflexes in Dahl salt-sensitive rats fed low salt

1984 ◽  
Vol 247 (1) ◽  
pp. H119-H123 ◽  
Author(s):  
A. Ferrari ◽  
F. J. Gordon ◽  
A. L. Mark
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Splanchnic Nerve ◽  
Left Ventricular ◽  
Low Salt ◽  
Circulatory Control ◽  
Cardiopulmonary Baroreflex

Abnormalities in neural circulatory control contribute to salt-induced hypertension in Dahl sensitive (DS) rats. This study tested the hypothesis that there is impairment in cardiopulmonary baroreflex function in prehypertensive DS rats. The study was performed in DS and Dahl resistant (DR) rats fed low-salt diet. Arterial baroreceptors were denervated. Sympathetic activity was recorded from the splanchnic nerve during stimulation of cardiopulmonary baroreceptors with volume expansion (iv dextran). Resting mean arterial pressure averaged 93 +/- 6 (SE) in DS vs. 98 +/- 5 mmHg in DR rats. Resting left ventricular end-diastolic pressure (LVEDP) was 13.5 +/- 1.0 in/DS vs. 11.4 +/- 0.9 mmHg in DR rats. Volume expansion with the same amount of dextran caused greater increases in LVEDP in DS (+13 +/- 1 mmHg) than DR (+10 +/- 1 mmHg) but less inhibition of sympathetic activity (-40 +/- 4 vs. -50 +/- 2%) in DS compared with DR rats, respectively. Cardiopulmonary baroreflex gain calculated as percent inhibition of sympathetic activity divided by increases in LVEDP was -3.2 +/- 0.2 in DS vs. -4.9 +/- 0.6%/mmHg in DR rats. Reflex responses to dextran were abolished by vagotomy. Volume expansion also induced increases in mean arterial pressure. These were/greater in DS than DR rats (+43 +/- 4 vs. +28 +/- 5 mmHg, respectively) before vagotomy but were similar in the two groups after vagotomy. The distensibility (delta volume/delta pressure) of the left atrium was similar in DS and DR rats. We conclude that prehypertensive DS rats have impairment of the cardiopulmonary baroreflex.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Effects of inspiratory loading on left ventricular myocardial blood flow and metabolism

1992 ◽  
Vol 72 (4) ◽  
pp. 1488-1492 ◽  
Author(s):  
S. Khilnani ◽  
L. M. Graver ◽  
K. Balaban ◽  
S. M. Scharf
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Venous Blood ◽  
Median Sternotomy ◽  
Left Ventricular ◽  
Coronary Resistance ◽  
Ventricular Afterload ◽  
Before And After

With airways obstruction, mean pleural pressure decreases. It has been postulated that associated increases in left ventricular afterload increase myocardial O2 demand (MvO2) and coronary blood flow (CBF). We tested this hypothesis in 12 anesthetized mixed-breed dogs. Through a median sternotomy, dogs were instrumented for the measurement of mean arterial pressure, cardiac output, and left anterior descending CBF. A catheter placed in the coronary sinus allowed sampling of left ventricular venous blood. MvO2 was calculated as CBF x (arteriovenous content difference), and coronary resistance was calculated as (mean arterial pressure)/CBF. After closure of the thoracotomy, animals were studied before and during inspiratory threshold loading (IL) of -20 to -25 cmH2O while breathing 100% O2 before and after bilateral cervical vagotomy. During IL, heart rate fell [approximately 20 beats/min (NS prevagotomy, P less than 0.05 postvagotomy)], arterial PCO2 increased [45 to 66 Torr prevagotomy, 45 to 50 Torr postvagotomy (P less than 0.01)], and arterial O2 content was unchanged. CBF increased with IL:41% prevagotomy (P less than 0.01), 18% postvagotomy (P less than 0.02). However, with IL, MvO2 did not increase significantly either pre- or postvagotomy. Coronary resistance decreased with IL [30% prevagotomy, 24% postvagotomy (P less than 0.01)]. In eight dogs, PCO2 was increased by increasing dead space while the animals were mechanically ventilated and paralyzed. Although there was little change in CBF, heart rate fell by an amount equal to that with IL. We conclude that 1) IL causes coronary vasodilation not related to changes in MvO2, PCO2, or vagal tone; 2) MvO2 does not increase with IL; and 3) decreased heart rate with IL is related to hypercapnia and/or acidosis.

Cardiovascular and Valsalva responses during parabolic flight

1998 ◽  
Vol 85 (5) ◽  
pp. 1957-1965 ◽  
Author(s):  
Todd T. Schlegel ◽  
Edgar W. Benavides ◽  
Donald C. Barker ◽  
Troy E. Brown ◽  
Deborah L. Harm ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Human Subjects ◽  
Parabolic Flight ◽  
Cardiovascular Responses ◽  
Systematic Evaluation ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Flight Measurements

We investigated the integrated cardiovascular responses of 15 human subjects to the acute gravitational changes (micro- and hypergravity portions) of parabolic flight. Measurements were made with subjects quietly seated and while subjects performed controlled Valsalva maneuvers. During quiet, seated, parabolic flight, mean arterial pressure increased during the transition into microgravity but decreased as microgravity was sustained. The decrease in mean arterial pressure was accompanied by immediate reflexive increases in heart rate but by absent (or later-than-expected) reflexive increases in total vascular resistance. Mean arterial pressure responses in Valsalva phases IIl, III, and IV were accentuated in hypergravity relative to microgravity ( P < 0.01, P < 0.01, and P < 0.05, respectively), but accentuations differed qualitatively and quantitatively from those induced by a supine-to-seated postural change in 1 G. This study is the first systematic evaluation of temporal and Valsalva-related changes in cardiovascular parameters during parabolic flight. Results suggest that arterial baroreflex control of vascular resistance may be modified by alterations of cardiopulmonary, vestibular, and/or other receptor activity.

scholarly journals Developmental Changes in Hemodynamic Responses and Cardiovagal Modulation during Isometric Handgrip Exercise

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Styliani Goulopoulou ◽  
Bo Fernhall ◽  
Jill A. Kanaley
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Isometric Contraction ◽  
Pressor Response ◽  
Reflex Response ◽  
Group Differences ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Isometric Handgrip Exercise ◽  
Pressor Reflex

The purpose of this study was to examine differences in pressor response and cardiovagal modulation during isometric handgrip exercise (IHG) between children and adults. Beat-to-beat heart rate (HR) and blood pressure were measured in 23 prepubertal children and 23 adults at baseline and during IHG. Cardiovagal modulation was quantified by analysis of HR variability. Mean arterial pressure responses to IHG were greater in adults compared to children (P<.05) whereas there were no group differences in HR responses (P>.05). Children had a greater reduction in cardiovagal modulation in response to IHG compared to adults (P<.05). Changes in mean arterial pressure during IHG were correlated with baseline cardiovagal modulation and force produced during isometric contraction (P<.05). In conclusion, differences in pressor reflex response between children and adults cannot be solely explained by differences in autonomic modulation and appear to be associated with factors contributing to the force produced during isometric contraction.

scholarly journals Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons

2015 ◽  
Vol 309 (10) ◽  
pp. R1273-R1284 ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Partial Loss ◽  
Rat Pups ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
Long Term Facilitation

The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.

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