0 trigemino-vagal reflex

Reflexology is the most fruitful part of neurology. With the accumulation of data in this area and the establishment of new principles and laws, our knowledge about the functions of the brain deepens, starting with simple reflexes of the medullae spinalis (Marschal ) and ending with complex reflexes of the cerebral hemispheres (combined, inhibited reflexes).

The 2021 Carl Ludwig Lecture. Unsympathetic autonomic regulation in heart failure: patient-inspired insights

Defined as a structural or functional cardiac abnormality accompanied by symptoms, signs or biomarkers of altered ventricular pressures or volumes, heart failure also is a state of autonomic disequilibrium. A large body of evidence affirms that autonomic disturbances are intrinsic to heart failure; that basal or stimulated sympathetic nerve firing or neural norepinephrine (NE) release more often than not exceed homeostatic need, such that an initially adaptive adrenergic or vagal reflex response, becomes maladaptive; and, that the magnitude of such maladaptation predicts prognosis. This Ludwig lecture develops two theses: that the elucidation and judiciously targeted amelioration of maladaptive autonomic disturbances offers opportunities to complement contemporary guideline-based heart failure therapy; and, that serendipitous single-participant insights, acquired in the course of experimental protocols with entirely different intent, can generate novel insight, inform mechanisms, and launch entirely new research directions. I précis 6 elements of our current synthesis of the causes and consequences of maladaptive sympathetic disequilibrium in heart failure, shaped by patient-inspired epiphanies: arterial baroreceptor reflex modulation; excitation stimulated by increased cardiac filling pressure; paradoxical muscle sympathetic activation as a peripheral neurogenic constraint on exercise capacity; renal sympathetic restraint of natriuresis; co-existing sleep apnea; and, augmented chemoreceptor reflex sensitivity, then conclude by envisaging translational therapeutic opportunities.

Reflex sympatho-vagal coactivation and concealed QTc prolongation: Lessons from hERG-blockers and long QT syndromes type 1 and type 2

Background and Purposes: Several hERG blocking molecules known for their propensity in triggering Torsades de Pointes (TdP) were reported as increasing High Frequency QT oscillations (HFQT). This effect was found as reflecting a sympatho-vagal coactivation. The present work aims to characterise the mechanism(s) leading to this particular state of the autonomic nervous system. Experimental approach: Effects of 20 hERG blockers including 15 torsadogenic molecules were assessed by telemetry in beagle dogs. Electrocardiogram and stroke volume modelled from the pulse contour method were analysed at the first dose level causing either QTc prolongation and/or HFQT increase. Cardiac autonomic control was analysed using the High Frequency Autonomic Modulation (HFAM) model in dogs and in untreated genotyped LQT1 and LQT2 individuals, for comparison. Key results: The sympatho-vagal coactivation induced by torsadogenic molecules is elicited by reflex compensatory mechanisms in response to changes in stroke volume or cardiac output related to hemodynamic off-targets and/or QT prolongation. QTc prolongation was concealed or markedly blunted by the sympathetic component activation in a large proportion of tested torsadogenic drugs. Sympathetic reflex mechanisms in LQT patients similar to that found for dofetilide was also revealed in both patients exhibiting QTc prolongation and concealed QTc prolongation, irrespective to LQT type. Conclusions and implications: QTc prolongation and/or drug-induced hemodynamic side effects enhance beat to beat ventricular repolarisation variability via sympatho-vagal reflex compensatory mechanisms. Considering the sympathetic reflex component via analysis of HFQT oscillations dramatically improves prediction, sensitivity and specificity of drug induced Torsades de pointes risk assessment.

Evaluación endometrial vía histeroscopia en pacientes con cáncer de mama – receptores hormonales positivos, tratadas con hormonoterapia

Objective: To know via hysteroscopy the endometrial pathology associated with the use of hormone therapy in patients with breast cancer. Methods: Research design: non-experimental, longitudinal, trend; based on patients who come randomly, from January to July 2014, to the consultation of Los Andes University Hospital. Results: The mean age of the patients was 55.3 years, mean time of menopause 8.03 years; 8 (26.6%) patients had associated chronic arterial hypertension and diabetes mellitus II, and 10% of the patients had arterial hypertension. The most common endometrial alterations were: 46.7 % endometrial polyps, 13.3 % simple hyperplasia without atypia, 6.6 % leiomyomas. Among 5 (16.6%) users of exemestane (all with normal ultrasound), 3 (10%) had endometrial polyps and 2 (6.7%) negative biopsies. Among the 23 (76.7%) patients taking tamoxifen, 9 (30%) had thickened endometrium, 12 (40%) normal ultrasound and 2 (6.7%) other findings; 10 (33.3 %) had polyps (6 with normal ultrasound and 4 with endometrial thickening) and 3 endometrial hyperplasia (all with thickened endometrium). Two patients receiving both treatments, one had hyperplasia and one had polyps (both with thickened endometrium). The population studies in 60% were luminal B breast cancer; 1 (3.3 %) patient had a vagal reflex as a complication of the procedure. Conclusion: Histeroscopic findings most often diagnosed were endometrial polyps, simple hyperplasia without atypia and submucosal myomas. Keywords: Hysteroscopy, endometrium, tamoxifen, cancer, breast.

Immunity and the carotid body: implications for metabolic diseases

Neuro-immune communication has gained enormous interest in recent years due to increasing knowledge of the way in which the brain coordinates functional alterations in inflammatory and autoimmune responses, and the mechanisms of neuron-immune cell interactions in the context of metabolic diseases such as obesity and type 2 diabetes. In this review, we will explain how this relationship between the nervous and immune system impacts the pro- and anti-inflammatory pathways with specific reference to the hypothalamus-pituitary-adrenal gland axis and the vagal reflex and will explore the possible involvement of the carotid body (CB) in the neural control of inflammation. We will also highlight the mechanisms of vagal anti-inflammatory reflex control of immunity and metabolism, and the consequences of functional disarrangement of this reflex in settlement and development of metabolic diseases, with special attention to obesity and type 2 diabetes. Additionally, the role of CB in the interplay between metabolism and immune responses will be discussed, with specific reference to the different stimuli that promote CB activation and the balance between sympathetic and parasympathetic in this context. In doing so, we clarify the multivarious neuronal reflexes that coordinate tissue-specific responses (gut, pancreas, adipose tissue and liver) critical to metabolic control, and metabolic disease settlement and development. In the final section, we will summarize how electrical modulation of the carotid sinus nerve may be utilized to adjust these reflex responses and thus control inflammation and metabolic diseases, envisioning new therapeutics horizons.

Bradycardia during laparoscopic surgeries: A cross-sectional study

Background: Bradycardia occurring during laparoscopic surgery potentially leads to cardiac arrest and adverse outcomes. Apart from the vagal reflex for its genesis, the knowledge on frequency and risk factors is limited. Objectives: To identify the bradycardia frequency and time points for its occurrence during laparoscopic surgeries. Methodology: In this hospital-based cross-sectional study, anaesthesia-related incident reports on bradycardia were collected from January to December 2019. Bradycardias (heart rate less than 60/minute) that occurred during laparoscopic surgeries were analyzed to characterize patient factors, the time point for occurrence, circumstantial events, management strategies, and outcomes. Results: Among 801 laparoscopic surgeries, 28 (3.4%) bradycardic incidents were identified, with one progressing to cardiac arrest. All bradycardias occurred in 26 patients undergoing laparoscopic cholecystectomy under general anaesthesia, with two patients each experiencing two bradycardic episodes. The mean patient age was 45 (±16.3) years and 17 (65.3%) were women. Fifteen (57.6%) patients had no co-morbidity. Controlled hypertension and hypothyroidism co-existed in seven (26.9%) and three (11.5%) cases respectively. Bradycardia occurred once each (3.5%) during laryngoscopy and endotracheal intubation. Six (21.4%) and twenty (71.4%) bradycardias respectively occurred before and during pneumoperitoneum. The mean of minimum heart rates was 43 (±8.8) per minute. Anticholinergics were administered in 25 (89.2%) incidents. Stopping surgery and pneumoperitoneum deflation included other major management strategies. The cardiac arrest case received chest compressions and adrenaline. Surgery resumed in all cases without adversity. Conclusion: Bradycardia occurs during laparoscopic surgery, more frequently during pneumoperitoneum and in healthy and younger females. Immediate cessation of surgical stimuli and atropine administration possibly prevent bradycardia from progressing to cardiac arrest.