CARDIOVASCULAR EFFECTS OF PENTOLINIUM BITARTRATE IN DOGS

1956 ◽  
Vol 34 (4) ◽  
pp. 747-755 ◽  
Author(s):  
W. E. G. A. Spoerel ◽  
C. W. Gowdey
Keyword(s):  
Pulse Rate ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Minute Volume ◽  
Initial Pulse ◽  
Pressor Responses ◽  
Pulmonary Arterial ◽  
Sinus Pressure

Pentolinium (5 mgm./kgm.) injected intravenously into dogs anesthetized with pentobarbital caused the pulse rate to approach that of dogs with surgical cardiac denervation. The higher the initial pulse rate, the greater the decrease after the drug; rates under 100/min. were increased. Changes in arterial pressure followed a similar pattern, and the changes in both systemic and pulmonary arterial pressures were correlated with the changes in pulse rate. The cardiac output was decreased. Pressor responses to injected adrenaline and noradrenaline were greater after pentolinium. Total peripheral resistance, respiratory rate, respiratory minute volume, and oxygen consumption were not changed significantly, but local (hind-leg) resistance was decreased in two of three experiments. Pentolinium abolished or reduced markedly the cardiovascular responses to reduced carotid sinus pressure, tilting, acute hypoxia, large doses of acetylcholine, and hemorrhage. The cardiac vagus and the cardiovascular part of the sympathetic nervous system are blocked, but the experiments suggest that the adrenal medulla may not be completely blocked by 5 mgm./kgm. pentolinium.

CARDIOVASCULAR EFFECTS OF PENTOLINIUM BITARTRATE IN DOGS

1956 ◽  
Vol 34 (1) ◽  
pp. 747-755
Author(s):  
W. E. G. A. Spoerel ◽  
C. W. Gowdey
Keyword(s):  
Pulse Rate ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Minute Volume ◽  
Initial Pulse ◽  
Pressor Responses ◽  
Pulmonary Arterial ◽  
Sinus Pressure

Pentolinium (5 mgm./kgm.) injected intravenously into dogs anesthetized with pentobarbital caused the pulse rate to approach that of dogs with surgical cardiac denervation. The higher the initial pulse rate, the greater the decrease after the drug; rates under 100/min. were increased. Changes in arterial pressure followed a similar pattern, and the changes in both systemic and pulmonary arterial pressures were correlated with the changes in pulse rate. The cardiac output was decreased. Pressor responses to injected adrenaline and noradrenaline were greater after pentolinium. Total peripheral resistance, respiratory rate, respiratory minute volume, and oxygen consumption were not changed significantly, but local (hind-leg) resistance was decreased in two of three experiments. Pentolinium abolished or reduced markedly the cardiovascular responses to reduced carotid sinus pressure, tilting, acute hypoxia, large doses of acetylcholine, and hemorrhage. The cardiac vagus and the cardiovascular part of the sympathetic nervous system are blocked, but the experiments suggest that the adrenal medulla may not be completely blocked by 5 mgm./kgm. pentolinium.

Cardiovascular responses to hypoxia and hypercapnia in barodenervated rats

1990 ◽  
Vol 68 (2) ◽  
pp. 678-686 ◽  
Author(s):  
B. R. Walker ◽  
B. L. Brizzee
Keyword(s):  
Blood Pressure ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Arterial Baroreflex ◽  
Conscious Rat ◽  
Hypercapnic Hypoxia ◽  
Intact Rats

Experiments were performed to examine the role of the arterial baroreceptors in the cardiovascular responses to acute hypoxia and hypercapnia in conscious rats chronically instrumented to monitor systemic hemodynamics. One group of rats remained intact, whereas a second group was barodenervated. Both groups of rats retained arterial chemoreceptive function as demonstrated by augmented ventilation in response to hypoxia. The cardiovascular effects to varying inspired levels of O2 and CO2 were examined and compared between intact and barodenervated rats. No differences between groups were noted in response to mild hypercapnia (5% CO2); however, the bradycardia and reduction in cardiac output observed in intact rats breathing 10% CO2 were eliminated by barodenervation. In addition, hypocapnic hypoxia caused a marked fall in blood pressure and total peripheral resistance (TPR) in barodenervated rats compared with controls. Similar differences in TPR were observed between the groups in response to isocapnic and hypercapnic hypoxia as well. It is concluded that the arterial baroreflex is an important component of the overall cardiovascular responses to both hypercapnic and hypoxic stimuli in the conscious rat.

Inhibition of hypoxic pulmonary vasoconstriction by antagonists of store-operated Ca2+ and nonselective cation channels

2005 ◽  
Vol 289 (1) ◽  
pp. L5-L13 ◽  
Author(s):  
Letitia Weigand ◽  
Joshua Foxson ◽  
Jian Wang ◽  
Larissa A. Shimoda ◽  
J. T. Sylvester
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Pulmonary Arteries ◽  
Cation Channels ◽  
Pulmonary Vasoconstriction ◽  
Nonselective Cation Channels ◽  
Pressor Responses ◽  
Intracellular Ca ◽  
Pulmonary Arterial

Previous studies indicated that acute hypoxia increased intracellular Ca2+ concentration ([Ca2+]i), Ca2+ influx, and capacitative Ca2+ entry (CCE) through store-operated Ca2+ channels (SOCC) in smooth muscle cells from distal pulmonary arteries (PASMC), which are thought to be a major locus of hypoxic pulmonary vasoconstriction (HPV). Moreover, these effects were blocked by Ca2+-free conditions and antagonists of SOCC and nonselective cation channels (NSCC). To test the hypothesis that in vivo HPV requires CCE, we measured the effects of SOCC/NSCC antagonists (SKF-96365, NiCl2, and LaCl3) on pulmonary arterial pressor responses to 2% O2 and high-KCl concentrations in isolated rat lungs. At concentrations that blocked CCE and [Ca2+]i responses to hypoxia in PASMC, SKF-96365 and NiCl2 prevented and reversed HPV but did not alter pressor responses to KCl. At 10 μM, LaCl3 had similar effects, but higher concentrations (30 and 100 μM) caused vasoconstriction during normoxia and potentiated HPV, indicating actions other than SOCC blockade. Ca2+-free perfusate and the voltage-operated Ca2+ channel (VOCC) antagonist nifedipine were potent inhibitors of pressor responses to both hypoxia and KCl. We conclude that HPV required influx of Ca2+ through both SOCC and VOCC. This dual requirement and virtual abolition of HPV by either SOCC or VOCC antagonists suggests that neither channel provided enough Ca2+ on its own to trigger PASMC contraction and/or that during hypoxia, SOCC-dependent depolarization caused secondary activation of VOCC.

Cardiovascular responses to arterial and venous hemorrhage in neonatal swine

1984 ◽  
Vol 247 (4) ◽  
pp. R626-R633 ◽  
Author(s):  
B. J. Buckley ◽  
N. Gootman ◽  
J. S. Nagelberg ◽  
P. G. Griswold ◽  
P. M. Gootman
Keyword(s):  
Blood Flow ◽  
Regional Blood Flow ◽  
Venous Blood ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Aortic Pressure ◽  
Carotid Occlusion ◽  
Pressor Responses ◽  
Age Dependent ◽  
Carotid Arterial

The cardiovascular effects of graded arterial or venous hemorrhage were evaluated in developing swine (less than or equal to 1 day, 2–5 days, 1 wk, and 2 wk of age) anesthetized with halothane in 50% N2O–50% O2. Serial 5-ml/kg aliquots of arterial or venous blood were removed at 3- to 4-min intervals to a cumulative total of 20 ml/kg. Tachycardia occurred in most animals. Decreases in aortic pressure to arterial, but not to venous, hemorrhage were age dependent. Renal, femoral, and carotid arterial flows decreased with hemorrhage in all animals; the decreases in blood flow did not differ among the three circulations and were not age dependent. Increases in femoral resistance were obtained to both arterial and venous hemorrhage only in the 2-wk-old group. As the degree of hemorrhage was increased, aortic pressure, regional blood flow, and femoral resistance (2 wk olds) responses were larger in magnitude. Aortic pressure in piglets 1-5 days of age could not be restored to within 20% of the prehemorrhage level at a smaller bleeding volume with arterial than with venous hemorrhage. Pressor responses to norepinephrine (0.5 micrograms/kg) and to bilateral common carotid occlusion were still present after 20-ml/kg hemorrhage. These responses indicate the presence of a progressive maturation-related compensation to the stress of arterial but not venous hemorrhage.

Correlation of acute with chronic hypoxic pulmonary hypertension in cattle

1975 ◽  
Vol 38 (3) ◽  
pp. 495-498 ◽  
Author(s):  
D. H. Will ◽  
J. L. Hicks ◽  
C. S. Card ◽  
J. T. Reeves ◽  
A. F. Alexander
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Acute Hypoxia ◽  
Common Mechanism ◽  
Mean Pulmonary Arterial Pressure ◽  
Pressor Responses ◽  
Pulmonary Arterial ◽  
Highly Correlated

We investigated acute and chronic hypoxic pulmonary pressor responses in two groups of calves, one bred to be susceptible, the other resistant to high-altitude pulmonary hypertension. Twelve 5-mo-old susceptible calves residing at 1,524 m increased their mean pulmonary arterial pressure from 26 +/- 2 (SE) to 55 +/- 4 mmHg during 2 h at a simulated altitude of 4,572 m. In 10 resistant calves pressure increased from 22 +/- 1 to 37 +/- 2 mmHg. Five calves were selected from each group for further study. When 9 mo old, the 5 susceptible calves again showed a greater pressor response to acute hypoxia (27 +/- 1 to 55 +/- 4 mmHg) than did 5 resistant calves (23 +/- 1 to 41 +/- 3 mmHg). When 12 mo old, the 5 susceptible calves also developed a greater increase in pulmonary arterial pressure (21 +/- 2 to 9 +/- 4 mmHg) during 18 days at 4,572 m than did the 5 resistant calves (21 +/- 1 to 64 +/- 4 mmHg). Acute and chronic hypoxic pulmonary pressor responses were highly correlated (r = 0.91; P less than 0.001) indicating that they were probably produced through a common mechanism.

Direct effects of acute hypoxia on the reactivity of peripheral arteries of the chicken embryo

2002 ◽  
Vol 283 (2) ◽  
pp. R331-R338 ◽  
Author(s):  
K. Ruijtenbeek ◽  
C. G. A. Kessels ◽  
E. Villamor ◽  
C. E. Blanco ◽  
J. G. R. De Mey
Keyword(s):  
Chicken Embryo ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Direct Effects ◽  
No Donor ◽  
Femoral Arteries ◽  
Contraction And Relaxation

In the chicken embryo, acute hypoxemia results in cardiovascular responses, including an increased peripheral resistance. We investigated whether local direct effects of decreased oxygen tension might participate in the arterial response to hypoxemia in the chicken embryo. Femoral arteries of chicken embryos were isolated at 0.9 of incubation time, and the effects of acute hypoxia on contraction and relaxation were determined in vitro. While hypoxia reduced contraction induced by high K+ to a small extent (−21.8 ± 5.7%), contractile responses to exogenous norepinephrine (NE) were markedly reduced (−51.1 ± 3.2%) in 80% of the arterial segments. This effect of hypoxia was not altered by removal of the endothelium, inhibition of NO synthase or cyclooxygenase, or by depolarization plus Ca2+ channel blockade. When arteries were simultaneously exposed to NE and ACh, hypoxia resulted in contraction (+49.8 ± 9.3%). Also, relaxing responses to ACh were abolished during acute hypoxia, while the vessels became more sensitive to the relaxing effect of the NO donor sodium nitroprusside (pD2: 5.81 ± 0.21 vs. 5.31 ± 0.27). Thus, in chicken embryo femoral arteries, acute hypoxia blunts agonist-induced contraction of the smooth muscle and inhibits stimulated endothelium-derived relaxation factor release. The consequences of this for in vivo fetal hemodynamics during acute hypoxemia depend on the balance between vasomotor influences of circulating catecholamines and those of the endothelium.

Cardiovascular responses to hemorrhage during acute and chronic hypoxia

1994 ◽  
Vol 267 (3) ◽  
pp. R619-R627 ◽  
Author(s):  
T. C. Resta ◽  
R. D. Russ ◽  
M. P. Doyle ◽  
J. M. Martinez ◽  
B. R. Walker
Keyword(s):  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Barometric Pressure ◽  
Ventricular Volume ◽  
Right Ventricular Hypertrophy ◽  
Hypoxic Conditions ◽  
Normal Increase

Previous work from our laboratory had demonstrated attenuation of systemic vasoreactivity to pressor agents in rats after acute or chronic exposure to hypoxia. Therefore we hypothesized that hemorrhage of acutely hypoxic (12% O2) or chronically hypoxic (barometric pressure 380 mmHg for 3 wk) rats would deter the normal increase in total peripheral resistance (TPR) and thus decrease the ability to maintain blood pressure. Progressive hemorrhage (2% of blood volume per min) was performed under conditions of either normoxia or acute hypoxia in conscious rats. In control animals, the increase in TPR observed during normoxic hemorrhage was absent when hemorrhage was performed in acute hypoxia. Furthermore, the amount of blood removal required to achieve hypotension was reduced under conditions of acute hypoxia. In contrast, chronically hypoxic rats exhibited no difference in the threshold for hypotension between conditions of acute normoxia and hypoxia and demonstrated an increased hypotensive threshold under both normoxic and hypoxic conditions compared with control animals. We next hypothesized that the prolonged threshold for hypotension observed in chronically hypoxic rats might be due to hypoxia-induced right ventricular hypertrophy. Such ventricular hypertrophy may minimize stimulation of ventricular volume receptors thought to elicit the reflex fall in heart rate and TPR occurring in extreme underfill conditions. Therefore we compared the cardiovascular responses to hemorrhage in rats with right ventricular hypertrophy resulting from administration of monocrotaline with those from rats treated with vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)

Stimulating intestinal afferents reflexly activates cardiovascular system in cats

1988 ◽  
Vol 254 (2) ◽  
pp. H354-H360 ◽  
Author(s):  
G. A. Ordway ◽  
K. R. Boheler ◽  
J. C. Longhurst
Keyword(s):  
Smooth Muscle ◽  
Cardiovascular System ◽  
Peripheral Resistance ◽  
Left Ventricular Pressure ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Dose Dependent Fashion ◽  
Visceral Smooth Muscle ◽  
Bethanechol Chloride

Capsaicin and bradykinin stimulate afferents from certain viscera to reflexly activate the cardiovascular system; however, whether these agents evoke similar reflex responses when applied topically to the intestine is not known. Therefore, in cats anesthetized with methoxyflurane, we applied capsaicin (10 micrograms) or bradykinin (0.5 microgram) to the serosal surface of the jejunum. Additionally, we topically applied bethanechol chloride, a synthetic choline ester with little direct cardiovascular effects, to evoke marked contraction of the smooth muscle of the jejunum. Capsaicin evoked significant (P less than 0.05) increases in mean arterial pressure (105 +/- 4 to 119 +/- 4 mmHg, mean +/- SE), first derivative left ventricular pressure (dP/dt) at 40 mmHg (2,698 +/- 134 to 3,105 +/- 155 mmHg/s), systemic vascular resistance (0.63 +/- 0.15 to 0.68 +/- 0.15 peripheral resistance units), and heart rate (196 +/- 14 to 205 +/- 15 beats/min), whereas aortic flow did not change. In a dose-dependent fashion, bradykinin and bethanechol each caused cardiovascular activation as well as a marked contraction of the smooth muscle in the segment of jejunum to which they were applied. In contrast, capsaicin produced no detectable contraction of visceral smooth muscle. Removal of the celiac and superior mesenteric ganglia abolished the cardiovascular responses evoked by capsaicin and bradykinin. Thus, in cats, stimulating intestinal afferents by topically applying capsaicin or bradykinin reflexly activates the cardiovascular system. Furthermore, although mechanoreceptors may contribute to the responses evoked by bradykinin and bethanechol, the capsaicin-related responses likely are mediated exclusively by chemically sensitive receptors.

Abated cardiovascular responses to chronic oral lisinopril treatment in conscious elderly rats

1999 ◽  
Vol 276 (5) ◽  
pp. R1408-R1415 ◽  
Author(s):  
Ruben Buñag ◽  
Jennifer Mellick ◽  
Brandy Allen
Keyword(s):  
Baroreflex Sensitivity ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Male Rats ◽  
Adrenergic Blockade ◽  
Reflex Bradycardia ◽  
Age Related ◽  
Pressor Responses ◽  
Mean Pressure ◽  
Old Rats

To determine whether the cardiovascular effects of chronic treatment with lisinopril are age related, we compared baroreflex sensitivity and pressor responsiveness in 4-mo- and 21-mo-old male rats that had been given oral lisinopril daily for 4 wk. Reflex bradycardia elicited by elevating blood pressure with phenylephrine was stronger in 4-mo-old rats than it was in 21-mo-old rats and also stronger in lisinopril-treated rats than it was in untreated rats of the same age. Pressor responses to angiotensin or norepinephrine were recorded after combined cholinergic and β-adrenergic blockade and then analyzed not only as absolute but also as percent increases in mean pressure. Although pressor responses seemed to be slightly reduced by lisinopril when expressed as absolute increases in mean pressure, corresponding percent increases were always larger in 4-mo-old rats than they were in 21-mo-old rats and were clearly enhanced by lisinopril more in younger rats. The stronger overall enhancement of pressor responsiveness and reflex bradycardia in younger rats suggests that the cardiovascular effects of lisinopril diminish with advancing age.

Pressor responses to vasopressin in rabbits with 3-day renal artery stenosis

1981 ◽  
Vol 240 (6) ◽  
pp. H862-H867 ◽  
Author(s):  
J. A. Johnson ◽  
S. Ichikawa ◽  
K. D. Kurz ◽  
W. L. Fowler ◽  
C. G. Payne
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Cardiovascular Responses ◽  
Artery Stenosis ◽  
Vasopressin Infusion ◽  
Pressor Responses

One-kidney rabbits were subjected to renal artery stenosis, and acute experiments were performed 3 days later on conscious animals; one-kidney rabbits without renal artery stenosis served as controls. Rabbits with 3-day renal artery stenosis were normotensive and had normal values for plasma renin activity. Intravenous infusion of arginine vasopressin at 5 mU.min-1.kg body wt-1 for 5 min resulted in a significantly (P less than 0.01) greater increase in mean arterial pressure and total peripheral resistance (TPR) in the renal artery stenosis rabbits than in the controls. Infusion of the angiotensin II (AII) competitive antagonist, [Sar1, Ile8]AII, before the vasopressin infusion abolished the hyperresponsiveness to vasopressin in the renal artery stenosis rabbits and resulted in changes in mean arterial pressure and TPR that were approximately of the same magnitude as the controls. Infusion of [SAr1, Ile8]AII before vasopressin infusion in control rabbits did not alter the cardiovascular responses to vasopressin. Because previous studies have shown that 3-day renal artery stenosis rabbits have exaggerated pressor responses to norepinephrine and that this hyperresponsiveness to norepinephrine is blocked by [Sar1, Ile8]-AII, the present study with vasopressin provided evidence that the increased responsiveness in this model is not specific for a single pressor agent. These studies also demonstrated that AII plays an important role in mediating the exaggerated pressor responses to vasopressin in this prehypertensive model.

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