Effect of prostaglandins on bradykinin-induced visceral-cardiac reflexes

1985 ◽  
Vol 249 (1) ◽  
pp. H155-H163 ◽  
Author(s):  
C. L. Stebbins ◽  
R. C. Smith ◽  
J. C. Longhurst
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Response ◽  
Serosal Surface ◽  
Abdominal Organs ◽  
Before And After ◽  
Stimulation Of

We examined the effect of prostaglandins on the reflex cardiovascular response to bradykinin applied to the abdominal organs of anesthetized cats. Bradykinin (10 micrograms/ml) was applied to the serosal surface of the stomach, gallbladder, or jejunum before and after injection of indomethacin (2-10 micrograms/ml iv) and after application of 1 microgram/ml of prostaglandins E1, E2, or F2 alpha (PGE1, PGE2, PGF2 alpha) or prostacyclin (PGI2). In six cats, stimulation of the stomach with bradykinin significantly increased mean arterial pressure (MAP) by 37 +/- 5 (SE) mmHg and maximal dP/dt by 633 +/- 101 mmHg/s. Following indomethacin the bradykinin-induced increases in MAP and dP/dt were significantly reduced to 19 +/- 4 mmHg and 191 +/- 58 mmHg/s, respectively. Treatment with PGE1, PGE2, or PGI2, but not PGF2 alpha, restored the initial bradykinin response. The gallbladder and jejunum responded similarly. Also application of exogenous prostaglandins, PGE2 or PGI2, to the stomach, gallbladder, or jejunum significantly augmented the cardiovascular response to bradykinin. Finally, PGE2 restored a portion of the cardiovascular response to bradykinin following the development of tachyphylaxis. We conclude that prostaglandins are necessary for the full manifestation of the cardiovascular response to bradykinin.

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.

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

1985 ◽  
Vol 63 (6) ◽  
pp. 937-943 ◽  
Author(s):  
David J. Boarini ◽  
Neal F. Kassell ◽  
James A. Sprowell ◽  
Julie J. Olin ◽  
Hans C. Coester
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Hypotension ◽  
Content Type ◽  
Blood Flows ◽  
Before And After ◽  
Regional Blood Flows ◽  
Fine Print

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

Effects of Ambulation and Nondependent Transfers on Vital Signs in Patients Receiving Norepinephrine

2017 ◽  
Vol 26 (1) ◽  
pp. 31-36 ◽  
Author(s):  
Rosario Arcaya Nievera ◽  
Ann Fick ◽  
Hilary K. Harris
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Physical Therapy ◽  
Arterial Pressure ◽  
Low Dose ◽  
Vital Signs ◽  
Activity Level ◽  
Significant Difference ◽  
Before And After ◽  
Norepinephrine Dose

Purpose To assess the safety of mobilizing patients receiving low-dose norepinephrine (0.05 μg/kg per min) by examining mean arterial pressure and heart rate before and after activity with parameters set by the physician. Background Norepinephrine is a peripheral vasoconstrictor administered for acute hypotension. During activity, blood flows to the periphery to supply muscles with oxygen, which may oppose the norepinephrine vasoconstriction. The safety of mobilizing patients receiving norepinephrine is unclear. Methods Heart rate, mean arterial pressure, norepinephrine dose, and activity performed were extracted retrospectively from charts of 47 cardiothoracic surgery patients during the first patient transfer to chair or ambulation with norepinephrine infusing. Mean arterial pressure and heart rate were compared before and after physical therapy (paired t tests). Differences among norepinephrine doses and physical activity levels were evaluated (Kruskal-Wallis test). Results Forty-one of the 47 patients (87%) tolerated the activity within safe ranges of vital signs. The change in patients’ mean arterial pressure from before to after activity was not significant (P = .16), but a significant increase in heart rate occurred after activity (P < .001). A Kruskal-Wallis test showed no significant difference in the norepinephrine dose and activity level (χ2 = 6.34, P = .17). No instances of cardiopulmonary or respiratory arrest occurred during any physical therapy sessions. Conclusions Infusion of low-dose norepinephrine should not be considered an automatic reason to keep patients on bed rest.

Effect of baroreceptor activity on ventilatory response to chemoreceptor stimulation

1975 ◽  
Vol 39 (3) ◽  
pp. 411-416 ◽  
Author(s):  
D. Heistad ◽  
F. M. Abboud ◽  
A. L. Mark ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Ventilatory Response ◽  
Carotid Bifurcation ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Baroreceptor Activation ◽  
Stimulation Of

This study tested the hypothesis that ventilatory responses to chemoreceptor stimulation are affected by the level of arterial pressure and degree of baroreceptor activation. Carotid chemoreceptors were stimulated by injection of nicotine into the common carotid artery of anesthetized dogs. Arterial pressure was reduced by bleeding the animals and raised by transient occlusion of the abdominal aorta. The results indicate that ventilatory responses to chemoreceptor stimulation were augmented by hypotension and depressed by hypertension. In additional studies we excluded the possibility that the findings were produced by a direct effect of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were perfused at constant flow. In one carotid bifurcation, perfusion pressure was raised to stimulate carotid sinus baroreceptors. In the other carotid bifurcation, pressure was constant and nicotine was injected to stimulate carotid chemoreceptors. Stimulation of baroreceptors on one side attenuated the ventilatory response to stimulation of contralateral chemoreceptors. This inhibition was observed before and after bilateral cervical vagotomy. We conclude that there is a major central interaction between baroreceptor and chemoreceptor reflexes so that changes in baroreceptor activity modulate ventilatory responses to chemoreceptor stimulation.

Effect of indomethacin on the pressor responses to sustained isometric contraction in humans

1993 ◽  
Vol 75 (1) ◽  
pp. 273-278 ◽  
Author(s):  
K. P. Davy ◽  
W. G. Herbert ◽  
J. H. Williams
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Voluntary Contraction ◽  
Plasma Norepinephrine ◽  
Isometric Handgrip ◽  
Double Blind ◽  
Muscle Ischemia ◽  
Stimulation Of

The purpose of this study was to test the hypothesis that prostaglandins participate in metaboreceptor stimulation of the pressor response to sustained isometric handgrip contraction in humans. To accomplish this, mean arterial pressure, heart rate (n = 10), and plasma norepinephrine levels (n = 8) were measured in healthy male subjects during sustained isometric handgrip at 40% of maximal voluntary contraction force to exhaustion and during a period of postcontraction muscle ischemia. The subjects were given a double-blind and counterbalanced administration of placebo or a single 100-mg dose of indomethacin. A period of 1 wk was allowed for systemic clearance of the drug. Mean arterial pressure increased 25 +/- 5 vs. 22 +/- 4 mmHg during the final minute of isometric handgrip contraction and 26 +/- 2 vs. 21 +/- 5 during the last minute of postcontraction muscle ischemia in the placebo vs. the indomethacin trial (P > 0.05), respectively. Heart rate was increased 21 +/- 4 vs. 17 +/- 3 beats/min during the final minute of isometric handgrip contraction in the placebo vs. the indomethacin trial (P > 0.05), respectively, and returned to control values during postcontraction muscle ischemia. Plasma norepinephrine levels increased 343 +/- 89 vs. 289 +/- 89 pg/ml after isometric handgrip contraction and 675 +/- 132 vs. 632 +/- 132 pg/ml after postcontraction muscle ischemia (P > 0.05) in the placebo vs. the indomethacin trial, respectively. These results suggest that prostaglandin inhibition does not significantly modulate muscle contraction-induced stimulation of mean arterial pressure, heart rate, or plasma norepinephrine levels.

scholarly journals Renal Denervation and Celiac Ganglionectomy Decrease Mean Arterial Pressure Similarly in Genetically Hypertensive Schlager (BPH/2J) Mice

Hypertension ◽  
2021 ◽  
Author(s):  
Ninitha Asirvatham-Jeyaraj ◽  
Madeline M. Gauthier ◽  
Christopher T. Banek ◽  
Abhismitha Ramesh ◽  
Hannah Garver ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Denervation ◽  
Before And After ◽  
Pressor Activity ◽  
Celiac Ganglionectomy ◽  
Surgical Treatments ◽  
Tissue Norepinephrine ◽  
Genetically Hypertensive

Renal denervation (RDNX) lowers mean arterial pressure (MAP) in patients with resistant hypertension. Less well studied is the effect of celiac ganglionectomy (CGX), a procedure which involves the removal of the nerves innervating the splanchnic vascular bed. We hypothesized that RDNX and CGX would both lower MAP in genetically hypertensive Schlager (BPH/2J) mice through a reduction in sympathetic tone. Telemeters were implanted into the femoral artery in mice to monitor MAP before and after RDNX (n=5), CGX (n=6), or SHAM (n=6). MAP, systolic blood pressure, diastolic blood pressure, and heart rate were recorded for 14 days postoperatively. The MAP response to hexamethonium (10 mg/kg, IP) was measured on control day 3 and postoperative day 10 as a measure of global neurogenic pressor activity. The efficacy of denervation was assessed by measurement of tissue norepinephrine. Control MAP was similar among the 3 groups before surgical treatments (≈130 mm Hg). On postoperative day 14, MAP was significantly lower in RDNX (−11±2 mm Hg) and CGX (−11±1 mm Hg) groups compared with their predenervation values. This was not the case in SHAM mice (−5±3 mm Hg). The depressor response to hexamethonium in the RDNX group was significantly smaller on postoperative day 10 (−10±5 mm Hg) compared with baseline control (−25±10 mm Hg). This was not the case in mice in the SHAM (day 10; −28±5 mm Hg) or CGX (day 10; −34±7 mm Hg) group. In conclusion, both renal and splanchnic nerves contribute to hypertension in BPH/2J mice, but likely through different mechanisms.

Baroreflex control of heart interval in conscious renal hypertensive dogs

1981 ◽  
Vol 241 (3) ◽  
pp. H332-H336
Author(s):  
M. D. Thames ◽  
C. L. Eastham ◽  
M. L. Marcus
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Hypertension ◽  
Conscious Dogs ◽  
Adrenergic Blockade ◽  
Cholinergic Mechanisms ◽  
Baroreflex Control ◽  
Control Heart ◽  
Before And After ◽  
Autonomic Blockade

The purpose of this study is to determine if baroreflex control of heart interval is abnormal in conscious dogs with renal hypertension. Changes in heart interval in response to transient nitroglycerin-induced decreases in arterial pressure and transient phenylephrine-induced increases in arterial pressure were determined in nine normotensive [mean arterial pressure 92 +/- 4 (SE) mmHg] and nine renal hypertensive conscious dogs (mean arterial pressure 139 +/- 10 mmHg). Data were acquired before and after beta-adrenergic blockade with 2 mg/kg iv propranolol and before and after parasympathetic blockade with 0.5 mg/kg iv atropine. Control heart rates for the normotensive and hypertensive dogs were not different (91 +/- 4 and 93 +/- 7 beats/min, respectively). Before autonomic blockade, the responses of normotensive and hypertensive dogs to nitroglycerin were not different. However, prolongation of the heart interval in response to phenylephrine in hypertensive dogs was significantly less than in normotensive dogs. In both groups, atropine nearly abolished the decrease in heart interval in response to nitroglycerin and the increase in heart interval in response to phenylephrine, although there were small but significant residual responses. Propranolol was without significant effect on heart interval responses to nitroglycerin and phenylephrine. We conclude that the baroreflex control of heart interval during transient decreases in arterial pressure is preserved in hypertensive dogs and is mediated mainly by decreases in parasympathetic outflow to the heart. In contrast, baroreflex control of heart interval during transient increases in arterial pressure is impaired in hypertension and is mediated mainly by activation of parasympathetic cholinergic mechanisms.

Cardiorespiratory response patterns to afferent stimulation of muscle nerves in the rabbit

1996 ◽  
Vol 81 (1) ◽  
pp. 266-273 ◽  
Author(s):  
G. Raimondi ◽  
J. M. Legramante ◽  
F. Iellamo ◽  
S. Cassarino ◽  
G. Peruzzi
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Venous Pressure ◽  
Response Patterns ◽  
Central Venous ◽  
Frequency Stimulation ◽  
End Tidal ◽  
Stimulation Of

The aim of this study was to test the hypothesis that stimulation of thin fiber muscle afferents is capable of matching the cardiovascular and ventilatory responses. In 46 anesthetized rabbits, the central end of the gastrocnemius nerves was electrically stimulated at 3 [low-frequency stimulation (LFS)] and 100 Hz [high-frequency stimulation (HFS)]. Intensities up to 200 times motor threshold were used. LFS induced a decrease in both mean arterial pressure (-19.9 +/- 2.9%) and systemic vascular resistance (-23.9 +/- 3.2%) an increase in cardiac output (CO) (6.4 +/- 1.7%), stroke volume (7.3 +/- 3.0%) and pulmonary ventilation (VE) (26.7 +/- 2.3%); heart rate and central venous pressure were not changed significantly. HFS induced an increase in mean arterial pressure (11.1 +/- 4.9%), CO (15.8 +/- 5.4%), stroke volume (13.4 +/- 5.4%), and VE but no significant changes in heart rate, systemic vascular resistance and central venous pressure. In both response patterns, arterial and end-tidal CO2 did not change significantly. The patterns of cardiorespiratory responses to both LFS and HFS were characterized by an increase in Co and VE without concomitant decreases in arterial and end-tidal PCO2 (isocapnic hyperpnea).

scholarly journals Abnormal cardiovascular response to nitroglycerin in migraine

Cephalalgia ◽  
2019 ◽  
Vol 40 (3) ◽  
pp. 266-277
Author(s):  
Willebrordus PJ van Oosterhout ◽  
Guus G Schoonman ◽  
Dirk P Saal ◽  
Roland D Thijs ◽  
Michel D Ferrari ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Initial Increase

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.

Delta Inferior Vena Cava Index Correlated with Mean Arterial Pressure (MAP) in Spinal Anesthesia

2021 ◽  
Vol 2 (2) ◽  
pp. 65-69
Author(s):  
Wiwi Jaya ◽  
◽  
Ulil Abshor ◽  
Buyung Hartiyo Laksono ◽  
Arie Zainul Fatoni ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Inferior Vena Cava ◽  
Arterial Pressure ◽  
Spinal Anesthesia ◽  
Inferior Vena ◽  
Vena Cava ◽  
Test Study ◽  
Significant Difference ◽  
Before And After ◽  
Post Test

Background: Spinal anesthesia has become an alternative to general anesthesia. However, spinal anesthesia has the most common side effects including, bradycardia and hypotension. The aim of this study was to determine the relationship between changes in the inferior vena cava index (delta inferior vena cava index) to changes in mean arterial pressure in spinal anesthesia. Methods: This study was an observational pre-post test study in thirty-two patients who received spinal anesthesia. The inferior vena cava index (inferior vena cava collectibility index and caval-aorta index) was measured before and after spinal anesthesia (5 and 10 minutes after onset). Data were analyzed using the Kolmogorov Smirnov test, Shapiro-Wilk test, T-test, and correlation test with α=5% Result: There was a significant difference in mean arterial pressure (MAP), delta inferior vena cava collectibility index (D-IVC-CI), and delta caval-aorta index (D-CAo-I) before and after spinal anesthesia. D-IVC-CI and D-CAo-I are significantly correlated with MAP. The correlation between D-IVC-CI and MAP had R = -0.371 (P <0.05) at 5 minutes post-anesthesia, while D-CAo-I and MAP had R = 0.472 (P <0.05) at 10 minutes post-anesthesia. Conclusion: The delta inferior vena cava index is correlated with the mean arterial pressure (MAP) value in spinal anesthesia.

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