Bezold-Jarisch Reflex Research Articles

A Heart Stopping Case of the Bezold-Jarisch Reflex.

The Bezold-Jarisch reflex is a parasympathetic reflex induced by intense mechanical stimulation of the ventricular myocytes. Exceptionally, cases have been described in patients receiving dobutamine infusion during a stress echocardiography. All were healthy middle-aged women and recovered without sequelae. A healthy 60-year-old woman suffered two 5.9-second episodes of asystole during her 20 mcg/kg/min infusion of dobutamine. Recovery was quick and without sequelae. Echocardiography and coronary angiography were both normal. In conclusion, this is the fourth documented case of a severe Bezold-Jarisch reflex causing asystole during dobutamine infusion. Diagnosis can only be made after excluding all other possible diagnoses, most importantly ischemia. This serves as a reminder of the importance of close monitoring during dobutamine infusion.

Effect of ondansetron on prevention of post-induction hypotension in elderly patients undergoing general anesthesia: A randomized, double-blind placebo-controlled clinical trial.

Background:Elderly patients are susceptible to post-induction hypotension. Volume loading and vasopressors for prevention of hypotension in elderly patients may increase perioperative cardiovascular risks. Ondansetron by blocking Bezold–Jarisch reflex (BJR) through inhibition of serotonin receptors has been effective in the prevention of post-spinal hypotension, and bradycardia. Bradycardia frequently accompanies post-induction hypotension in elderly patients, which signifies a possible preventing role for ondansetron. No previous study has evaluated the prophylactic effects of ondansetron for the prevention of post-induction hypotension.Materials and Methods:In this randomized placebo-controlled clinical trial, ondansetron 4 mg was given intravenously to 65 elderly patients, 20 min before induction of general anesthesia, and the rate of post-induction hypotension defined as 25% or more reduction in mean arterial blood pressure, compared with a placebo groups.Results:A total of 114 patients completed the study (58 in ondansetron and 56 in the placebo group). Proportions of post-induction hypotension were 9 (16%) and 25 (45%) in ondansetron and placebo groups, respectively, (P = 0.001). Forty-five patients (40%) developed bradycardia. Rates of bradycardia were not significantly different between two groups.Conclusions:The results of this study show the effectiveness of intravenous ondansetron for prevention of post-induction hypotension in elderly patients. The mechanism of this effect largely is unknown. Role of ondansetron for prevention of post-induction hypotension may not fully understandable by its interaction with BJR, as has been shown in post-spinal hypotension.

Role of sympathetic nerve activity in the process of fainting.

Syncope is defined as a transient loss of consciousness and postural tone, characterized by rapid onset, short duration, and spontaneous recovery, and the process of syncope progression is here described with two types of sympathetic change. Simultaneous recordings of microneurographically-recorded muscle sympathetic nerve activity (MSNA) and continuous and noninvasive blood pressure measurement has disclosed what is going on during the course of syncope progression. For vasovagal or neurally mediated syncope, three stages are identified in the course of syncope onset, oscillation, imbalance, and catastrophe phases. Vasovagal syncope is characterized by sympathoexcitation, followed by vagal overcoming via the Bezold-Jarisch reflex. Orthostatic syncope is caused by response failure or a lack of sympathetic nerve activity to the orthostatic challenge, followed by fluid shift and subsequent low cerebral perfusion. Four causes are considered for the compensatory failure that triggers orthostatic syncope: hypovolemia, increased pooling in the lower body, failure to activate sympathetic activity, and failure of vasoconstriction against sympathetic vasoconstrictive stimulation. Many pathophysiological conditions have been described from the perspectives of (1) exaggerated sympathoexcitation and (2) failure to activate the sympathetic nerve. We conclude that the sympathetic nervous system can control cardiovascular function, and its failure results in syncope; however, responses of the system obtained by microneurographically-recorded MSNA would determine the pathophysiology of the onset and progression of syncope, explaining the treatment effect that could be achieved by the analysis of this mechanism.

No intention to cheat: Coping with unintentional Anti-Doping Rule Violations

Anabolic-androgenic steroids are misused, including women, but little is known about the cardiovascular effects of these drugs on females.Evaluated the effects of nandrolone decanoate (ND), physical exercise and estrogen deficiency on female rats.Female Wistar rats were divided into 8 groups: S and OVX: (SHAM: sham surgery; OVX: ovariectomy, vehicle), SE and OVXE (resistance exercise 5 times a week, vehicle), SD and OVXD (treated with ND, 20 mg/kg/week for 4 weeks); SDE and OVXDE. Treatments were initiated 21 days after surgery. The Bezold–Jarisch reflex was assessed by Phenylbiguanide administration. The right atrium, kidney, and serum were collected for molecular analyses by RT-PCR of atrial natriuretic peptide (ANP), A-type natriuretic peptide receptor (NPR-A) and NPR-C. ELISA assay to estradiol and testosterone concentrations. The gastrocnemius muscle, heart and kidney weights/tibia length were measured. Morphometric analysis of heart was made (H/E) and collagen content of heart and kidney were evaluated using Pirossirius Red.ND treatment increased ANP expression on atrium and decreased NPR-A expression in kidney. Physical exercise and ovariectomy did not alter this parameter. NPR-C level was reduced in the SDE and OVXDE. Renal and cardiac hypertrophy was observed after ND treatment, with collagen deposition. Plasma estrogen concentrations were reduced and serum testosterone concentrations were increased after ND treatment.ANP has an important role in modulating the cardiovascular effects of ND in females. This modulating may have occurred by the increasing ANP expression, reducing NPR-A and NPR-C expression levels, and changing sex hormone levels.

The discovery of diazepinone-based 5-HT3 receptor partial agonists

Serotonin type 3 (5-HT3) receptor partial agonists have been targeted as potential new drugs for the symptomatic relief of irritable bowel syndrome (IBS). Multiple diazepinone-based compounds have been discovered, which exhibit nanomolar binding affinity for the h5-HT3A receptor and display a range of intrinsic activities (IA=7–87% of 5-HT Emax) in HEK cells heterologously expressing the h5-HT3A receptor. Favorable physicochemical properties and in vitro ADME profile coupled with oral activity in the murine von Bezold–Jarisch reflex model demonstrates the series has promise for producing low to moderate IA partial agonists suitable for an IBS indication.

Triphasic cardiovascular response to cannabinoids – Focus on underlying mechanisms

The endocannabinoid anandamide exerts complex effects on the cardiovascular system [Malinowska et al., Br J Pharmacol, 2011]. Thus, rapid intravenous injection of anandamide and its stable analogue methanandamide in anaesthetized rats and mice induces typical triphasic changes. Phase I, the so-called BezoldJarisch reflex, is characterized by a rapid bradycardia and hypotension associated with a decrease in cardiac contractility and an increase in total peripheral resistance. Phase II is a brief pressor response associated with an increase in cardiac contractility and blood flow in the mesenteric and renal arteries. Phase III comprises a prolonged (lasting up to 10 min) and marked decrease in blood pressure, mesenteric and renal blood flow, a marked decrease in cardiac contractility and a slight decrease in heart rate and total peripheral resistance. Phase I is mediated via vanilloid TRPV1 receptors since it was induced also by the TRPV1 receptor agonist capsaicin (but not by the CB1 receptor agonist CP55940), blocked by the TRPV1 receptor antagonists capsazepine and ruthenium red (but not by the CB1 receptor antagonist rimonabant) and absent in TRPV1 / mice. Phase II consists of a peripheral component that is most probably located in blood vessels, is sensitive to nifedipine, ruthenium red and pentobarbitone and, hence, probably represents a Ca-dependent mode of action and a central component. The paraventricular nucleus of the hypothalamus (PVN) may contribute to the latter since a pressor effect was obtained after injection of anandamide, methanandamide or CP55940 (intraventricularly or directly into the PVN). This effect only occurred when the peripheral CB1 receptors were blocked by administration of CB1 receptor antagonists, including AM6545 that does not reach the brain. It was sensitive to adrenalectomy and counteracted by antagonists of CB1, NMDA, thromboxane A2 and b2adrenergic receptors [AM251 (directly into the PVN), MK-801, SQ29548 and ICI118551, respectively] suggesting that the latter four receptors are involved in the events ultimately leading to the anandamide-induced adrenal secretion of catecholamines. Importantly, the hypotensive effect of intravenously administered CP55940 was reversed into a hypertensive one in the presence of AM6545 and both responses were abolished by chemical lesion of the PVN by kainic acid. Phase III is mediated mainly by presynaptic inhibitory CB1 receptors located on the postganglionic (although a preganglionic localization cannot be excluded) sympathetic nerve endings innervating resistance vessels and heart. The CB1 receptor antagonist-sensitive inhibitory effect of these receptors was detected after electrical stimulation of the preganglionic sympathetic nerve fibres in pithed rabbits or rats or following injection of nicotine but not phenylephrine/noradrenaline or isoprenaline (increasing blood pressure and heart rate, respectively). The prolonged hypotension might also be related to the activation of CB1 and/or vanilloid TRPV1 receptors in the spinal cord or to a direct vasodilatation via O-1918 sensitive receptors. In conscious rats anandamide and methanandamide induced a brief pressor (phase II) response connected with renal and mesenteric vasoconstriction and hindquarters vasodilatation. In addition, higher doses of anandamide elicited an initial bradycardia, hypotension and hindquarters vasoconstriction (phase I). However, unlike in anaesthetized rats, none of the cannabinoids led to a prolonged hypotension (phase III). Cardiovascular effects of anandamide are changed under pathophysiological conditions. Thus, in anaesthetized rats myocardial ischemia enhanced phase I and reduced phase III whereas hypertension enhanced phase III. Acknowledgement: B.M. and E.S. would like to express their gratitude to Professor Manfred Gothert for his continuous encouragement extending over a time period of decades.

Near fatal bradycardia during cesarean section under spinal anesthesia: "High spinal" may not be only risk factor.

Sir, Bradycardia during cesarean section under spinal anesthesia is not uncommon and usually associated with a high sympathetic block. We are reporting a case of severe near fatal bradycardia in 31-year-old parturient undergoing cesarean section under spinal anesthesia without a “high spinal” block. A 31-year-old parturient, weighing 67 kg and height 164 cm, third gravida at 38 completed week pregnancy, was posted for an elective cesarean section for a history of previous two cesarean section and breech presentation in this pregnancy. She did not have any comorbid illness and all the preoperative investigations were within the normal limit. Preoperative blood pressure was 134/86 mm Hg and pulse rate was 86 beats per minute (bpm). In the operating room spinal anesthesia was administered in left lateral posture in L3-L4 intervertebral space by a 25G Qunicke's spinal needle. 10 mg 0.5% hyperbaric bupivacaine and 15 mcg fentanyl was used for spinal anesthesia. 500 ml of Ringer's Lactate was infused during spinal anesthesia. After 5 min of spinal anesthesia, when a T8 height of sensory block was achieved, surgery was started. No significant drop in the blood pressure was note after spinal anesthesia. Ten minutes later, a healthy male baby was delivered uneventfully. Soon after baby delivery, when the obstetrician was massaging the uterus and giving traction to the umbilical cord to take out the placenta, we noticed a sudden severe bradycardia, heart rate dropped to 29 bpm from 68 bpm and the patient complained of nausea. Immediately, we asked the surgeon to stop manipulation and 0.6 mg atropine was given intravenously. She also received 100% oxygen through anesthesia circuit. Sooner, heart rate came to 85 bpm and the patient was fully awake. We checked the height of sensory block again then, and found to be T6. Obstetrician then delivered the placenta; again drop of heart rate from 90 to 65 bpm was noted during this procedure. However, again it came up to 90 bpm without any intervention. Rest of the surgery was uneventful and no episode of bradycardia or hypotension was noted throughout the surgery. Reported incidence of bradycardia during cesarean section under spinal anesthesia is 2.5%.[1] It is classically associated with a “high spinal block”;[2] a sensory block height more than T4 has been described as a risk factor.[1] Cardiac arrest has been reported during cesarean section under spinal anesthesia at the time of placental expulsion.[3] Manipulations of the abdominal viscera, peritoneum or traction of the visceral ligaments during abdominal surgeries can cause a severe bradycardia and hypotension.[4] Bradycardia during surgery under spinal anesthesia is due to a reflex cardiovascular depression mostly due to a decrease in the venous return, known as Bezold-Jarisch reflex or neurocardiogenic syncope.[5] Prompt intervention is the key to the success of management of bradycardia and maternal mortality can be prevented. We treated bradycardia by intravenous atropine as per current advanced cardiovascular life support protocol and it was successful.[6] To best of our knowledge, bradycardia from uterine massage at the time of cesarean section has not been reported until now. Anesthesiologists caring pregnant women must remember that severe bradycardia may occur even without a “high spinal” and timely intervention is the only key to maternal safety.

Animal studies on the mechanisms and radiofrequency catheter ablation of the syncope with vasovaga1 syncope -radiofrequency ablation of cardiac nerve attenuates bezold-jarisch reflex in canine

Background: The Bezold–Jarisch Reflex (BJR) is one of the main causes for Vasovaga1 Syncope (VVS). Blocking the efferent pathways of the vagus ganglia in the heart may attenuate the BJR. Objective: To observe the influence of radiofrequency catheter ablation of the interventricular sulcus fat and endocardial nerve potential on Bezold-Jarisch Reflex (BJR) induced by veratridine in canine. Methods: Six mongrel dogs were anesthetized and their chest were opened through a right thoracotomy to expose the Interventricular sulcus fat. Veratridine was injected into the left ventricle at bolus doses of 15 ug/kg through a catheter to induce BJR. The Sinus Cycle Length (SCL), Systolic Arterial Pressure (SAR), Diastolic Arterial Pressure (DAP), Mean Arterial Pressure (MAP), Left Ventricle Systolic Pressure (LVSP), Left Ventricle Diastolic Pressure (LVDP) and Mean Left Ventricle Pressure (MLVP) were measured under the baseline and after ablation of fat pad; the changes of the above parameters (ΔSCL, ΔSAP, ΔDAP, ΔMAP, ΔLVSP, ΔLVDP and ΔMLVP) were calculated. Then the same dose of veratridine was injected under mapping along the mitral annulus, and potential nerve ablation and the changes of the above parameters were observed. Results: BJR was successfully induced in the 6 animals; the animals has prolonged Sinus Cycle Length (SCL) and decreased MAP and MLVP. After ablation, the prolongation of SCL after injection of veratridine was markedly reduced [229.2±92.3] ms vs [39.3±14.1] ms, p< 0.01.All the pressures were decreased after injection of veratridine, with significant decrease found only for DAP and MAP both p< 0.05. Conclusion: Ablation of the interventricular sulcus fat and endocardial nerve potential fat can effectively attenuate the decrement of heart rate and the decrement of DAP and MAP during the BJR induced by veratridine, which provides a basis for the treatment of VVS.

Dopamine‐induced bradycardia in two dogs under isoflurane anaesthesia

Dopamine is a commonly used positive inotropic agent for the treatment of hypotension in small animals. Two dogs that had undergone surgery, under isoflurane anaesthesia, developed a sudden and profound bradycardia when a dopamine infusion was administered. Bradycardia was attributed to the activation of the Bezold-Jarisch reflex, an inhibitory reflex, characterised by bradycardia and hypotension.

Bezold-Jarish reflex and cardiac arrest under spinal anaesthesia

Background: Cardiac arrests during spinal anaesthesia (SA) are described as “very rare”, but are actually relatively common. 1 Hemodynamic instability is expected with the onset of the block, but delayed bradycardia or asystole may be more sinister. 2 The Bezold-Jarisch reflex (BJR) includes the triad of bradycardia, hypotension and peripheral vasodilation triggered by cardiac mechanoreceptor activation. 2 We report a successful intraoperative resuscitation during SA. Case report: Male patient, 75 years old, 90Kg, ASA II, with hypertension (medicated with ACEI) and a sinus bradycardia of 57 bpm was admit ted for suprapubic prostatectomy. No other medical or surgical history. A SA was performed using hyperbaric bupivacaine 8 mg plus sufentanil 2mcg. At the incision a T6 sensitive block level was documented and developed hypotension (MAP 60mmHg. Blood loss was minimal and until the time of cardiac arrest the patient had received 1L of ringer lactate solution. Af ter surgery he was transferred to the ICU, heart disease was excluded and was discharged 1 week later af ter a iatrogenic pneumothorax. Discussion: During SA the cardiac vagal tone is enhanced and the ef fect on venous return can be profound.1 The BJR can be triggered by reduced venous return.2 Strong resting vagal tone (bradycardia) and dermatomal block to T5/6 or higher, increases the risk of cardiac arrest during SA.1,2 Volume loading is critical in maintaining adequate preload to decrease the risk of severe bradycardia and cardiac arrest. Inadequate volume loading was most probably the culprit. Early administration of a powerful alpha-adrenergic agonist to increase venous return and improve cardiac output, as recommended by Caplan et al2 was performed.

Astrocyte damage but not microglial infiltration in the nucleus tractus solitarii attenuates cardiovascular reflexes

Nucleus tractus solitarii (NTS) injections of saporin (SAP) conjugates that kill neurokinin‐1 receptor (NK1R) or tyrosine hydroxylase (TH)/dopamine‐β‐hydroxylase (DBH) neurons attenuate baroreflexes, lead to loss of NTS astrocytes with glial fibrillary acidic protein (GFAP), and lead to increased microglial staining with OX42. We sought to determine if SAP alone altered cardiovascular reflexes due to loss of astrocytes, loss of neurons or proliferation of microglia. NTS injection of SAP led to loss of GFAP as well as connexin 43 (CX43) immunofluorescent labeling but did not affect neuronal markers NMDAR1 (NMDA receptor subunit 1), GluR2 (AMPA receptor subunit 2), neuronal nitric oxide synthase (nNOS), TH, DBH, vesicular glutamate transporter 2 (VGluT2), NK1R, and protein gene product 9.5 (PGP 9.5). In contrast, SAP led to increased OX42. Bilateral NTS injections of SAP decreased baroreflex, chemoreflex, and von Bezold Jarisch reflex responses. Decreases in baroreflex responses seen in rats treated with SAP were comparable to responses when SAP conjugates targeted TH/DBH neurons or NK1R neurons. Baroreflexes were unaffected by 6‐hydroxydopamine (6‐OHDA), which did not reduce GFAP staining, but did increase OX42. Thus, full cardiovascular reflex expression relies on intact NTS astrocytes. Reflex changes after SAP are independent of microglial proliferation. Support: NIH R01 HL088090 and VA Merit Review.

Hypotension and ischaemic stroke associated with aliskiren in the ALTITUDE trial: Sensitisation of the Bezold–Jarisch reflex?

Hypotension and syncopal attacks have been reported in association with drugs which block the renin-angiotensin-aldosterone system (RAAS). It has been proposed that the underlying mechanism is due to sensitisation of the Bezold-Jarisch reflex leading to withdrawal of sympathetic tone, profound and prolonged bradycardia, and hypotension. Sensitisation of this reflex occurs in the presence of blockade of the RAAS. In the ALTITUDE trial the use of the direct renin inhibitor, aliskiren, was associated with hypotensive episodes and an excess of ischaemic stroke. It is hypothesised that this is best explained by activation of the Bezold-Jarisch reflex, which may be particularly important in circumstances where there is dual blockade of the RAAS.

A cardiovascular collapse occurred in the beach chair position for shoulder arthroscopy under general anesthesia -A case report-

The occurrence of severe hypotension and bradycardia, following placing to the beach chair position from supine during general anesthesia for repair of tendon injury of the rotator cuff of shoulder in a healthy 50 year-old man was described. The Bezold-Jarisch reflex, which is known to inhibit cardiovascular reflex and composed of three kinds of symptoms such as vasodilation, bradycardia and hypotension, has been reported mainly in peripheral nerve block, and may occur during orthostasis, hypovolemia, hemorrhage, supine inferior vena cava compression in pregnancy, interscalene block for shoulder surgery in the sitting position and so on. The bradycardia and hypotension can be more aggravated when causative elements overlaps each other. Anticholinergics and vasopressor were injected intravenously, and position of the patient was changed to the supine position immediately resulting in a normal vital signs dramatically.

Nandrolone decanoate determines cardiac remodelling and injury by an imbalance in cardiac inflammatory cytokines and ACE activity, blunting of the Bezold–Jarisch reflex, resulting in the development of hypertension

The aims of this study were to evaluate the effects of nandrolone (ND) on cardiac inflammatory cytokines, ACE activity, troponin I, and the sensitivity of the Bezold–Jarisch reflex (BJR). Male Wistar rats were administered either ND (20mg/kg; DECA) or vehicle (control animals; CONT) for 4weeks. BJR was analyzed by measuring the bradycardia and hypotension responses elicited by serotonin administration (2–32μg/kg). Mean arterial pressure (MAP) was assessed and myocyte hypertrophy was determined by the heart weight/body weight ratio and by morphometric analysis. Matrix collagen deposition was assessed by histological analysis of the picrosirius red-stained samples. Mesenteric vascular reactivity was performed and central venous pressure (CVP) evaluated. Cardiac inflammatory cytokine levels and angiotensin-converting enzyme (ACE) activity were studied as well the biomarker of cardiac lesion, troponin I. DECA group showed enhancement of matrix type I collagen deposition (p<0.01) and cardiac ACE activity (p<0.01) compared with the CONT. Interleukin (IL)-10 was reduced (p<0.01) and pro-inflammatory cytokines (TNF-α and IL-6; p<0.01) were increased in the DECA group compared with CONT. Cardiac injury was observed in the DECA group shown by the reduction in cardiac troponin I (p<0.01) compared with the CONT group. Animals in the DECA group also developed myocyte hypertrophy and reduction of BJR sensitivity. The MAP of animals treated with ND reached hypertensive levels (p<0.01; compared with CONT). No changes in CVP and vascular reactivity were observed in both experimental groups. We conclude that high doses of ND elicit cardiotoxic effects with cardiac remodelling and injury. Cardiac changes reduce the BJR sensitivity. Together, these abnormalities contributed to the development of hypertension in animals in the DECA group.

The treatment with pyridostigmine improves the cardiocirculatory function in rats with chronic heart failure

Sympathetic hyperactivity and its outcome in heart failure have been thoroughly investigated to determine the focus of pharmacologic approaches targeting the sympathetic nervous system in the treatment of this pathophysiological condition. On the other hand, therapeutic approaches aiming to protect the reduced cardiac parasympathetic function have not received much attention. The present study evaluated rats with chronic heart failure (six to seven weeks after coronary artery ligation) and the effects of an increased parasympathetic function by pyridostigmine (an acetylcholinesterase inhibitor) on the following aspects: arterial pressure (AP), heart rate (HR), baroreceptor and Bezold-Jarisch reflex, pulse interval (PI) and AP variability, cardiac sympathetic and parasympathetic tonus, intrinsic heart rate (i-HR) and cardiac function. Conscious rats with heart failure exhibited no change in HR, Bezold-Jarisch reflex, PI variability and cardiac sympathetic tonus. On the other hand, these animals presented hypotension and reduced baroreflex sensitivity, power in the low frequency (LF) band of the systolic AP spectrum, cardiac parasympathetic tonus and i-HR, while anesthetized rats exhibited reduced cardiac performance. Pyridostigmine prevented the attenuation of all the parameters examined, except basal AP and cardiac performance. In conclusion, the blockade of acetylcholinesterase with pyridostigmine was revealed to be an important pharmacological approach, which could be used to increase parasympathetic function and to improve a number of cardiocirculatory parameters in rats with heart failure.

Reflejos cardiopulmonares. Implicación en anestesiología

The baroreflex, chemoreflex, pulmonary reflexes, Bezold-Jarisch and Bainbridge reflexes and their interaction with local mechanisms, are a demonstration of the richness of cardiovascular responses that occur in human beings. As well as these, the anesthesiologist must contend with other variables that interact by attenuating or accentuating cardiopulmonary reflexes such as, anesthetic drugs, surgical manipulation, and patient positioning. In the present article we review these reflexes and their clinical relevance in anesthesiology.

85 INSIGHTS INTO VAGAL GANGLIONIC SYNAPTIC INTEGRATION FROM THE VON BEZOLD-JARISCH REFLEX

Background: The von Bezold-Jarisch reflex (vBJR) elicits a vagally-mediated, cardioprotective bradycardia, which is attenuated in hypertensive models1. The cardiac ganglia gate vagal drive and impaired ganglionic signal transmission is also found in hypertensive models2. We therefore extended our recent intracellular study of cardiac vagal ganglion neurone (CVN) responses to cardiorespiratory reflexes3 to include the vBJR. Methods: Intracellular recordings were made from CVNs in the working heart-brainstem preparation of Wistar rats (P18-25, n = 6). They were classified as tonic or phasic based on their firing responses. We compared their response to vBJR activation using phenylbiguanide (PBG, 200/ug i.a.) with baro-, chemo- and diving reflex responses. Results: PBG produced robust bradycardias (-98 ± 29bpm). Tonic cell (n = 4) EPSP and spike rates were increased by activation of all reflexes indicating convergence through a single population of CVNs. Strikingly, the increase in EPSP/spike frequency was ∼2.5x higher during the vBJR than the chemoreflex (16 ± 10 vs 7 ± 4 Hz, n = 4), despite similar bradycardias (-98 ± 29 vs -98 ± 35bpm). PBG-responses depended on intact brainstem function, and no evidence of direct depolarisation or activation of local cardiac ganglionic circuits was found. PBG never excited phasic cells (putative interneurones, n = 10). Conclusions: vBJR activation excites a common pool of vagal postganglionic neurones shared with the other cardiorespiratory reflexes. The relatively augmented excitation of CVNs by the vBJR means that the intrinsic integrative properties of the ganglion cells are important in determining the magnitude of end organ response and thus changes at the level of the ganglion may play a role in its depression in hypertension.

Corrigendum: Role of the renin–angiotensin system on the nandrolone-decanoate-induced attenuation of Bezold-Jarisch reflex

Corrigendum: Role of the renin–angiotensin system on the nandrolone-decanoate-induced attenuation of Bezold-Jarisch reflex

Bezold-Jarisch反射発現後に脊髄くも膜下麻酔を行い無脈性電気活動に至った1例

膀胱出血をしている患者に脊髄くも膜下麻酔を行ったところ，脊髄くも膜下麻酔施行中に心拍数と血圧が低下し，脊髄くも膜下腔へ薬液注入時に無脈性電気活動となった．臨床経過と術後の心拍変動解析から，脊髄くも膜下麻酔施行中の心拍数と血圧の低下の原因は循環血液量減少と交感神経過緊張を誘因とする迷走神経反射（Bezold-Jarisch反射）とわかった．Bezold-Jarisch反射が発現した状態で，脊髄くも膜下腔へ薬液を注入したため無脈性電気活動を生じたと考えた．循環血液量減少を伴う交感神経過緊張状態ではBezold-Jarisch反射に注意する必要がある．

Hypotensive bradycardic events during shoulder arthroscopic surgery under interscalene brachial plexus blocks

Sudden, profound hypotensive and bradycardic events (HBEs) have been reported in more than 20% of patients undergoing shoulder arthroscopy in the sitting position. Although HBEs may be associated with the adverse effects of interscalene brachial plexus block (ISBPB) in the sitting position, the underlying mechanisms responsible for HBEs during the course of shoulder surgery are not well understood. The basic mechanisms of HBEs may be associated with the underlying mechanisms responsible for vasovagal syncope, carotid sinus hypersensitivity or orthostatic syncope. In this review, we discussed the possible mechanisms of HBEs during shoulder arthroscopic surgery, in the sitting position, under ISBPB. In particular, we focused on the relationship between HBEs and various types of syncopal reactions, the relationship between HBEs and the Bezold-Jarisch reflex, and the new contributing factors for the occurrence of HBEs, such as stellate ganglion block or the intraoperative administration of intravenous fentanyl.