Sympathetic Nerve Stimulation Research Articles

Optogenetic Stimulation of Kidney Sympathetic Nerves as a New Protective Approach to AKI

Optogenetic Stimulation of Kidney Sympathetic Nerves as a New Protective Approach to AKI

Sympathetic structural and electrophysiological remodeling in a rabbit model of reperfused myocardial infarction.

Chondroitin sulfate proteoglycans (CSPGs) inhibit sympathetic reinnervation in rodent hearts post-myocardial infarction (MI), causing regional hypoinnervation that is associated with supersensitivity of β-adrenergic receptors and increased arrhythmia susceptibility. To investigate the role of CSPGs and hypoinnervation in the heart of larger mammals, we used a rabbit model of reperfused MI and tested electrophysiological responses to sympathetic nerve stimulation (SNS). Innervated hearts from MI and sham rabbits were optically mapped using voltage and Ca2+-sensitive dyes. SNS was performed with electrical stimulation of the spinal cord, and β-adrenergic responsiveness was tested using isoproterenol. Sympathetic nerve density and CSPG expression were evaluated using immunohistochemistry. CSPGs were robustly expressed in the infarct region of all MI hearts, and the presence of CSPGs was associated with reduced sympathetic nerve density in the infarct versus remote region. Action potential duration (APD) dispersion and tendency for induction of ventricular tachycardia/fibrillation (VT/VF) were increased with SNS in MI but not sham hearts. SNS decreased APD at 80% repolarization (APD80) in MI but not sham hearts, whereas isoproterenol decreased APD80 in both groups. Isoproterenol also shortened Ca2+ transient duration at 80% repolarization in both groups but to a greater extent in MI hearts. Our data suggest that sympathetic remodeling post-MI is similar between rodents and rabbits, with CSPGs associated with sympathetic hypoinnervation. Despite a reduction in sympathetic nerve density, the infarct region of MI hearts remained responsive to both physiological SNS and isoproterenol, potentially through preserved or elevated β-adrenergic responsiveness, which may underlie increased APD dispersion and tendency for VT/VF.NEW & NOTEWORTHY Here, we show that CSPGs are present in the infarcts of rabbit hearts with reperfused MI, where they are associated with reduced sympathetic nerve density. Despite hypoinnervation, sympathetic responsiveness is maintained or enhanced in MI rabbit hearts, which also demonstrate increased APD dispersion and tendency for arrhythmias following sympathetic modulation. Together, this study indicates that the mechanisms of sympathetic remodeling post-MI are similar between rodents and rabbits, with hypoinnervation likely associated with enhanced β-adrenergic sensitivity.

First, a seat; then, an upgrade.

The Sir Stanley Peart Essay Competition is an annual event run by the British and Irish Hypertension Society to encourage Early Career Researchers to continue the ethos of Sir Stanley Peart. Sir Stanley Peart was a clinician and clinical researcher who made a major contribution to our understanding of blood pressure regulation. He was the first to demonstrate the release of noradrenaline in response to sympathetic nerve stimulation. He was also the first to purify, and determine the structure of, angiotensin and he later isolated the enzyme, renin, and carried out many important investigations of the factors controlling its release in the body. This year, the essay topic was "Do we need new classes of antihypertensive drugs?". In his prize-winning essay, "First, a seat; then, an upgrade", Dr Sathyanarayanan argues that we do not need new classes of antihypertensive drugs, instead we should focus our attention on addressing the factors that lead to high blood pressure in the first place and use our existing drug classes more effectively.

The Effect of Prenatal Yoga on Emesis Gravidarum in the First Trimester Pregnant Women

Background: Increased levels of progesterone, estrogen, and HCG (chorionic gonadotropin hormone) during the first trimester of pregnancy can produce morning sickness, also known as emesis gravidarum (nausea and vomiting). To lessen the release of hormones that induce anxiety, severe nausea, and vomiting, prenatal yoga practitioners can block the stimulation of sympathetic nerves by practicing muscle relaxation. This study aims to ascertain how prenatal yoga affects first-trimester emesis gravidarum. Method: This study used a pre-experimental design with a pretest-posttest design in one group, involving 16 mothers who had emesis gravidarum at PMB Fatimah Bandung Rejosari, Sukun, Malang. Data collection was done using the questionnaire. Results: The result was that two prenatal yoga sessions over two weeks demonstrated significant benefits. Prenatal yoga affects emesis gravidarum in the first trimester of pregnancy, as indicated by the independent t-test technique (2-tailed) of 0.000 <0.005. Discussion: Steroid hormones can slow down stomach emptying, which causes emesis gravidarum. Excessive or low cortisol levels can be brought back to normal with yoga. Yoga offers numerous mental and physical health advantages. Conclusion We can conclude that the course of treatment impacts the severity of emesis gravidarum, or nausea and vomiting, during the first trimester of pregnancy.

Heart rate dynamics and asymmetry during sympathetic activity stimulation and post-stimulation recovery in ski mountaineers-a pilot exploratory study.

There is a lack of studies on non-linear heart rate (HR) variability in athletes. We aimed to assess the usefulness of short-term HR dynamics and asymmetry parameters to evaluate the neural modulation of cardiac activity based on non-stationary RR interval series by studying their changes during sympathetic nervous system activity stimulation (isometric handgrip test) and post-stimulation recovery in professional ski mountaineers. The correlation between the changes in the parameters and the respiratory rate (RespRate) and also the duration of the career was analyzed. Short-term (5 min) and ultra-short-term (1 min) rates of patterns with no variations (0V), number of acceleration runs of length 1 (AR1), and short-term Porta's Index were greater, whereas Guzik's Index (GI) was smaller during sympathetic stimulation compared to rest. GI increased and the number of AR1 decreased during recovery. Greater increases in GI and RMSSD were associated with greater decreases in RespRate during recovery. Greater increases in RespRate from rest to short-term sympathetic stimulation were associated with greater increases in 0V (Max-min method) and AR1 but also with greater decreases in decelerations of short-term variance and accelerations and decelerations of long-term variance. Greater increases in 0V (Max-min method) and number of AR1 during sympathetic stimulation were associated with a shorter career duration. Greater decreases in these parameters during recovery were associated with a longer career duration. Changes in measures of HR dynamics and asymmetry, calculated based on short-term non-stationary RRi time series induced by sympathetic stimulation and post-stimulation recovery, reflected sympathovagal shift and were associated with condition-related alterations in RespRate and career duration in athletes who practice ski mountaineering.

Regulation of nerve-evoked contractions of the murine vas deferens

Stimulation of sympathetic nerves in the vas deferens yields biphasic contractions consisting of a rapid transient component resulting from activation of P2X1 receptors by ATP and a secondary sustained component mediated by activation of α1-adrenoceptors by noradrenaline. Noradrenaline can also potentiate the ATP-dependent contractions of the vas deferens, but the mechanisms underlying this effect are unclear. The purpose of the present study was to investigate the mechanisms underlying potentiation of transient contractions of the vas deferens induced by activation of α1-adrenoceptors. Contractions of the mouse vas deferens were induced by electric field stimulation (EFS). Delivery of brief (1s duration) pulses (4 Hz) yielded transient contractions that were inhibited tetrodotoxin (100 nM) and guanethidine (10 µM). α,β-meATP (10 µM), a P2X1R desensitising agent, reduced the amplitude of these responses by 65% and prazosin (100 nM), an α1-adrenoceptor antagonist, decreased mean contraction amplitude by 69%. Stimulation of α1-adrenoceptors with phenylephrine (3 µM) enhanced EFS and ATP-induced contractions and these effects were mimicked by the phorbol ester PDBu (1 µM), which activates PKC. The PKC inhibitor GF109203X (1 µM) prevented the stimulatory effects of PDBu on ATP-induced contractions of the vas deferens but only reduced the stimulatory effects of phenylephrine by 40%. PDBu increased the amplitude of ATP-induced currents recorded from freshly isolated vas deferens myocytes and HEK-293 cells expressing human P2X1Rs by 93%. This study indicates that: (1) potentiation of ATP-evoked contractions of the mouse vas deferens by α1-adrenoceptor activation were not fully blocked by the PKC inhibitor GF109203X and (2) that the stimulatory effect of PKC on ATP-induced contractions of the vas deferens is associated with enhanced P2X1R currents in vas deferens myocytes.

Diet induced obesity alters the excitability of liver-related PVN neurons

Stimulation of hepatic sympathetic nerves increases glucose production and glycogenolysis. Activity of pre-sympathetic neurons in the paraventricular nucleus (PVN) of the hypothalamus and in the ventrolateral and ventromedial medulla (VLM/VMM) largely influence the sympathetic output. Despite the importance of these central circuits, the cellular properties of pre-sympathetic liver-related neurons remain to be determined. Here, we tested the hypotheses that the activity of pre-sympathetic liver-related neurons in the PVN and VLM/VMM is altered in diet induced obese (DIO) mice, as well as their sensitivity to insulin. Whole-cell patch-clamp recordings were conducted from liver-related neurons in male DIO (15–19-week-old) and control mice. During a step protocol, current steps (0-30pA, duration 1s) were applied to reveal the firing activity of neurons. Our data showed increased excitability of liver-related PVN neurons in DIO mice (n=9) compared to Control mice (n=10) (simple linear regression, different elevation, p=0.04). Moreover, in DIO mice, insulin decreased the frequency of action potentials (basal: 0.83±0.28 Hz vs insulin: 0.47±0.22 Hz, n=10; Wilcoxon test, p=0.01), while it had no effect on the firing in control mice (basal: 0.79±0.37 Hz vs insulin: 0.51±0.26 Hz, n=8, Wilcoxon test, p=0.11). Similarly, in DIO mice, insulin decreased the firing of liver-related PVN neurons after current injection (simple linear regression, different elevation, p=0.01, n=9). Next, liver-related PVN neurons were identified based on their projection to the VLM/VMM, and we found that the excitability of pre-sympathetic liver-related PVN neurons (n=7) was increased compared to liver-related PVN neurons (n=10) (simple linear regression, different elevation, p=0.00). Intriguingly, insulin did not alter the excitability of pre-sympathetic liver-related PVN neurons neither in control (n=8) or DIO mice (n=7) (simple linear regression, different elevation (Control: p=0.27; DIO: p=0.21). Since insulin sensitivities of liver-related PVN and pre-sympathetic liver-related PVN neurons were different, recordings were conducted from liver-related neurons in the VLM/VMM, which is well-known for its control over the sympathetic tone. In control mice, during the step protocol insulin had no effect on the excitability (simple linear regression, different elevation, p=0.37 n=7) whereas it decreased the firing rate of liver-related VLM/VMM neurons in DIO mice (nonlinear fit, different curve, p=0.03, n=4). Additionally, insulin receptor expression was confirmed by single cell digital droplet PCR in a subset of liver-related neurons by collecting mRNA from the cytoplasm of the recorded neurons. In summary, these results demonstrate that the firing activity of liver-related neurons are altered in DIO mice as well as their sensitivity to insulin. These data provide further evidence for cellular changes involving neurons regulating the sympathetic output to the liver. This work was supported by the NIH (DK-122842 to AZs and AVD), and Marko Spark Innovation Research Fund to AZs and AVD. We also thank the Tulane Brain Institute Cell and Tissue Imaging Core and the NIH Center for Neuroanatomy and Neurotropic viruses for the PRVs (P40 OD010996). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

High-Fat Diet Modulates the Excitability of Neurons within the Brain-Liver Pathway.

Stimulation of hepatic sympathetic nerves increases glucose production and glycogenolysis. Activity of pre-sympathetic neurons in the paraventricular nucleus (PVN) of the hypothalamus and in the ventrolateral and ventromedial medulla (VLM/VMM) largely influence the sympathetic output. Increased activity of the sympathetic nervous system (SNS) plays a role in the development and progression of metabolic diseases; however, despite the importance of the central circuits, the excitability of pre-sympathetic liver-related neurons remains to be determined. Here, we tested the hypothesis that the activity of liver-related neurons in the PVN and VLM/VMM is altered in diet-induced obese mice, as well as their response to insulin. Patch-clamp recordings were conducted from liver-related PVN neurons, VLM-projecting PVN neurons, and pre-sympathetic liver-related neurons in the ventral brainstem. Our data demonstrate that the excitability of liver-related PVN neurons increased in high-fat diet (HFD)-fed mice compared to mice fed with control diet. Insulin receptor expression was detected in a population of liver-related neurons, and insulin suppressed the firing activity of liver-related PVN and pre-sympathetic VLM/VMM neurons in HFD mice; however, it did not affect VLM-projecting liver-related PVN neurons. These findings further suggest that HFD alters the excitability of pre-autonomic neurons as well as their response to insulin.

Phospholipase C-ε defines a PACAP-stimulated pathway for secretion in the chromaffin cell.

Adrenomedullary chromaffin cells respond to splanchnic (sympathetic) nerve stimulation by releasing stress hormones into the circulation. The signal for hormone secretion is encoded in the neurotransmitters - especially acetylcholine (ACh) and pituitary adenylate cyclase activating polypeptide (PACAP) - that are released into the splanchnic-chromaffin cell synapse. However, functional differences in the effects of ACh and PACAP on the chromaffin cell secretory response are not well defined. Here, selective agonists of PACAP receptors or nicotinic and muscarinic acetylcholine receptors were applied to chromaffin cells. The major differences in the effects of these agents were not on exocytosis, per se, but rather on the steps upstream of exocytosis. In almost every respect, the properties of individual fusion events triggered by PACAP and cholinergic agonists were similar. On the other hand, the properties of the Ca2+ transients evoked by PACAP differed in several ways from those evoked by muscarinic and nicotinic receptor stimulation. A defining feature of the PACAP-stimulated secretory pathway was its dependence on signaling through exchange protein directly activated by cAMP (Epac) and PLCε. However, the absence of PLCε did not disrupt Ca2+ transients evoked by cholinergic agonists. Accordingly, inhibition of Epac activity did not disrupt secretion triggered by acetylcholine or specific agonists of muscarinic and nicotinic receptors. Thus, PACAP and acetylcholine stimulate chromaffin cell secretion via separate and independent pathways. This feature of stimulus-secretion coupling may be important for sustaining hormone release from the adrenal medulla under conditions associated with the sympathetic stress response.

Stimulation of extrinsic sympathetic nerves differentially affects neurogenic motor activity in guinea pig distal colon.

The speed of pellet propulsion through the isolated guinea pig distal colon in vitro significantly exceeds in vivo measurements, suggesting a role for inhibitory mechanisms from sources outside the gut. The aim of this study was to investigate the effects of sympathetic nerve stimulation on three different neurogenic motor behaviors of the distal colon: transient neural events (TNEs), colonic motor complexes (CMCs), and pellet propulsion. To do this, segments of guinea pig distal colon with intact connections to the inferior mesenteric ganglion (IMG) were set up in organ baths allowing for simultaneous extracellular suction electrode recordings from smooth muscle, video recordings for diameter mapping, and intraluminal manometry. Electrical stimulation (1-20 Hz) of colonic nerves surrounding the inferior mesenteric artery caused a statistically significant, frequency-dependent inhibition of TNEs, as well as single pellet propulsion, from frequencies of 5Hz and greater. Significant inhibition of CMCs required stimulation frequencies of 10Hz and greater. Phentolamine (3.6μM) abolished effects of colonic nerve stimulation, consistent with a sympathetic noradrenergic mechanism. Sympathetic inhibition was constrained to regions with intact extrinsic nerve pathways, allowing normal motor behaviors to continue without modulation in adjacent extrinsically denervated regions of the same colonic segments. The results demonstrate differential sensitivities to sympathetic input among distinct neurogenic motor behaviors of the colon. Together with findings indicating CMCs activate colo-colonic sympathetic reflexes through the IMG, these results raise the possibility that CMCs may paradoxically facilitate suppression of pellet movement in vivo, through peripheral sympathetic reflex circuits.

The denervation or activation of renal sympathetic nerve and renal blood flow.

The denervation or activation of the sympathetic nerve in the kidney can affect renal hemodynamics. The sympathetic nervous system regulates the physiological functions of the kidneys. Stimulation of sympathetic efferent nerves affects various parameters related to renal hemodynamics, including sodium excretion, renin secretion, and renal blood flow (RBF). Hence, renal sympathetic fibers may also play an essential role in regulating systemic vascular resistance and controlling blood pressure. In the absence of renal nerves, the hemodynamics response to stimuli is negligible or absent. The effect of renal sympathetic denervation on RBF is dependent on several factors such as interspecies differences, the basic level of nerve activity in the vessels or local density of adrenergic receptor in the vascular bed. The role of renal denervation has been investigated therapeutically in hypertension and related disorders. Hence, the dynamic impact of renal nerves on RBF enables using RBF dynamic criteria as a marker for renal denervation therapy.

Dynamic accentuated antagonism of heart rate control during different levels of vagal nerve stimulation intensity in rats.

Accentuated antagonism refers to a phenomenon in which the vagal effect on heart rate (HR) is augmented by background sympathetic tone. The dynamic aspect of accentuated antagonism remains to be elucidated during different levels of vagal nerve stimulation (VNS) intensity. We performed VNS on anesthetized rats (n = 8) according to a binary white noise signal with a switching interval of 500 ms at three different stimulation rates (low-intensity: 0-10 Hz, moderate-intensity: 0-20 Hz, and high-intensity: 0-40 Hz). The transfer function from VNS to HR was estimated with and without concomitant tonic sympathetic nerve stimulation (SNS) at 5 Hz. The asymptotic low-frequency (LF) gain (in beats/min/Hz) of the transfer function increased with SNS regardless of the VNS rate [low-intensity: 3.93 ± 0.70 vs. 5.82 ± 0.65 (P = 0.021), moderate-intensity: 3.87 ± 0.62 vs. 5.36 ± 0.53 (P = 0.018), high-intensity: 4.77 ± 0.85 vs. 7.39 ± 1.36 (P = 0.011)]. Moreover, SNS slightly increased the ratio of high-frequency (HF) gain to the LF gain. These effects of SNS were canceled by the pretreatment of ivabradine, an inhibitor of hyperpolarization-activated cyclic nucleotide-gated channels, in another group of rats (n = 6). Although background sympathetic tone antagonizes the vagal effect on mean HR, it enables finer HR control by increasing the dynamic gain of the vagal HR transfer function regardless of VNS intensity. When interpreting the HF component of HR variability, the augmenting effect from background sympathetic tone needs to be considered.

Stress exacerbates pancreatic cancer both directly and indirectly by creating an immunosuppressive environment.

Sympathetic nerve stimulation by stress exacerbates various solid tumors, including pancreatic cancer (PCa). The relationship between cancer and immunity has been suggested; however, there is limited information about the effects of nerve stimulation on immunity and cancer. We aimed to investigate the involvement of sympathetic nerve stimulation in immune cells and its effects on PCa using a restraint stress mouse model. In the in vitro experiment, the mouse-derived PCa cell line (LTPA) was cultured in a noradrenalin-supplemented medium. In the in vivo experiment, mice were divided into non-stress and stress groups. LTPA proliferated significantly more when cultured in a noradrenalin-supplemented medium than in a normal medium. Flow cytometry analysis of blood immune cells revealed a significant decrease in B cells, T cells, and macrophages and a significant increase in myeloid-derived suppressor cells (MDSCs) in the stress group. Furthermore, a significant increase in blood noradrenaline levels was observed in the stress group (p< .01). In the PCa mice model, immune cells in the blood showed a similar trend, and the stress group had a poor prognosis. Furthermore, immunostaining at the tumor site showed that there was a lower number of B and T cells in the stress group. In addition, MDSCs were present at the tumor margins. These results suggest that sympathetic nerve stimulation is not only directly involved in PCa growth but also exacerbates PCa by creating an immunosuppressive environment in the blood and tumor tissue.

Sympathetic nervous stimulation promotes complex rotational ventricular fibrillation events in guinea pig hearts

Sympathetic nervous stimulation promotes complex rotational ventricular fibrillation events in guinea pig hearts

Amount of Pannexin 1 in Smooth Muscle Cells Regulates Sympathetic Nerve-Induced Vasoconstriction.

Panx1 (pannexin 1) forms high conductance channels that secrete ATP upon stimulation. The role of Panx1 in mediating constriction in response to direct sympathetic nerve stimulation is not known. Additionally, it is unknown how the expression level of Panx1 in smooth muscle cells (SMCs) influences α-adrenergic responses. We hypothesized that the amount of Panx1 in SMCs dictates the levels of sympathetic constriction and blood pressure. To test this hypothesis, we used genetically modified mouse models enabling expression of Panx1 in vascular cells to be varied. Electrical field stimulation on isolated arteries and blood pressure were assessed. Genetic deletion of SMC Panx1 prevented constriction by electric field stimulation of sympathetic nerves. Conversely, overexpression of Panx1 in SMCs using a ROSA26 transgenic model increased sympathetic nerve-mediated constriction. Connexin 43 hemichannel inhibitors did not alter constriction. Next, we evaluated the effects of altered SMC Panx1 expression on blood pressure. To do this, we created mice combining a global Panx1 deletion, with ROSA26-Panx1 under the control of an inducible SMC specific Cre (Myh11). This resulted in mice that could express only human Panx1, only in SMCs. After tamoxifen, these mice had increased blood pressure that was acutely decreased by the Panx1 inhibitor spironolactone. Control mice genetically devoid of Panx1 did not respond to spironolactone. These data suggest Panx1 in SMCs could regulate the extent of sympathetic nerve constriction and blood pressure. The results also show the feasibility humanized Panx1-mouse models to test pharmacological candidates.

An Artifact-Resistant Feature SKNAER for Quantifying the Burst of Skin Sympathetic Nerve Activity Signal.

Evaluation of sympathetic nerve activity (SNA) using skin sympathetic nerve activity (SKNA) signal has attracted interest in recent studies. However, signal noises may obstruct the accurate location for the burst of SKNA, leading to the quantification error of the signal. In this study, we use the Teager–Kaiser energy (TKE) operator to preprocess the SKNA signal, and then candidates of burst areas were segmented by an envelope-based method. Since the burst of SKNA can also be discriminated by the high-frequency component in QRS complexes of electrocardiogram (ECG), a strategy was designed to reject their influence. Finally, a feature of the SKNA energy ratio (SKNAER) was proposed for quantifying the SKNA. The method was verified by both sympathetic nerve stimulation and hemodialysis experiments compared with traditional heart rate variability (HRV) and a recently developed integral skin sympathetic nerve activity (iSKNA) method. The results showed that SKNAER correlated well with HRV features (r = 0.60 with the standard deviation of NN intervals, 0.67 with low frequency/high frequency, 0.47 with very low frequency) and the average of iSKNA (r = 0.67). SKNAER improved the detection accuracy for the burst of SKNA, with 98.2% for detection rate and 91.9% for precision, inducing increases of 3.7% and 29.1% compared with iSKNA (detection rate: 94.5% (p < 0.01), precision: 62.8% (p < 0.001)). The results from the hemodialysis experiment showed that SKNAER had more significant differences than aSKNA in the long-term SNA evaluation (p < 0.001 vs. p = 0.07 in the fourth period, p < 0.01 vs. p = 0.11 in the sixth period). The newly developed feature may play an important role in continuously monitoring SNA and keeping potential for further clinical tests.

High resolution optical mapping of cardiac electrophysiology in pre-clinical models

Optical mapping of animal models is a widely used technique in pre-clinical cardiac research. It has several advantages over other methods, including higher spatial resolution, contactless recording and direct visualisation of action potentials and calcium transients. Optical mapping enables simultaneous study of action potential and calcium transient morphology, conduction dynamics, regional heterogeneity, restitution and arrhythmogenesis. In this dataset, we have optically mapped Langendorff perfused isolated whole hearts (mouse and guinea pig) and superfused isolated atria (mouse). Raw datasets (consisting of over 400 files) can be combined with open-source software for processing and analysis. We have generated a comprehensive post-processed dataset characterising the baseline cardiac electrophysiology in these widely used pre-clinical models. This dataset also provides reference information detailing the effect of heart rate, clinically used anti-arrhythmic drugs, ischaemia-reperfusion and sympathetic nervous stimulation on cardiac electrophysiology. The effects of these interventions can be studied in a global or regional manner, enabling new insights into the prevention and initiation of arrhythmia.

Takotsubo cardiomyopathy

Takotsubo cardiomyopathy (TTC) is a clinical condition of transient acute heart failure correlated to regional wall motion abnormalities extending beyond the distribution of a single epicardial coronary artery. It is classified into four major types: apical, basal, mid-ventricular and focal. Sympathetic nerve stimulation and catecholamine storm are the main players in the pathogenesis of TTC. The clinical course of disease is generally benign but it may end with life-threatening complications. Coronary angiography, left ventriculogram, transthoracic echocardiography and cardiac magnetic resonance imaging (CMR) are the main tools for making diagnosis. Except for critical cases with hemodynamic instability and/or complications, the overall management is limited to conventional heart failure therapy.

Acute lung injury after pulmonary resection surgery for lung cancer and anesthetic management

Although the outcome of patients undergoing pulmonary resection surgeries for lung cancer has improved, postoperative acute lung injury (ALI) remains the leading cause of death. High oxygen concentration, high peak airway pressure, and hyper-perfusion due to hypoxic pulmonary vasoconstriction play a major role in the development of ALI in the ventilated dependent lung during one-lung ventilation. In the collapsed non-dependent lung, mechanical stress induced by re-expansion, ischemia-reperfusion injury, and direct surgical manipulation are associated with the onset of ALI. These contributing factors to ALI elicit local inflammatory responses, resulting in pulmonary edema that resembles acute respiratory distress syndrome histologically. Some preventive strategies to reduce ALI are recommended during mechanical ventilation, OLV support in particular. A lung protective strategy, including sufficient positive end-expiratory pressure, low tidal volume, and lower inspiratory oxygen concentration, should be adopted to attenuate lung damage. The application of continuous positive airway pressure to the collapsed non-dependent lung has been shown to reduce inflammatory cytokines. Given that excessive fluid administration is associated with the risk of postoperative pulmonary complications, a fluid restrictive strategy should be considered to prevent ALI. Anesthetic management may affect the onset of postoperative ALI. Compared to propofol anesthesia, volatile anesthetics have been shown to attenuate local inflammatory responses in both lungs during thoracic surgeries. Thoracic epidural analgesia may attenuate a local inflammatory response in the lung through the blockade of sympathetic nerve stimulation. Thus, more effective strategies to prevent ALI should be investigated to improve the prognosis of patients undergoing thoracic surgeries.

Phagocytic activity of leukocytes in peptic ulcer and stomach cancer

N.V. Puchkov and G.G. Golodets found that the perfusion fluid collected during stimulation of the frog's sympathetic nerves (sympathy) increased the phagocytic activity of blood leukocytes, and that collected during irritation of the vagus nerve (acetylcholine) decreased ... These data were later confirmed by other researchers (S. M. Titova, R. U. Lipshitz, A. D. Ado et al., Etc.).