Bupivacaine Inhibits Baroreflex Control of Heart Rate in Conscious Rats

2000 ◽  
Vol 92 (1) ◽  
pp. 197-197 ◽  
Author(s):  
Kyoung S. K. Chang ◽  
Don R. Morrow ◽  
Kazuyo Kuzume ◽  
Michael C. Andresen
Keyword(s):  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Cardiovascular Reflexes ◽  
Pulse Interval ◽  
Dependent Manner ◽  
Baroreflex Control ◽  
Conscious Rats ◽  
Reflex Bradycardia ◽  
Adrenergic Antagonist ◽  
Dose Dependent

Background Because exposure to intravenously administered bupivacaine may alter cardiovascular reflexes, the authors examined bupivacaine actions on baroreflex control of heart rate in conscious rats. Methods Baroreflex sensitivity (pulse interval vs. systolic blood pressure in ms/mmHg) was determined before, and 1.5 and 15.0 min after rapid intravenous administration of bupivacaine (0.5, 1.0, and 2.0 mg/kg) using heart rate changes evoked by intravenously administered phenylephrine or nitroprusside. The actions on the sympathetic and parasympathetic autonomic divisions of the baroreflex were tested in the presence of a muscarinic antagonist methyl atropine and a beta-adrenergic antagonist atenolol. Results Within seconds of injection of bupivacaine, mean arterial pressure increased and heart rate decreased in a dose-dependent manner. Baroreflex sensitivity was unaltered after administration of 0.5 mg/kg bupivacaine. In addition, 1 mg/kg bupivacaine at 1.5 min depressed phenylephrine-evoked reflex bradycardia (0.776 +/- 0.325 vs. 0.543 +/- 0.282 ms/mmHg, P < 0.05) but had no effect on nitroprusside-induced tachycardia. Bupivacaine (2 mg/kg), however, depressed reflex bradycardia and tachycardia (phenylephrine, 0.751 +/- 0.318 vs. 0.451 +/- 0.265; nitroprusside, 0.839 +/- 0.256 vs. 0.564 +/- 0.19 ms/mmHg, P < 0.05). Baroreflex sensitivity returned to prebupivacaine levels by 15 min. Bupivacaine (2 mg/kg), in the presence of atenolol, depressed baroreflex sensitivity (phenylephrine, 0.633 +/- 0.204 vs. 0.277 +/- 0.282; nitroprusside, 0.653 +/- 0.142 vs. 0.320 +/- 0.299 ms/mmHg, P < 0.05). In contrast, bupivacaine did not alter baroreflex sensitivity in the presence of methyl atropine. Conclusions Bupivacaine, in clinically relevant concentrations, inhibits baroreflex control of heart rate in conscious rats. This inhibition appears to involve primarily vagal components of the baroreflex-heart rate pathways.

Isoflurane Depresses Baroreflex Control of Heart Rate in Decerebrate Rats

2002 ◽  
Vol 96 (5) ◽  
pp. 1214-1222 ◽  
Author(s):  
Jong S. Lee ◽  
Don Morrow ◽  
Michael C. Andresen ◽  
Kyoung S. K. Chang
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Baroreflex Sensitivity ◽  
Baroreflex Control ◽  
Beta Adrenoceptor ◽  
Reflex Bradycardia ◽  
Reflex Tachycardia ◽  
Map Data ◽  
Regulatory Sites

Background Isoflurane inhibits baroreflex control of heart rate (HR) by poorly understood mechanisms. The authors examined whether suprapontine central nervous system cardiovascular regulatory sites are required for anesthetic depression. Methods The effects of isoflurane (1 and 2 rat minimum alveolar concentration [MAC]) on the baroreflex control of HR were determined in sham intact and midcollicular-transected decerebrate rats. Intravenous phenylephrine (0.2-12 microg/kg) and nitroprusside (1-60 microg/kg) were used to measure HR responses to peak changes in mean arterial pressure (MAP). Sigmoidal logistic curve fits to HR-MAP data assessed baroreflex sensitivity (HR/MAP), HR range, lower and upper HR plateau, and MAP at half the HR range (BP50). Four groups (two brain intact and two decerebrate) were studied before, during, and after isoflurane. To assess sympathetic and vagal contributions to HR baroreflex, beta-adrenoceptor (1 mg/kg atenolol) or muscarinic (0.5 mg/kg methyl atropine) antagonists were administered systemically. Results Decerebration did not alter resting MAP and HR or baroreflex parameters. Isoflurane depressed baroreflex slope and HR range in brain-intact and decerebrate rats. In both groups, 1 MAC reduced HR range by depressing peak reflex tachycardia. Maximal reflex bradycardia during increases in blood pressure was relatively preserved. Atenolol during 1 MAC did not alter maximum reflex tachycardia. In contrast, atropine during 1 MAC fully blocked reflex bradycardia. Therefore, 1 MAC predominantly depresses sympathetic components of HR baroreflex. Isoflurane at 2 MAC depressed both HR plateaus and decreased BP50 in both groups. Conclusions Isoflurane depresses HR baroreflex control by actions that do not require suprapontine central nervous system sites. Isoflurane actions seem to inhibit HR baroreflex primarily by the sympathetic nervous system.

Baroreflex modulation by angiotensins at the rat rostral and caudal ventrolateral medulla

2006 ◽  
Vol 290 (4) ◽  
pp. R1027-R1034 ◽  
Author(s):  
Andréia C. Alzamora ◽  
Robson A. S. Santos ◽  
Maria J. Campagnole-Santos
Keyword(s):  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Opposite Effect ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Differential Modulation ◽  
Baroreflex Control ◽  
Caudal Ventrolateral Medulla ◽  
Angiotensin Peptides ◽  
Reflex Bradycardia

We determined the effect of microinjection of ANG-(1–7) and ANG II into two key regions of the medulla that control the circulation [rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively)] on baroreflex control of heart rate (HR) in anesthetized rats. Reflex bradycardia and tachycardia were induced by increases and decreases in mean arterial pressure produced by intravenous phenylephrine and sodium nitroprusside, respectively. The pressor effects of ANG-(1–7) and ANG II (25 pmol) after RVLM microinjection (11 ± 0.8 and 10 ± 2 mmHg, respectively) were not accompanied by consistent changes in HR. In addition, RVLM microinjection of these angiotensin peptides did not alter the bradycardic or tachycardic component of the baroreflex. CVLM microinjections of ANG-(1–7) and ANG II produced hypotension (−11 ± 1.5 and −11 ± 1.9 mmHg, respectively) that was similarly not accompanied by significant changes in HR. However, CVLM microinjections of angiotensins induced differential changes in the baroreflex control of HR. ANG-(1–7) attenuated the baroreflex bradycardia (0.26 ± 0.06 ms/mmHg vs. 0.42 ± 0.08 ms/mmHg before treatment) and facilitated the baroreflex tachycardia (0.86 ± 0.19 ms/mmHg vs. 0.42 ± 0.10 ms/mmHg before treatment); ANG II produced the opposite effect, attenuating baroreflex tachycardia (0.09 ± 0.06 ms/mmHg vs. 0.31 ± 0.07 ms/mmHg before treatment) and facilitating the baroreflex bradycardia (0.67 ± 0.16 ms/mmHg vs. 0.41 ± 0.05 ms/mmHg before treatment). The modulatory effect of ANG II and ANG-(1–7) on baroreflex sensitivity was completely abolished by peripheral administration of methylatropine. These results suggest that ANG II and ANG-(1–7) at the CVLM produce a differential modulation of the baroreflex control of HR, probably through distinct effects on the parasympathetic drive to the heart.

Acute effects of ethanol on baroreceptor reflex control of heart rate and on pressor and depressor responsiveness in rats

1987 ◽  
Vol 65 (5) ◽  
pp. 834-841 ◽  
Author(s):  
A-R. A. Abdel-Rahman ◽  
Roy Russ ◽  
J. A. Strickland ◽  
W. R. Wooles
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Baroreflex Sensitivity ◽  
Pressor Response ◽  
Base Line ◽  
Response Curves ◽  
Baroreflex Control ◽  
Conscious Rats ◽  
Upward Shift ◽  
The Right

In rats anesthetized with α-chloralose, doses of 0.1, 0.5, and 1 g/kg of ethanol produced an upward shift of baroreflex curves constructed by plotting the heart rate response against mean arterial pressure following evoked rises in mean arterial pressures by phenylephrine or angiotensin II. Whereas the upward shift of baroreceptor curves may be related, at least in part, to a higher base-line heart rate after ethanol, the data showed that the 1 g/kg dose of ethanol significantly depressed baroreflex sensitivity, suggesting that higher doses of ethanol impair baroreflex-mediated bradycardia. The phenylephrine, but not the angiotensin II or the nitroprusside, dose–response curves were shifted to the right after ethanol, indicating a decreased pressor responsiveness and suggesting that ethanol may have α-adrenergic blocking activity. This effect was also obtained in conscious rats. That this effect was not influenced by changes in baroreflex sensitivity was supported by the finding that a similar shift of the phenylephrine pressor–response curve was obtained in bilaterally vagotomized and hexamethonium-treated rats. Whether this effect of ethanol on baroreflex control of heart rate was influenced by anesthesia was investigated in conscious rats; the 1 g/kg dose of ethanol that produced the most significant decrease in baroreflex sensitivity was used in these experiments. Ethanol was still able to significantly inhibit baroreflex sensitivity in conscious rats, but the upward shift of the baroreflex curve and the elevated base-line heart rate no longer occurred. On the other hand, none of the three doses of ethanol had any significant effect on baroreflex-mediated tachycardia (in response to nitroprusside-evoked hypotension). The data suggest that high doses of ethanol selectively inhibit baroreflex-mediated bradycardia and that ethanol has an α-blocking-like activity in conscious and anesthetized rats.

Effects of aging on 24-h dynamic baroreceptor control of heart rate in ambulant subjects

1995 ◽  
Vol 268 (4) ◽  
pp. H1606-H1612 ◽  
Author(s):  
G. Parati ◽  
A. Frattola ◽  
M. Di Rienzo ◽  
P. Castiglioni ◽  
A. Pedotti ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Blood Pressure ◽  
Baroreflex Sensitivity ◽  
Regression Line ◽  
Domain Analysis ◽  
Pulse Interval ◽  
Alpha Coefficient ◽  
Baroreflex Control ◽  
Effects Of Aging

The effects of aging on the dynamic modulation of baroreflex sensitivity over 24 h was assessed in eight elderly (mean age +/- SD, 63.9 +/- 3.2 yr) and in eight young (23.9 +/- 6.1 yr) mild or moderate essential hypertensive patients, who were subject to a 24-h intra-arterial (Oxford technique) blood pressure recording in ambulatory conditions. The sensitivity of baroreflex control of the heart rate was dynamically assessed by quantifying 1) the slope of the regression line between pulse interval (the reciprocal of heart rate) and systolic blood pressure changes over spontaneously occurring hypertension-bradycardia or hypotension-tachycardia sequences (time domain analysis) and 2) the ratio between spectral-powers of pulse interval and systolic blood pressure around 0.1 Hz (alpha-coefficient: frequency domain analysis). The 24-h average sequence slope was lower in old than in young individuals (4.4 +/- 0.5 vs. 9.9 +/- 1.3 and 4.8 +/- 0.7 vs. 8.4 +/- 1.4 ms/mmHg for hypertension-bradycardia and hypotension-tachycardia sequences, respectively; P < 0.05 for both). Similar results were obtained by using the alpha-coefficient approach. The marked nighttime increase in baroreflex sensitivity observed in young individuals was much less evident in the elderly. Thus 24-h baroreflex sensitivity is markedly impaired by aging. The impairment becomes manifest also as an inability to increase baroreflex sensitivity at night.

Parasympathetic impairment of baroreflex control of heart rate in Dahl S rats

1990 ◽  
Vol 259 (1) ◽  
pp. R76-R83 ◽  
Author(s):  
S. A. Whitescarver ◽  
C. E. Ott ◽  
T. A. Kotchen
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Sodium Nitroprusside ◽  
Baroreflex Sensitivity ◽  
Parasympathetic Nervous System ◽  
Baroreflex Control ◽  
High Salt Diet ◽  
Salt Diet ◽  
Reflex Bradycardia ◽  
Before And After

To test the hypothesis that impaired baroreflex control of heart rate in Dahl salt-sensitive (S) rats is due to an impairment of the parasympathetic limb of the bradycardic response, baroreflex sensitivity was evaluated in conscious, chronically instrumented Dahl S and salt-resistant (R) animals. Sensitivity was impaired in Dahl S rats when bolus doses of phenylephrine were administered (0.863 +/- 0.042 vs. 1.43 +/- 0.055 ms/mmHg), but it was not different than in R rats when tested with sodium nitroprusside. When the sensitivities before and after blocking the parasympathetic nervous system with atropine were compared, it was revealed that 82% of the reflex bradycardia resulting from bolus doses of phenylephrine was due to the parasympathetic nervous system, whereas the majority (73%) of the bradycardia induced by 5-min infusions of phenylephrine was due to withdrawal of sympathetic tone. Neither baroreflex sensitivity to infusions of phenylephrine (73% sympathetic) or to infusions after atropine (100% sympathetic) were significantly different between S and R rats. Therefore, the impairment of the heart rate reflex in Dahl S rats is due to an impairment of the parasympathetic limb of the response. In addition, a high-salt diet before the development of hypertension did not alter baroreflex sensitivity in either Dahl S or R rats.

scholarly journals Blockade of Cerebral Blood Flow Response to Insulin-Induced Hypoglycemia by Caffeine and Glibenclamide in Conscious Rats

1997 ◽  
Vol 17 (12) ◽  
pp. 1309-1318 ◽  
Author(s):  
Naoaki Horinaka ◽  
Tang-Yong Kuang ◽  
Hazel Pak ◽  
Robert Wang ◽  
Jane Jehle ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Degradation Products ◽  
Dependent Manner ◽  
Conscious Rats ◽  
Intravenous Injections ◽  
Adenosine Receptor Antagonist ◽  
Flow Response ◽  
Arterial Plasma ◽  
Dose Dependent

The possibility that adenosine and ATP-sensitive potassium channels (KATP) might be involved in the mechanisms of the increases in cerebral blood flow (CBF) that occur in insulin-induced hypoglycemia was examined. Cerebral blood flow was measured by the [14C]iodoantipyrine method in conscious rats during insulin-induced, moderate hypoglycemia (2 to 3 mmol/L glucose in arterial plasma) after intravenous injections of 10 to 20 mg/kg of caffeine, an adenosine receptor antagonist, or intracisternal infusion of 1 to 2 μmol/L glibenclamide, a KATP channel inhibitor. Cerebral blood flow was also measured in corresponding normoglycemic and drug-free control groups. Cerebral blood flow was 51% higher in untreated hypoglycemic than in untreated normoglycemic rats ( P < 0.01). Caffeine had a small, statistically insignificant effect on CBF in normoglycemic rats, but reduced the CBF response to hypoglycemia in a dose-dependent manner, i.e., 27% increase with 10 mg/kg and complete elimination with 20 mg/kg. Chemical determinations by HPLC in extracts of freeze-blown brains showed significant increases in the levels of adenosine and its degradation products, inosine and hypoxanthine, during hypoglycemia ( P < 0.05). Intracisternal glibenclamide had little effect on CBF in normoglycemia, but, like caffeine, produced dose-dependent reductions in the magnitude of the increases in CBF during hypoglycemia, i.e., +66% with glibenclamide-free artificial CSF administration, +25% with 1 μmol/L glibenclamide, and almost complete blockade (+5%) with 2 μmol/L glibenclamide. These results suggest that adenosine and KATP channels may play a role in the increases in CBF during hypoglycemia.

Abstract 477: Chronic Baroreflex Activation Improves Baroreflex Control of Heart Rate In Obesity

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Radu Iliescu ◽  
Ionut Tudorancea ◽  
Eric Irwin ◽  
Thomas Lohmeier
Keyword(s):  
Heart Rate ◽  
Pulse Interval ◽  
Vagal Activity ◽  
Fat Intake ◽  
High Fat ◽  
Baroreflex Control ◽  
Systolic Blood Pressure Variability ◽  
Body Weight Increase ◽  
Obesity Hypertension ◽  
Fat Feeding

Impaired baroreflex control of heart rate (BRS) and attendant risk for cardiac arrhythmias are associated with sympathetically-mediated obesity hypertension. Since both global and renal-specific sympathoinhibition have sustained antihypertensive effects in obesity, we compared BRS in obese dogs subjected to 7 days of electrical baroreflex activation (BA) and, after recovery (REC), to bilateral surgical renal denervation (RDX). After control (C) measurements and 4 weeks of high fat diet, fat intake was reduced (RF) to maintain a body weight increase of ∼ 50%, which led to an increase in mean arterial pressure (MAP) from 100±2 to 117±3 mmHg and heart rate (HR) from 86±3 to 130±4 bpm. Obesity hypertension was associated with decreased sensitivity of 24h spontaneous BRS (determined by the sequence technique from daily beat-to-beat time series) and pulse interval (PI) variability (24h SD). While both BA and RDX abolished hypertension, only BA diminished tachycardia and normalized BRS, consequently improving HR variability. Short-term systolic blood pressure variability (5 min SD) also decreased with high fat feeding and was restored to control upon reduction of fat intake (RF) during established obesity hypertension, suggesting a vasoplegic effect of fat. These data suggest that in addition to the antihypertensive effects of sympathoinhibition, BA corrects cardiac baroreflex dysfunction in obesity hypertension, presumably by enhancing cardiac vagal activity. This in turn markedly improves depressed HR variability, a known risk factor for cardiac arrhythmic events.

Alterations in Blood Pressure and Heart Rate Variabililty in Transgenic Rats with Low Brain Angiotensinogen

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 727-727
Author(s):  
Ovidiu Baltatu ◽  
Ben J Janssen ◽  
Ralph Plehm ◽  
Detlev Ganten ◽  
Michael Bader
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Circadian Variation ◽  
Ang Ii ◽  
Transgenic Rats ◽  
Short Term ◽  
Baroreflex Control ◽  
Sd Rats ◽  
The Brain

P191 The brain renin-angiotensin system (RAS) system may play a functional role in the long-term and short-term control of blood pressure (BPV) and heart rate variability (HRV). To study this we recorded in transgenic rats TGR(ASrAOGEN) with low brain angiotensinogen levels the 24-h variation of BP and HR during basal and hypertensive conditions, induced by a low-dose s.c. infusion of angiotensin II (Ang II, 100 ng/kg/min) for 7 days. Cardiovascular parameters were monitored by telemetry. Short-term BPV and HRV were evaluated by spectral analysis and as a measure of baroreflex sensitivity the transfer gain between the pressure and heart rate variations was calculated. During the Ang II infusion, in SD but not TGR(ASrAOGEN) rats, the 24-h rhythm of BP was inverted (5.8 ± 2 vs. -0.4 ± 1.8 mm Hg/group of day-night differences of BP, p< 0.05, respectively). In contrast, in both the SD and TGR(ASrAOGEN) rats, the 24-h HR rhythms remained unaltered and paralleled those of locomotor activity. The increase of systolic BP was significantly reduced in TGR(ASrAOGEN) in comparison to SD rats as previously described, while the HR was not altered in TGR(ASrAOGEN) nor in SD rats. The spectral index of baroreflex sensitivity (FFT gain between 0.3-0.6 Hz) was significantly higher in TGR(ASrAOGEN) than SD rats during control (0.71 ± 0.1 vs. 0.35 ± 0.06, p<0.05), but not during Ang II infusion (0.6 ± 0.07 vs. 0.4 ± 0.1, p>0.05). These results demonstrate that the brain RAS plays an important role in mediating the effects of Ang II on the circadian variation of BP. Furthermore these data are consistent with the view that the brain RAS modulates baroreflex control of HR in rats, with AII having an inhibitory role.

Comparison of phenylephrine bolus and infusion methods in baroreflex measurements

1990 ◽  
Vol 69 (3) ◽  
pp. 962-967 ◽  
Author(s):  
J. T. Sullebarger ◽  
C. S. Liang ◽  
P. D. Woolf ◽  
A. E. Willick ◽  
J. F. Richeson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Heart Rate Response ◽  
Pressor Response ◽  
Plasma Catecholamines ◽  
Systolic Arterial Pressure ◽  
Normal Subjects ◽  
Vagus Nerves ◽  
Baroreflex Control

Phenylephrine (PE) bolus and infusion methods have both been used to measure baroreflex sensitivity in humans. To determine whether the two methods produce the same values of baroreceptor sensitivity, we administered intravenous PE by both bolus injection and graded infusion methods to 17 normal subjects. Baroreflex sensitivity was determined from the slope of the linear relationship between the cardiac cycle length (R-R interval) and systolic arterial pressure. Both methods produced similar peak increases in arterial pressure and reproducible results of baroreflex sensitivity in the same subjects, but baroreflex slopes measured by the infusion method (9.9 +/- 0.7 ms/mmHg) were significantly lower than those measured by the bolus method (22.5 +/- 1.8 ms/mmHg, P less than 0.0001). Pretreatment with atropine abolished the heart rate response to PE given by both methods, whereas plasma catecholamines were affected by neither method of PE administration. Naloxone pretreatment exaggerated the pressor response to PE and increased plasma beta-endorphin response to PE infusion but had no effect on baroreflex sensitivity. Thus our results indicate that 1) activation of the baroreflex by the PE bolus and infusion methods, although reproducible, is not equivalent, 2) baroreflex-induced heart rate response to a gradual increase in pressure is less than that seen with a rapid rise, 3) in both methods, heart rate response is mediated by the vagus nerves, and 4) neither the sympathetic nervous system nor the endogenous opiate system has a significant role in mediating the baroreflex control of heart rate to a hypertensive stimulus in normal subjects.

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