Effects of long-term pretreatment with isoproterenol on bromocriptine-induced tachycardia in conscious rats

2000 ◽  
Vol 78 (3) ◽  
pp. 260-265 ◽  
Author(s):  
Saad Lahlou ◽  
Guilherme C Lima ◽  
Carmelo SC Leão-Filho ◽  
Gloria P Duarte
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Pressure ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Perfused Heart ◽  
Maximal Increase ◽  
Ventricular Systolic Pressure ◽  
Conscious Rats ◽  
Left Ventricular Systolic Pressure

It has been shown that bromocriptine-induced tachycardia, which persisted after adrenalectomy, is (i) mediated by central dopamine D2 receptor activation and (ii) reduced by 5-day isoproterenol pretreatment, supporting therefore the hypothesis that this effect is dependent on sympathetic outflow to the heart. This study was conducted to examine whether prolonged pretreatment with isoproterenol could abolish bromocriptine-induced tachycardia in conscious rats. Isoproterenol pretreatment for 15 days caused cardiac hypertrophy without affecting baseline blood pressure and heart rate. In control rats, intravenous bromocriptine (150 µg/kg) induced significant hypotension and tachycardia. Bromocriptine-induced hypotension was unaffected by isoproterenol pretreatment, while tachycardia was reversed to significant bradycardia, an effect that was partly reduced by i.v. domperidone (0.5 mg/kg). Neither cardiac vagal nor sympathetic tone was altered by isoproterenol pretreatment. In isolated perfused heart preparations from isoproterenol-pretreated rats, the isoproterenol-induced maximal increase in left ventricular systolic pressure was significantly reduced, compared with saline-pretreated rats (the EC50 of the isoproterenol-induced increase in left ventricular systolic pressure was enhanced ~22-fold). These results show that 15-day isoproterenol pretreatment not only abolished but reversed bromocriptine-induced tachycardia to bradycardia, an effect that is mainly related to further cardiac beta-adrenoceptor desensitization rather than to impairment of autonomic regulation of the heart. They suggest that, in normal conscious rats, the central tachycardia of bromocriptine appears to predominate and to mask the bradycardia of this agonist at peripheral dopamine D2 receptors.Key words: bromocriptine, blood pressure, heart rate, isoproterenol pretreatment, peripheral dopamine D2 receptors, desensitization.

Increased cardiac contractility in acute uremia: interrelationships with hypertension

1975 ◽  
Vol 229 (2) ◽  
pp. 501-505 ◽  
Author(s):  
T Nivatpumin ◽  
T Yipintsoi ◽  
S Penpargkul ◽  
J Scheuer
Keyword(s):  
Blood Pressure ◽  
Systolic Hypertension ◽  
Diastolic Pressure ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Ventricular Systolic Pressure ◽  
Inotropic State ◽  
Left Ventricular Systolic Pressure

To study the effects of acute uremia on the inotropic state of the rat heart, we subjected rats to bilateral nephrectomy and studied their hearts in the open chest 24 h later. Uremic rats had significantly higher systolic blood pressure than sham-operated animals. Left ventricular systolic pressure and maximum dP/dt, both during ejection and isovolumic contrations, were higher for any given end-diastolic pressure in hearts of uremic rats than in sham-operated animals. This difference in performance charcteristics was not abolished by doses of propranolol that blocked the heart rate response to isoproterenol. The administration of phenoxybenzamine during the 24 h of uremia abolished the blood pressure rise in uremic rats, but the increased contractile state persisted. Treatment of sham-operated animals with methoxamine to produce the same course of blood pressure as observed in uremic rats was also associated with an increased inotropic state. These results indicate that in the rat, acute uremia is associated with an increased inotropic state that is not mediated by beta-adrenergic mechanisms. The systolic hypertension of acute uremia is not the major cause of the increased contractility, although systolic hypertension without uremia can mimic the performance characteristics found in hearts of uremic rats.

Gender differences in the cardiac response to dietary conjugated linoleic acid isomers

2006 ◽  
Vol 84 (2) ◽  
pp. 257-264 ◽  
Author(s):  
Paramjit S. Tappia ◽  
Rabban Mangat ◽  
Cindy Gabriel ◽  
Melissa R. Dent ◽  
Nina Aroutiounova ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Heart Rate ◽  
Heart Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Female Rats ◽  
Male Rats ◽  
Control Group ◽  
Ventricular Systolic Pressure ◽  
Left Ventricular Systolic Pressure

The present study was undertaken to assess the heart function, by the in vivo catheterization technique, of healthy male and female Sprague–Dawley rats fed different conjugated linoleic acid (CLA) isomers, (cis-9, trans-11 (c9,t11) and trans-10, cis-12 (t10,c12)) individually and in combination (50:50 mix as triglyceride or fatty acids) from 4 to 20 weeks of age. Whereas the triglyceride form of the CLA isomer mix lowered the heart rate, the rate of contraction (+dP/dt) and rate of relaxation (–dP/dt), systolic and diastolic pressures, mean arterial pressure, and the left ventricular systolic pressure were higher in male rats as compared with all the other dietary groups. In contrast, there were no significant effects in the cardiac function of the female rats in response to the CLA isomer mix in triglyceride form. Whereas the heart rate, +dP/dt, and left ventricular systolic pressure were lower in male rats fed the t10,c12 CLA isomer alone, the heart rate of the female rats was higher, but the systolic pressure, +dP/dt, and mean arterial pressure were lower compared with the control group. Also, the left ventricular end-diastolic pressure was specifically higher in the female rats in response to free fatty acids-containing CLA mix. Furthermore, an additive effect of the free fatty acids-containing CLA mix was seen in the +dP/dt and –dP/dt of female rats compared with the control group. These results indicate that CLA isomers exert differential effects on heart function and suggest the need for a complete evaluation of the benefits, interactions, and potential side effects of each isomer.

Cardiac changes during behavioral stress in dogs

1979 ◽  
Vol 236 (5) ◽  
pp. H750-H758 ◽  
Author(s):  
R. A. Galosy ◽  
L. K. Clarke ◽  
J. H. Mitchell
Keyword(s):  
Heart Rate ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Avoidance Task ◽  
Base Line ◽  
Sidman Avoidance ◽  
Ventricular Systolic Pressure ◽  
Behavioral Stress ◽  
Left Ventricular Systolic Pressure

Alterations in heart rate (HR), left ventricular systolic pressure (LVP), and maximum rate of left ventricular pressure development (LV dP/dtmax) during a Sidman avoidance task were studied in eight chronically prepared dogs. Four of these animals comprised a nonstressed control group. In the experimental group, in addition to phasic increases in HR, LVP, and LV dP/dtmax during the avoidance period of each day, tonic increases in these measures were also observed over the 13 days of the experiment. Left ventricular systolic pressure was found to be least sensitive to the stress procedure inasmuch as the phasic changes were no longer present after the 10th day and tonic levels were within base-line values by the 13th day. When alterations in cardiac activity were observed in the nonstressed animals, there were decreases in function. It was concluded that controlled behavioral stress produces increased cardiac performance without increased bodily activity. It was also hypothesized that preavoidance increases in heart rate in experimental animals were the result of vagal influences on the heart, whereas avoidance increases in HR, LV dP/dtmax, and LVP were functions of increased beta-sympathetic activity on the heart and adaptive peripheral vascular changes.

Metabolism of the perfused rabbit heart. IV. Effects of β-adrenergic blockade on enzyme release and late energy stores during postanoxic reoxygenation

1980 ◽  
Vol 58 (5) ◽  
pp. 469-476 ◽  
Author(s):  
Miguel A. Chiong ◽  
Henry Stefaniszyn
Keyword(s):  
Heart Rate ◽  
Energy Charge ◽  
Systolic Pressure ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Enzyme Release ◽  
Ventricular Systolic Pressure ◽  
Energy Stores ◽  
Left Ventricular Systolic Pressure

The effects of 80 μM dl-propranolol on left ventricular (LV) performance, energy stores, and creatine kinase (CK) release were studied in a modified Langendorff rabbit heart preparation during 75 min of aerobic perfusion and postanoxic reoxygenation.The data showed that this concentration of propranolol, which blocked the effects of β-adrenergic stimulation without affecting LV performance, coronary sinus flow (CSF), or oxygen consumption [Formula: see text], was associated with greater stores of glycogen and adenine nucleotides at the end of aerobic perfusion. Similar effects were observed during postanoxic reoxygenation, when recoveries of left ventricular systolic pressure, heart rate, heart rate - left ventricular systolic pressure product, CSF, and [Formula: see text] remained unchanged during propranolol administration, but myocardial concentrations of glycogen, creatine phosphate, and ATP were greater and the ATP:AMP ratio and the energy charge were higher than in untreated hearts. In addition, the rate of CK loss was lower in the blocked postanoxic hearts than in the unblocked group. These results indicate that propranolol had a beneficial effect on cardiac metabolism during postanoxic recovery tending to normalize energy stores and to reduce enzyme loss during reoxygenation of perfused rabbit hearts without affecting mechanical performance, coronary flow, or O2 metabolism.

Abstract 13421: Ventricular and Arterial Elastance During Isometric Handgrip Exercise and Post-exercise Circulatory Arrest in Heart Failure With and Without Preserved Ejection Fraction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Naoki Fujimoto ◽  
Keishi Moriwaki ◽  
Issei Kameda ◽  
Masaki Ishiyama ◽  
Taku Omori ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Circulatory Arrest ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Isometric Handgrip ◽  
Arterial Elastance ◽  
Post Exercise

Introduction: Isometric handgrip (IHG) training at 30% maximal voluntary contraction (MVC) lowers blood pressure in hypertensive patients. Impacts of IHG exercise and post-exercise circulatory arrest (PECA), which isolates metaboreflex control, have been unclear in heart failure (HF). Purpose: To investigate the impacts of IHG exercise and PECA on ventricular-arterial stiffness and left ventricular (LV) relaxation in HF with preserved (HFpEF) and reduced ejection fraction (HFrEF). Methods: We invasively obtained LV pressure-volume (PV) loops in 20 patients (10 HFpEF, 10 HFrEF) using conductance catheter with microtip-manometer during 3 minutes of IHG at 30%MVC and 3 minutes of PECA. Hemodynamics and LV-arterial function including LV end-systolic elastance (Ees) by the single-beat method, effective arterial elastance (Ea), and time constant of LV relaxation (Tau) were evaluated every minute. Results: At rest, HFpEF had higher LV end-systolic pressure (ESP) and lower heart rate than HFrEF with similar LV end-diastolic pressure (EDP). The coupling ratio (Ees/Ea) was greater in HFpEF than HFrEF (1.0±0.3 vs. 0.6±0.3, p<0.01). IHG for 3minutes similarly increased heart rate in HFpEF (by 10±8 bpm) and HFrEF (by 14±6 bpm). IHG also increased end-diastolic and LVESP (134±21 vs. 158±30 mmHg and 113±25 vs. 139±25 mmHg) in both groups (groupхtime effect p≥0.25). In HFpEF, Ees, Ea and Ees/Ea (1.0±0.3 vs. 1.1±0.4) were unaffected during IHG. In HFrEF, IHG induced variable increases in Ea. LV end-systolic volume and the ESPV volume-axis intercept were larger, and Ees at IHG 3 rd min was greater (1.30±0.7 vs. 3.1±2.1 mmHg/ml, p<0.01) than baseline, resulting in unchanged Ees/Ea at IHG 3 rd min (0.6±0.3 vs. 0.8±0.4, p≥0.37). Tau was prolonged only in HFrEF during IHG and was returned to the baseline value during PECA. During the first 2 minutes of PECA, LVESP was lower than that at IHG 3 rd min only in HFpEF, suggesting less metaboreflex control of blood pressure in HFpEF during IHG. Conclusions: IHG exercise at 30%MVC induced modest increases in LV end-systolic and end-diastolic pressures in HFpEF and HFrEF. Although the prolongation of LV relaxation was observed only in HFrEF, the ventricular and arterial coupling was maintained throughout the IHG exercise in both groups.

Role of reflexes following myocardial necrobiosis

1965 ◽  
Vol 209 (6) ◽  
pp. 1081-1088 ◽  
Author(s):  
G. Ascanio ◽  
F. Barrera ◽  
E. V. Lautsch ◽  
M. J. Oppenheimer
Keyword(s):  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Hemodynamic Changes ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood ◽  
Bilateral Vagotomy ◽  
Left Ventricular Systolic Pressure

Intracoronary administration of hexachlorotetrafluorobutane (Hexa) into non-thoracotomized dogs produced a statistically significant decrease in left ventricular systolic pressure (LVSP), mean femoral arterial blood pressure (MFAP), first derivative of left ventricular pressure pulse (dP/d t), total peripheral resistance (TPR), and cardiac output (C.O.) lasting up to 1 hr after injection. Femoral vascular resistance decreased during the first 3 min after production of necrobiosis. Fifty percent of the dogs died of ventricular fibrillation (VF) after Hexa infarction. Prereserpinized dogs did not show significant changes in the parameters which were significantly changed in normal dogs after Hexa necrobiosis except in the case of VF which was almost absent in this group. Bilateral vagotomy prior to Hexa administration prevented most hemodynamic changes after necrobiosis whereas atropine did not. Bilateral vagotomy and atropine 1 hr after necrobiosis increased MFAP, dP/d t, LVSP, C.O., and TPR. Apparently excitatory efferent sympathetic activity on heart and femoral arterial vessels is reflexly inhibited by the effects of intracoronary injection of Hexa. The afferent pathway is via the vagus nerve.

Modulation of cardiovascular response to dynamic exercise by fastigial nucleus

1984 ◽  
Vol 56 (5) ◽  
pp. 1369-1377 ◽  
Author(s):  
K. J. Dormer
Keyword(s):  
Blood Pressure ◽  
Repeated Measures ◽  
Cardiovascular Response ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Fastigial Nucleus ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood

Mongrel dogs (n = 34) were used to record the cardiovascular responses during submaximal exercise-tolerance tests (ETT) before and after the placement of lesions in rostral portions of the cerebellar fastigial nucleus (FN). Sterile surgical procedures were used to implant solid-state pressure transducers into the left ventricle or descending aorta (anesthesia 1% halothane in O2) and multipolar stainless steel electrodes into FN (anesthesia alpha-chloralose 115 mg/kg iv). Heart rate (HR), maximal left ventricular systolic pressure ( LVPmax ) and its first derivative ( dLVP /dt), and mean arterial blood pressure (MAP) were recorded during a motorized treadmill ETT. Electrolytic direct-current or radio-frequency lesions were made through the indwelling FN electrodes, and the ETT was repeated following 10–14 days recovery. Two-way analysis of variance (ANOVA), with repeated measures on one, and one-way ANOVA for simple effects indicated a significant reduction in HR and MAP (P less than 0.01) but not LVPmax and dLVP /dt occurred during exercise as a result of rostral FN lesions. Although the trend for reduced LVPmax and dLVP /dt was also evident, a relatively greater decrease in blood pressure occurred in the peripheral vasculature during exercise. It was concluded that FN acts as a modulator of HR and MAP during dynamic exercise because of the observed deficits, and because FN is known to both send efferent projections to medullary vasomotor areas and receive projections from motor cortex and muscle and joint afferents.

Effects of sympathetic stimulation during cooling on hypothermic as well as posthypothermic hemodynamic function

2006 ◽  
Vol 84 (10) ◽  
pp. 985-991 ◽  
Author(s):  
T.V. Kondratiev ◽  
T. Tveita
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Saline Solution ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Mechanical Function ◽  
Ventricular Systolic Pressure ◽  
Hemodynamic Variables ◽  
Left Ventricular Systolic Pressure

This experimental study was performed to explore hemodynamic effects of a moderate dose epinephrine (Epi) during hypothermia and to test the hypothesis whether sympathetic stimulation during cooling affects myocardial function following rewarming. Two groups of male Wistar rats (each, n = 7) were cooled to 15 °C, maintained at this temperature for 1 h, and then rewarmed. Group 1 received 1 μg/min Epi, i.v., for 1 h during cooling to 28 °C, a dose known to elevate cardiac output (CO) by approximately 25% at 37 °C. Group 2 served a saline solution control. At 37 °C, Epi infusion elevated CO, left ventricular systolic pressure, maximum rate of left ventricle pressure rise, and mean arterial pressure. During cooling to 28 °C, these variables, with the exception of mean arterial pressure, decreased in parallel to those in the saline solution group. In contrast, in the Epi group, mean arterial pressure remained increased and total peripheral resistance was significantly elevated at 28 °C. Compared with corresponding prehypothermic values, most hemodynamic variables were lowered after 1 h at 15 °C in both groups (except for stroke volume). After rewarming, alterations in hemodynamic variables in the Epi-treated group were more prominent than in saline solution controls. Thus, before cooling, continuous Epi infusion predominantly stimulates myocardial mechanical function, materialized as elevation of CO, left ventricular systolic pressure, and maximum rate of left ventricle pressure rise. Cooling, on the other hand, apparently eradicates central hemodynamic effects of Epi and during stable hypothermia, elevation of peripheral vascular vasopressor effects seem to take over. In contrast to temperature-matched, non-Epi stimulated control rats, a significant depression of myocardial mechanical function occurs during rewarming following a moderate sympathetic stimulus during initial cooling.

A Physiological Controller for Turbodynamic Ventricular Assist Devices Based on Left Ventricular Systolic Pressure

2016 ◽  
Vol 40 (9) ◽  
pp. 842-855 ◽  
Author(s):  
Anastasios Petrou ◽  
Gregor Ochsner ◽  
Raffael Amacher ◽  
Panagiotis Pergantis ◽  
Mathias Rebholz ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Assist Devices ◽  
Ventricular Assist ◽  
Ventricular Systolic Pressure ◽  
Assist Devices ◽  
Left Ventricular Systolic Pressure

Muscle metaboreflex attenuates spontaneous heart rate baroreflex sensitivity during dynamic exercise

2007 ◽  
Vol 292 (6) ◽  
pp. H2867-H2873 ◽  
Author(s):  
Javier A. Sala-Mercado ◽  
Masashi Ichinose ◽  
Robert L. Hammond ◽  
Tomoko Ichinose ◽  
Marco Pallante ◽  
...  
Keyword(s):  
Heart Rate ◽  
Exercise Intensity ◽  
Baroreflex Sensitivity ◽  
Pressor Response ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Moderate Exercise ◽  
Ventricular Systolic Pressure ◽  
Muscle Metaboreflex

Hypoperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex. Dynamic exercise attenuates spontaneous baroreflex sensitivity (SBRS) in the control of heart rate (HR) during rapid, spontaneous changes in blood pressure (BP). Our objective was to determine whether muscle metaboreflex activation (MRA) further diminishes SBRS. Conscious dogs were chronically instrumented for measurement of HR, cardiac output, mean arterial pressure, and left ventricular systolic pressure (LVSP) at rest and during mild (3.2 km/h) or moderate (6.4 km/h at 10% grade) dynamic exercise before and after MRA (via partial reduction of hindlimb blood flow). SBRS was evaluated as the slopes of the linear relations (LRs) between HR and LVSP during spontaneous sequences of at least three consecutive beats when HR changed inversely vs. pressure (expressed as beats·min−1·mmHg−1). During mild exercise, these LRs shifted upward, with a significant decrease in SBRS (−3.0 ± 0.4 vs. −5.2 ± 0.4, P < 0.05 vs. rest). MRA shifted LRs upward and rightward and decreased SBRS (−2.1 ± 0.1, P < 0.05 vs. mild exercise). Moderate exercise shifted LRs upward and rightward and significantly decreased SBRS (−1.2 ± 0.1, P < 0.05 vs. rest). MRA elicited further upward and rightward shifts of the LRs and reductions in SBRS (−0.9 ± 0.1, P < 0.05 vs. moderate exercise). We conclude that dynamic exercise resets the arterial baroreflex to higher BP and HR as exercise intensity increases. In addition, increases in exercise intensity, as well as MRA, attenuate SBRS.

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