Excess tachycardia: heart rate after antimuscarinic agents in conscious dogs

1984 ◽  
Vol 246 (2) ◽  
pp. H168-H173 ◽  
Author(s):  
D. F. Rigel ◽  
D. Lipson ◽  
P. G. Katona
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Atropine Sulfate ◽  
Conscious Dogs ◽  
Adrenergic System ◽  
Antimuscarinic Agent ◽  
Antimuscarinic Agents ◽  
Arterial Blood ◽  
Charged Derivative ◽  
Bilateral Vagotomy

In conscious dogs the heart rate after atropine is higher than after bilateral vagotomy; we have termed the additional heart rate with atropine "excess tachycardia" (ET). In six dogs the cervical vagosympathetic trunks were exteriorized in skin tubes, and arterial and venous catheters were chronically implanted. Atropine sulfate (0.1 mg/kg iv) injected during cold blockade of the vagi increased the heart rate by only 6 +/- 4 (SE) beats/min (NS) but rewarming the vagi in five of the six dogs after atropine resulted in an additional heart rate increase (ET) of 26 +/- 6 beats/min (P less than 0.005). The ET (41 +/- 11 beats/min) tended to be larger when the animals were pretreated with 1 mg/kg propranolol (P = 0.09). Similar results were obtained when atropine methylbromide, a charged derivative of atropine sulfate, or glycopyrrolate, a synthetic antimuscarinic agent, was substituted for atropine sulfate (ET: 51 +/- 6 and 51 +/- 16 beats/min, respectively). Raising the arterial blood pressure with phenylephrine increased the heart rate further; lowering the blood pressure with sodium nitroprusside attenuated or abolished the ET. Our results show that ET is produced by antimuscarinic agents in general and is not mediated by the beta-adrenergic system. Furthermore, ET is present only when the cervical vagi are intact, probably because ET is mediated by cholinergic vagal efferent fibers via a mechanism that has not yet been recognized in cardiac rate control.

Effects of l-arginine on systemic and renal haemodynamics in conscious dogs

1991 ◽  
Vol 81 (6) ◽  
pp. 727-732 ◽  
Author(s):  
Marohito Murakami ◽  
Hiromichi Suzuki ◽  
Atsuhiro Ichihara ◽  
Mareo Naitoh ◽  
Hidetomo Nakamoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Renal Haemodynamics ◽  
Conscious Dogs ◽  
Arginine Infusion ◽  
Arterial Blood

1. The effects of l-arginine on systemic and renal haemodynamics were investigated in conscious dogs. l-Arginine was administered intravenously at doses of 15 and 75 μmol min−1 kg−1 for 20 min. 2. Mean arterial blood pressure, heart rate and cardiac output were not changed significantly by l-arginine infusion. However, l-arginine infusion induced a significant elevation of renal blood flow from 50 ± 3 to 94 ± 12 ml/min (means ± sem, P < 0.01). 3. Simultaneous infusion of NG-monomethyl-l-arginine (0.5 μmol min−1 kg−1) significantly inhibited the increase in renal blood flow produced by l-arginine (15 μmol min−1 kg−1) without significant changes in mean arterial blood pressure or heart rate. 4. Pretreatment with atropine completely inhibited the l-arginine-induced increase in renal blood flow, whereas pretreatment with indomethacin attenuated it (63 ± 4 versus 82 ± 10 ml/min, P < 0.05). 5. A continuous infusion of l-arginine increased renal blood flow in the intact kidney (55 ± 3 versus 85 ± 9 ml/min, P < 0.05), but not in the contralateral denervated kidney (58 ± 3 versus 56 ± 4 ml/min, P > 0.05). 6. These results suggest that intravenously administered l-arginine produces an elevation of renal blood flow, which may be mediated by facilitation of endogenous acetylcholine-induced release of endothelium-derived relaxing factor and vasodilatory prostaglandins.

Rhythmicity of urinary sodium excretion, mean arterial blood pressure, and heart rate in conscious dogs

1992 ◽  
Vol 262 (1) ◽  
pp. H149-H156 ◽  
Author(s):  
U. Palm ◽  
W. Boemke ◽  
H. W. Reinhardt
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Conscious Dogs ◽  
Arterial Blood ◽  
Infusion Regimen

The existence of urinary excretion rhythms in dogs, which is a matter of controversy, was investigated under strictly controlled intake and environmental conditions. In seven conscious dogs, 14.5 mmol Na, 3.55 mmol K, and 91 ml H2O.kg body wt-1.24 h-1 were either administered with food at 8:30 A.M. or were continuously infused at 2 consecutive days. During these 3 days, automatized 20-min urine collections, mean arterial blood pressure (MABP), and heart rate (HR) recordings were performed without disturbing the dogs. Fundamental and partial periodicities, the noise component of urinary sodium excretion (UNaV), MABP, and HR were analyzed using a method derived from Fourier and Cosinor analysis. Oral intake (OI) leads to powerful 24-h periodicities in all dogs and seems to synchronize UNaV. UNaV on OI peaked between 1 and 3 P.M. Under the infusion regimen, signs of nonstationary rhythms and desynchronization predominated. UNaV under the infusion regimen could be separated into two components: a rather constant component continuously excreted and superimposed to this an oscillating component. No direct coupling between UNaV and MABP periodicities could be demonstrated. On OI, an increase in HR seems to advance the peak UNaV in the postprandial period. HR and MABP signals were both superimposed with noise. We conclude that UNaV rhythms are present in dogs. They are considerably more pronounced on OI.

Augmentation of respiratory sinus arrhythmia in response to progressive hypercapnia in conscious dogs

2001 ◽  
Vol 280 (5) ◽  
pp. H2336-H2341 ◽  
Author(s):  
Fumihiko Yasuma ◽  
Jun-Ichiro Hayano
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Respiratory Sinus Arrhythmia ◽  
Physiological Response ◽  
Minute Ventilation ◽  
Control Level ◽  
Conscious Dogs ◽  
Sinus Arrhythmia ◽  
Arterial Blood

Respiratory sinus arrhythmia (RSA) may serve to enhance pulmonary gas exchange efficiency by matching pulmonary blood flow with lung volume within each respiratory cycle. We examined the hypothesis that RSA is augmented as an active physiological response to hypercapnia. We measured electrocardiograms and arterial blood pressure during progressive hypercapnia in conscious dogs that were prepared with a permanent tracheostomy and an implanted blood pressure telemetry unit. The intensity of RSA was assessed continuously as the amplitude of respiratory fluctuation of heart rate using complex demodulation. In a total of 39 runs of hypercapnia in 3 dogs, RSA increased by 38 and 43% of the control level when minute ventilation reached 10 and 15 l/min, respectively ( P < 0.0001 for both), and heart rate and mean arterial pressure showed no significant change. The increases in RSA were significant even after adjustment for the effects of increased tidal volume, respiratory rate, and respiratory fluctuation of arterial blood pressure ( P < 0.001). These observations indicate that increased RSA during hypercapnia is not the consequence of altered autonomic balance or respiratory patterns and support the hypothesis that RSA is augmented as an active physiological response to hypercapnia.

Mechanisms involved in central cardiovascular effects of prostaglandin F2 alpha

1982 ◽  
Vol 242 (5) ◽  
pp. R545-R551 ◽  
Author(s):  
G. Feuerstein ◽  
C. J. Helke ◽  
R. L. Zerbe ◽  
D. M. Jacobowitz ◽  
I. J. Kopin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rectal Temperature ◽  
Cardiovascular Effects ◽  
Plasma Norepinephrine ◽  
Central Administration ◽  
Prostaglandin F2 Alpha ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
Bilateral Vagotomy

Prostaglandin F2 alpha (PGF2 alpha) injected into the cerebroventricular system (icv) of halothane-anesthetized rats increased the arterial blood pressure, heart rate, and rectal temperature. These effects were accompanied by a preferential increase in plasma norepinephrine concentration. Plasma levels of epinephrine, renin, and vasopressin were not changed in the PGF2 alpha-icv-treated rats. Bilateral vagotomy did not affect the PGF2 alpha-induced hypertension and tachycardia nor was there any change in the selective increase in plasma norepinephrine concentration. Hexamethonium pretreatment suppressed, in a dose-response manner, the increases in blood pressure, heart rate, and rectal temperature in response to PGF2 alpha-icv. Plasma norepinephrine and epinephrine levels were not altered by PGF2 alpha-icv in hexamethonium-treated rats, but plasma vasopressin concentration was markedly elevated in all hexamethonium-infused rats. These results suggest that selective central activation of the sympathetic nervous system underlies the profound cardiovascular and temperature responses elicited by central administration of PGF2 alpha.

Reflex inhibition of plasma renin activity by increased left ventricular pressure in conscious dogs

1989 ◽  
Vol 256 (6) ◽  
pp. R1299-R1307
Author(s):  
A. J. Gorman ◽  
J. S. Chen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Left Atrial ◽  
Plasma Renin ◽  
Left Ventricular ◽  
Renin Activity ◽  
Conscious Dogs ◽  
Arterial Blood

The purpose of the present study was to determine the effects of left ventricular (LV) outflow obstruction on plasma renin activity (PRA) and the contribution from afferent receptors located in the LV myocardium. In chronically instrumented, conscious dogs (n = 12), changes in PRA during a 15- to 20-mmHg decrease in arterial blood pressure were assessed during 1) intravenous infusions of nitroprusside (NP) alone and 2) infusions of NP while peak systolic LV pressure was elevated by acute ascending aortic occlusion (AAO + NP). Infusions of NP alone elicited significant increases in heart rate (24.9 +/- 5.1 beats/min; P less than 0.01) and in PRA [3.31 +/- 0.53 ng angiotensin I (ANG I).ml-1.h-1; P less than 0.01]. These were accompanied by decreases in both LV pressure (-13.8 +/- 3.6 mmHg; P less than 0.05) and left atrial pressure (-3.0 +/- 0.7 mmHg; P less than 0.05). During AAO + NP, LV pressure was elevated to an absolute level of 169.2 +/- 4.6 mmHg (+53.3 +/- 4.2 mmHg; P less than 0.001), whereas left atrial pressure was not changed. Both the hypotension-induced rise in PRA and tachycardia were significantly inhibited during AAO + NP (+0.59 +/- 0.29 ng ANG I.ml-1.h-1 and +6.3 +/- 4.6 beats/min, respectively; NS). The topical application of a local anesthetic in the region of the main coronary artery, sufficient to block the heart rate and arterial blood pressure responses to selective LV receptor stimulation by intracoronary veratridine (0.1-0.4 microgram/kg), resulted in significant increases in PRA and heart rate during AAO + NP.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac inotropic, chronotropic, and dromotropic actions of subretrofacial neurons of cat RVLM

1999 ◽  
Vol 276 (4) ◽  
pp. R1102-R1111 ◽  
Author(s):  
R. R. Campos ◽  
R. M. McAllen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Left Ventricular Pressure ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Ventrolateral Medulla ◽  
Diastolic Filling ◽  
Arterial Blood ◽  
Premotor Neurons ◽  
Bilateral Vagotomy

The cardiac actions of microinjecting sodium glutamate (0.5–2 nmol) among sympathetic premotor neurons of the subretrofacial nucleus in the rostral ventrolateral medulla (RVLM) were studied in chloralose-anesthetized cats after bilateral vagotomy, sinoaortic denervation, adrenalectomy, and α1-receptor blockade. Glutamate microinjections increased heart rate by 25.9 ± 1.8 beats/min (17.5%), systolic rate of rise in left ventricular pressure (LVdP/d t) by 1,443 ± 110 mmHg/s (119%), and arterial blood pressure by 26.9 ± 1.7 mmHg (50%), whereas they shortened the electrocardiogram P–R interval in 85 of 103 cases by 7.5 ± 1.2 ms (11.4%), triggering junctional rhythms on five occasions. The increase in LVdP/d tusually led the rise in blood pressure, and its magnitude greatly exceeded any increase attributable to changes in heart rate, diastolic filling, or afterload. Right-sided microinjections caused significantly greater tachycardias than did left-sided microinjections, but only left-sided microinjections triggered junctional rhythms (5 of 52 vs. 0 of 51; P < 0.05), whereas microinjections on either side raised LVdP/d tequally. Subretrofacial neurons thus drive positive chronotropic, inotropic, and dromotropic actions via the cardiac sympathetic nerves, whereas subsets among them preferentially control different aspects of cardiac function.

Neural contribution to the effect of glucagon-like peptide-1-(7—36) amide on arterial blood pressure in rats

1999 ◽  
Vol 277 (5) ◽  
pp. E784-E791 ◽  
Author(s):  
José Manuel Barragán ◽  
John Eng ◽  
Raquel Rodríguez ◽  
Enrique Blázquez
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Intravenous Administration ◽  
Cardiovascular Parameters ◽  
Arterial Blood ◽  
Neural Information ◽  
Bilateral Vagotomy ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

This study was designed to determine the contribution of the central nervous system (CNS) to the effects of glucagon-like peptide-1-(7—36) amide (tGLP-1) on arterial blood pressure and heart rate in rats. Accordingly, intracerebroventricular administration of the peptide produced an increase in cardiovascular parameters, which was blocked by previous administration of exendin-(9—39) through the same route, but not when it was intravenously injected. Intravenous administration of tGLP-1 produced a significant increase in arterial blood pressure and heart rate, which was blocked by the previous intracerebroventricular or intravenous administration of exendin-(9—39). Bilateral vagotomy blocked the stimulating effect of intracerebroventricular tGLP-1 administration on arterial blood pressure and heart rate. Also, bilateral vagotomy prevented the blocking effect of intracerebroventricular but not of intravenous exendin-(9—39) on cardiovascular parameters after intravenous administration of tGLP-1. These findings suggest that the action of tGLP-1 on cardiovascular parameters is under a dual control generated in the CNS and in peripheral structures and that the neural information emerging in the brain is transmitted to the periphery through the vagus nerve.

Compression Stocking Length Effects on Arterial Blood Pressure and Heart Rate Following Head-Up Tilt in Healthy Volunteers

2014 ◽  
Vol 63 (6) ◽  
pp. 435-438 ◽  
Author(s):  
Kunihiko Tanaka ◽  
Shiori Tokumiya ◽  
Yumiko Ishihara ◽  
Yumiko Kohira ◽  
Tetsuro Katafuchi
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Healthy Volunteers ◽  
Arterial Blood Pressure ◽  
Compression Stocking ◽  
Arterial Blood ◽  
Head Up Tilt ◽  
Length Effects
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