scholarly journals Role of Baroreflex Sensitivity in Predicting Tilt Training Response in Patients with Neurally Mediated Syncope

2016 ◽  
Vol 57 (2) ◽  
pp. 313 ◽  
Author(s):  
Kwang Jin Chun ◽  
Hye Ran Yim ◽  
Jungwae Park ◽  
Seung-Jung Park ◽  
Kyoung-Min Park ◽  
...  
Keyword(s):  
Baroreflex Sensitivity ◽  
Neurally Mediated Syncope ◽  
Training Response

Role of vasopressin in acutely altered baroreflex sensitivity during hemorrhage in rats

1991 ◽  
Vol 261 (3) ◽  
pp. R677-R685 ◽  
Author(s):  
B. L. Brizzee ◽  
R. D. Russ ◽  
B. R. Walker
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Blood Loss ◽  
Baroreflex Sensitivity ◽  
Peripheral Resistance ◽  
Conscious Rat ◽  
Arterial Blood ◽  
Arterial Hemorrhage ◽  
Moderate Elevation

Experiments were performed to examine the potential role of circulating arginine vasopressin (AVP) on baroreflex sensitivity during hypotensive and nonhypotensive hemorrhage in the conscious rat. Animals were chronically instrumented for measurement of cardiac output, blood pressure, and heart rate (HR). Three potential stimuli for release of AVP were utilized: 1) rapid 20% arterial hemorrhage that resulted in hypotension, 2) nonhypovolemic hypotension induced by intravenous infusion of nitroprusside, and 3) nonhypotensive hemorrhage (rapid 10% arterial blood withdrawal). Hypotensive hemorrhage was associated with significant reductions in blood pressure, cardiac output, HR, and calculated total peripheral resistance, an increase in baroreflex (BRR) bradycardia in response to pressor infusions of phenylephrine, and a moderate elevation in circulating AVP. Prior intravenous administration of a specific V1-vasopressinergic antagonist augmented the hypotensive response to hemorrhage; however, neither V1- nor V2-blockade affected hemorrhage-induced augmentation of the BRR. Inducement of hypotension by infusion of nitroprusside did not alter subsequent BRR sensitivity. Finally, nonhypotensive hemorrhage was associated with an increase in resting HR and augmented BRR sensitivity. However, in contrast to hypotensive hemorrhage, either V1- or V2-antagonism attenuated the increase in BRR sensitivity seen with 10% hemorrhage. These data suggest that, although AVP may play a role in blood pressure maintenance via its direct vasoconstrictor actions during hypotensive hemorrhage, the observed augmentation of BRR sensitivity associated with severe blood loss is not attributable to a vasopressinergic mechanism activated by circulating AVP. However, blood-borne AVP may contribute to BRR sensitivity alterations in response to mild blood loss.

The role of pacing for the management of neurally mediated syncope: Carotid sinus syndrome and vasovagal syncope

1994 ◽  
Vol 127 (4) ◽  
pp. 1030-1037 ◽  
Author(s):  
James D. Maloney ◽  
Fredrick J. Jaeger ◽  
Carlos Rizo-Patron ◽  
Dennis W.X. Zhu
Keyword(s):  
Carotid Sinus ◽  
Vasovagal Syncope ◽  
Carotid Sinus Syndrome ◽  
Neurally Mediated Syncope

scholarly journals Additive effects of heating and exercise on baroreflex control of heart rate in healthy males

2017 ◽  
Vol 123 (6) ◽  
pp. 1555-1562 ◽  
Author(s):  
Tiago Peçanha ◽  
Cláudia L. M. Forjaz ◽  
David. A. Low
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Baroreflex Sensitivity ◽  
Whole Body ◽  
Additive Effects ◽  
Passive Heating ◽  
Baroreflex Control ◽  
Rr Intervals ◽  
Body Heat

This study assessed the additive effects of passive heating and exercise on cardiac baroreflex sensitivity (cBRS) and heart rate variability (HRV). Twelve healthy young men (25 ± 1 yr, 23.8 ± 0.5 kg/m2) randomly underwent two experimental sessions: heat stress (HS; whole body heat stress using a tube-lined suit to increase core temperature by ~1°C) and normothermia (NT). Each session was composed of a preintervention rest (REST1); HS or NT interventions; postintervention rest (REST2); and 14 min of cycling exercise [7 min at 40%HRreserve (EX1) and 7 min at 60%HRreserve (EX2)]. Heart rate and finger blood pressure were continuously recorded. cBRS was assessed using the sequence (cBRSSEQ) and transfer function (cBRSTF) methods. HRV was assessed using the indexes standard deviation of RR intervals (SDNN) and root mean square of successive RR intervals (RMSSD). cBRS and HRV were not different between sessions during EX1 and EX2 (i.e., matched heart rate conditions: EX1 = 116 ± 3 vs. 114 ± 3 and EX2 = 143 ± 4 vs. 142 ± 3 beats/min but different workloads: EX1 = 50 ± 9 vs. 114 ± 8 and EX2 = 106 ± 10 vs. 165 ± 8 W; for HS and NT, respectively; P < 0.01). However, when comparing EX1 of NT with EX2 of HS (i.e., matched workload conditions but with different heart rates), cBRS and HRV were significantly reduced in HS (cBRSSEQ = 1.6 ± 0.3 vs. 0.6 ± 0.1 ms/mmHg, P < 0.01; SDNN = 2.3 ± 0.1 vs. 1.3 ± 0.2 ms, P < 0.01). In conclusion, in conditions matched by HR, the addition of heat stress to exercise does not affect cBRS and HRV. Alternatively, in workload-matched conditions, the addition of heat to exercise results in reduced cBRS and HRV compared with exercise in normothermia. NEW & NOTEWORTHY The present study assessed cardiac baroreflex sensitivity during the combination of heat and exercise stresses. This is the first study to show that prior whole body passive heating reduces cardiac baroreflex sensitivity and autonomic modulation of heart rate during exercise. These findings contribute to the better understanding of the role of thermoregulation on cardiovascular regulation during exercise.

scholarly journals Nicotinamide attenuates streptozotocin-induced diabetes complications and increases survival rate in rats: role of autonomic nervous system

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Paula L. Cruz ◽  
Ivana C. Moraes-Silva ◽  
Amanda A. Ribeiro ◽  
Jacqueline F. Machi ◽  
Marcelo Dantas Tavares de Melo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Survival Rate ◽  
Baroreflex Sensitivity ◽  
Diabetes Complications ◽  
Body Weight Loss ◽  
Diabetic Rats ◽  
Male Wistar Rats ◽  
Streptozotocin Induced Diabetes

Abstract Background To evaluate the effect of nicotinamide prior to streptozotocin-induced (STZ) diabetes in baroreflex sensitivity and cardiovascular autonomic modulation, and its association with hemodynamics and metabolic parameters. Methods Methods: Male Wistar rats were divided into control (Cont) and STZ-induced diabetes (Diab). Half of the rats from each group received a single dose of nicotinamide (100 mg/Kg) before STZ injection (Cont+NicA and Diab+NicA). All groups were followed-up for 5 weeks. Results Body weight loss of more than 40% was observed in Diab throughout the period (Diab: 271.00 ± 12.74 g; Diab+NicA: 344.62 ± 17.82). Increased glycemia was seen in Diab rats (541.28 ± 18.68 mg/dl) while Diab+NicA group had a slight decrease (440.87 ± 20.96 mg/dl). However, insulin resistance was observed only in Diab. In relation to Cont, heart rate, mean blood pressure and diastolic function were reduced when compared to Diab, together with parasympathetic modulation and baroreflex sensitivity. All of these parameters were improved in Diab+NicA when compared to Diab. Improved baroreflex sensitivity and parasympathetic modulation were correlated with glycemia, insulin resistance, and body weight mass. Additionally, Diab+NicA group increased survival rate. Conclusions Results suggest that the association of nicotinamide in STZ-induced diabetic rats prevents most of the expected derangements mainly by preserving parasympathetic and baroreflex parameters.

scholarly journals Pregnancy impairs baroreflex control of heart rate in rats: role of insulin sensitivity

2010 ◽  
Vol 298 (2) ◽  
pp. R419-R426 ◽  
Author(s):  
Virginia L. Brooks ◽  
Julia M. Mulvaney ◽  
Afaf S. Azar ◽  
Ding Zhao ◽  
Robert K. Goldman
Keyword(s):  
Insulin Resistance ◽  
Heart Rate ◽  
Standard Deviation ◽  
Insulin Sensitivity ◽  
Baroreflex Sensitivity ◽  
Late Gestation ◽  
Baroreflex Control ◽  
Sequence Method ◽  
Method Analysis

Recent studies in rabbits suggest that insulin resistance and reduced brain insulin contribute to impaired baroreflex control of heart rate (HR) during pregnancy; however, the mechanisms are unknown. The rat model is ideal to investigate these mechanisms because much is known about rat brain baroreflex neurocircuitry and insulin receptor locations. However, it is unclear in rats whether pregnancy impairs the HR baroreflex or whether insulin resistance is involved. Therefore, this study tested the hypothesis that in rats pregnancy decreases HR baroreflex sensitivity (BRS) and that this decrease is related to concurrent decreases in insulin sensitivity (IS). BRS was quantified before, during, and after pregnancy using complementary methods: 1) spontaneous BRS (sBRS) derived from sequence method analysis of telemetric, continuous arterial pressure recordings; and 2) maximal BRS of complete sigmoidal baroreflex relationships. IS was measured (hyperinsulinemic euglycemic clamp) to determine whether BRS and IS change in parallel. sBRS was reduced at midgestation [pregnancy day 10 (P10)], returned to nonpregnant (NP) levels on P18, and fell again at late gestation (P20) (sBRS in ms/mmHg: NP, 1.66 ± 0.04; P10, 1.17 ± 0.11; P18, 1.55 ± 0.12; P20, 1.31 ± 0.05; n = 5; P < 0.05). Similar triphasic patterns were observed for both maximal BRS [in beats·min−1·mmHg−1: NP, 4.45 ± 0.52 ( n = 10); P11–12, 2.76 ± 0.11 ( n = 7); P17–18, 3.79 ± 0.14 ( n = 5); P19–20, 2.32 ± 0.40 ( n = 8); P < 0.0001] and previous and current measurements of IS (in mg glucose·kg−1·min−1: NP, 32 ± 2; P19–20, 15 ± 1; P < 0.0005). Furthermore, during pregnancy, the standard deviation (SD) of MAP increased, and the SD of HR decreased, indirectly suggesting baroreflex impairment. sBRS increased transiently during parturition, and sBRS, maximal BRS, and IS normalized 3–4 days postpartum. In conclusion, pregnancy decreases HR BRS in rats. The parallel temporal changes in BRS and IS suggest a mechanistic link.

Role of endogenous opioids in syncope induced by head-up tilt test and its relationship with isoproterenol-dependent and isoproterenol-independent neurally-mediated syncope

1998 ◽  
Vol 67 (3) ◽  
pp. 211-218 ◽  
Author(s):  
Matı́as Pérez-Paredes ◽  
Francisco Picó-Aracil ◽  
Teo Fuentes-Jiménez ◽  
José G Sánchez-Villanueva ◽  
Elena Expósito-Ordoñez ◽  
...  
Keyword(s):  
Endogenous Opioids ◽  
Tilt Test ◽  
Neurally Mediated Syncope ◽  
Head Up Tilt ◽  
Head Up Tilt Test

scholarly journals ACTH Infusion Impairs Baroreflex Sensitivity—Implications for Cardiovascular Hypoglycemia-Associated Autonomic Failure

2020 ◽  
Vol 105 (7) ◽  
pp. 2345-2353
Author(s):  
Janet H Leung ◽  
Omar F Bayomy ◽  
Istvan Bonyhay ◽  
Johanna Celli ◽  
Jeffrey White ◽  
...  
Keyword(s):  
Outcome Measures ◽  
Baroreflex Sensitivity ◽  
Autonomic Failure ◽  
Random Order ◽  
Double Blind ◽  
Clinical Research Center ◽  
Early Afternoon ◽  
Treatment Analysis ◽  
Placebo Infusion

Abstract Context Hypoglycemia attenuates cardiovascular homeostatic autonomic control. This attenuation, known as the cardiovascular component of hypoglycemia-associated autonomic failure (HAAF), is characterized most notably by decreased baroreflex sensitivity (BRS) that begins during hypoglycemia and persists until at least the next day, despite return to euglycemia. Understanding the mechanisms underlying this reduction in BRS is important because BRS attenuation is associated with increased morbidity and mortality. Objective The objective of this work is to investigate the role of the adrenocorticotropin (ACTH)-adrenal axis in decreasing BRS. We tested the hypothesis that infusion of ACTH 1–24 (cosyntropin), as compared to placebo, would acutely suppress BRS, and that this decrease in BRS would be present the next day. Design A double-blind, placebo-controlled, random-order, cross-over study was conducted. Setting This study took place in a clinical research center. Participants Participants included healthy men and women. Interventions Interventions included an intravenous infusion of cosyntropin (70 μg/hour for 2.5 hours in the morning and again in the early afternoon) vs normal saline placebo. Main Outcome Measures Outcome measures included BRS during and 16 hours after cosyntropin vs placebo infusions. Results Cosyntropin infusion attenuated BRS (mm Hg/ms) as compared to placebo (baseline 17.8 ± 1.38 vs 17.0 ± 2.07; during 14.4 ± 1.43 vs 17.3 ± 1.65; and next day 14.8 ± 1.42 vs 18.9 ± 2.04; P &lt; .05, time by treatment, analysis of variance). BRS was decreased during the final 30 minutes of the morning cosyntropin infusion as compared to baseline (P &lt; .01) and remained suppressed the next day (16 hours after afternoon infusion) (P &lt; .025). Placebo infusion did not significantly change BRS. Corrected QT interval was not affected. Conclusions ACTH attenuates BRS, raising the possibility that hypoglycemia-induced increases in ACTH may contribute to the cardiovascular component of HAAF.

Endogenous opiate modulation of baroreflexes in normotensive and hypertensive rats

1988 ◽  
Vol 255 (5) ◽  
pp. H987-H991 ◽  
Author(s):  
J. E. Szilagyi
Keyword(s):  
Blood Pressure ◽  
Renovascular Hypertension ◽  
Baroreflex Sensitivity ◽  
Baroreceptor Reflex ◽  
Hypertensive Rats ◽  
Endogenous Opiates ◽  
Endogenous Opiate ◽  
The Brain ◽  
Naloxone Treatment

It is evident that hypertension is associated with elevated endogenous opiates. This study was designed to examine the role of endogenous opiates in the development and/or maintenance of two-kidney renovascular hypertension and in baroreceptor reflex function in conscious hypertensive rats. Naloxone administration during the onset of hypertension significantly attenuated the rise in blood pressure. After one week, systolic blood pressure in naloxone-treated rats was 27 mmHg lower than in 0.9% NaCl-treated hypertensive rats. Acute naloxone infusions in chronic hypertensive animals also significantly lowered blood pressure (-10%) and heart rate (-26%). Baroreceptor function was significantly enhanced in both normotensive (+135%) and hypertensive (+207%) rats after administration of naloxone. Furthermore, naloxone treatment also caused the baroreflex response to shift from the higher reset state toward that seen in normotensive counterparts. The inability of naloxone methyl bromide to alter baroreflex sensitivity indicates that the site(s) of action of opiates resides in the brain. These data support a role for opiates in the development and/or maintenance of renovascular hypertension, which may be related to alterations in baroreceptor reflex function.

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