Primary diffuse large B-cell lymphoma of adrenal gland: A case report.

INTRODUCTION: Most adrenal tumors are benign and primary adrenal malignancies are relatively rare. Primary adrenal lymphoma (PAL) is a very rare and highly aggressive malignant tumor with unknown etiology, atypical clinical symptoms, nonspecific imaging manifestations, difficult disease diagnosis and poor prognosis. CASE REPORT: This case report details a 42-year-old woman who was admitted to the hospital with a 1-year-old bilateral adrenal mass and 1-month-old left upper abdominal pain. Enhanced CT of the abdomen showed a right adrenal nodule and a large occupying lesion in the left adrenal region, with a high probability of pheochromocytoma. Intraoperatively, a huge tumor measuring about 12*12*10 cm was found in the left adrenal region, infiltrating the left kidney, spleen and pancreatic tail. Postoperative pathology: lymphocytes were found in the renal capsule and subcapsule, lymphocytes were found in the pancreas; lymphocytes were found in the spleen. Consider a tumor of the lymphohematopoietic system, possibly lymphoma. CONCLUSION: This case demonstrates that primary adrenal diffuse large B-cell lymphoma (PADLBCL) is highly aggressive, has a poor prognosis, is prone to recurrence, has poor therapeutic outcomes, and is difficult to diagnose. Clinicians should consider the possibility of PADLBCL when encountering huge adrenal-occupying lesions and consider chemotherapy before surgery. Reducing the tumor size before surgery is a more favorable therapeutic approach, thus prolonging the patient life and improving the quality of survival.

Atox1 regulates macrophage polarization in intestinal inflammation via ROS-NLRP3 inflammasome pathway.

BACKGROUND: Inflammation and oxidative stress play an important role in the pathophysiology of inflammatory bowel disease (IBD). This study aimed to explore the effects of copper chaperone Antioxidant-1 (Atox1) on macrophages in a mouse model of intestinal inflammation. METHODS: A mouse model of TNBS-induced colitis was established and verified using the disease activity index. Atox1 conditional knockout mice were applied. The proportion of macrophages in colonic lamina propria mononuclear cells and ROS production were analyzed using flow cytometry. Inflammatory cytokines were measured using ELISA. Expression of macrophage M1/M2 polarization markers, p47phox, NLRP3, and Caspase-1 p20 was measured using quantitative RT-PCR and Western blotting. RESULTS: Atox1 expression was up-regulated in colon tissues of TNBS-induced colitis mice. Macrophages isolated from TNBS-induced colitis mice showed M1 polarization and nuclear translocation of Atox1. Inhibiting copper chaperone activity decreased p47phox, ROS production, and M1 polarization induced by CuCl2 in macrophages. TNBS induced up-regulation of inflammatory cytokines, M1 polarization markers, and p47phox expression in mice, an effect which was preempted by Atox1 knockout. Inflammatory cytokines and expression of M1 polarization markers, p47phox, NLRP3, Caspase-1 p20 were also increased in macrophages isolated from TNBS-induced colitis mice. These changes were alleviated in mice with Atox1 knockout. The effects of Atox1 on macrophage polarization were mediated via the ROS-NLRP3 inflammasome pathway. CONCLUSION: Atox1 plays a pro-inflammatory role, promotes M1 polarization of macrophages, and increases the concentrations of pro-inflammatory cytokines in intestinal tissue by regulating the ROS-NLRP3 inflammasome pathway. Atox1 is a potential therapeutic target in IBD.

The effects of cognitive-motor dual-task training on athletes' cognition and motor performance.

Background: Cognitive-Motor Dual Task (CMDT) training has been widely utilized in rehabilitation and sports practice. However, whether CMDT training can better enhance athletes' cognitive-motor performance compared to traditional single-task (ST) training remains unclear. Method: A systematic review that complied with PRISMA was carried out (Prospero registration number: CRD42023443594). The electronic databases used for the systematic literature search from the beginning through 13 June 2023, included Web of Science, Embase, PubMed, and the Cochrane Library. After obtaining the initial literature, two researchers independently assessed it based on inclusion and exclusion criteria. Finally, the included literature was analyzed to compare the differences between ST training and CMDT training. Results: After screening 2,094 articles, we included 10 acute studies and 7 chronic studies. Conclusion: This systematic review shows that athletes typically show a degradation of performance in CMDT situations as opposed to ST when evaluated transversally. However, this performance decline is notably reduced following longitudinal training in CMDT, indicating the effectiveness of sustained CMDT training in enhancing cognitive-motor performance under dual-task conditions. Our study provides new insights into the application of CMDT in the field of sports training. Practitioners can utilize CMDT to assess athletic skill levels or optimize cognitive-motor performance of athletes, taking into account the specific needs of each sport. Systematic review registration: https://www.crd.york.ac.uk/prospero, identifier CRD42023443594.

Subarachnoid haemorrhage-induced reversible cardiac dysfunction: time course and potential mechanisms.

AIMS: Cardiac dysfunction is commonly observed in patients with subarachnoid haemorrhage (SAH). However, the specific timeline of cardiac remodelling and the underlying mechanisms responsible for this effect following SAH remain unknown. This study aims to explore the impact of SAH on cardiac dysfunction and its potential mechanisms over time. METHODS AND RESULTS: In Protocol 1, we investigated cardiac function and potential mechanisms in a Sprague-Dawley rat model of SAH at six time points (baseline and Days 1, 3, 7, 14, and 28) while exploring the underlying mechanisms. Our assessments included the haemodynamic profile, echocardiography, and the concentrations of plasma biomarkers at various time points post-SAH. We determined neuropeptide Y (NPY) 1-5 receptor protein expression levels through western blotting. In Protocol 2, we administered an NPY1 receptor antagonist to evaluate the effects of cardiac dysfunction induced by SAH on Day 3. In Protocol 1, SAH gradually provoked cardiac systolic dysfunction during the acute phase, reaching its peak on Day 3 without concurrent alterations in wall thickness. However, no significant changes were observed from Days 14 to 28 compared with Day 0. The changes in cardiac dysfunction were consistent with myocardial injury, inflammatory biomarkers, and NPY levels. SAH resulted in a heightened heart rate and systolic blood pressure, correlating with elevated epinephrine and norepinephrine levels. In Protocol 2, the administration of the NPY1 receptor antagonist effectively ameliorated cardiac dysfunction. CONCLUSIONS: SAH induces transient cardiac dysfunction in the acute phase, and the underlying mechanisms for this response involve the NPY-NPY1 receptor pathway, otherwise known as catecholamines.

Intramyocardial Hemorrhage Leads to Higher MACE Rate by Increasing Myocardial Infarction Volume in Patients with STEMI.

Background and Aims: Whether IMH can directly cause persistent myocardial necrosis after reperfusion therapy in STEMI patients is still unclear. We conducted a prospective study to compare the cardiovascular parameters in patients with STEMI with and without IMH to explore the potential correlations between IMH and poor outcomes. Methods and Results: We prospectively enrolled 65 consecutive patients with newly diagnosed STEMI admitted to the CCU of the Second Xiangya Hospital of Central South University between April 2019 and November 2021, all of whom underwent primary PCI. Of these, 38 (58.5%) and 27 (41.5%) patients were in the IMH-absent and IMH-present groups, respectively. At a mean time of 5-7 days after reperfusion therapy, the volume of MI measured using LGE sequence was larger in STEMI patients with IMH than in patients without IMH (34.2 ± 12.7 cm3 vs 21.1 ± 13.1 cm3, P<0.001). HsTNT levels were significantly higher in the IMH-present group than in the IMH-absent [2500.0 (1681.5-4307.0) pg/mL vs 1710.0 (203.0-3363.5) pg/mL, P=0.021] group during hospitalization. The LVEF measured using CMR in the IMH-present group was lower than that in the IMH-absent group (30.7 ± 9.8% vs 42.3 ± 11.0%, P < 0.001). The rate of MACE at 12 months in IMH-present group was significantly higher than in the IMH-absent group (9/27 VS 2/38, P = 0.012). Conclusion: IMH can lead to further expansion of MI volumes in patients with STEMI, resulting in lower LVEF and higher MACE rate in the post-discharge follow-up.

The comparison between the novel technique and conventional method in the catheter ablation of premature ventricular contractions originating from the free wall of tricuspid annulus.

BACKGROUND: This study aimed to assess the safety and effectiveness of a novel technique for catheter ablation in patients with premature ventricular contraction (PVC) from the free wall of tricuspid annulus (TV). HYPOTHESIS: We hypothesized that the novel technique is more efficacious than the traditional approach. METHODS: We retrospectively investigated 59 consecutive patients with PVC originating from the free wall of TV between January 2013 and November 2021. The patients were divided into two groups: the reversed S-curve technique group (RST, n = 26) and the reversed C-curve technique group (RCT, n = 33). The RST under the support of a steerable sheath was used in RST group, while the RCT under the support of a nonsteerable sheath was used in the RCT group. Systematic mapping and radiofrequency ablation were preferentially performed under the valve in all patients. RESULTS: Compared to the RCT group, total procedural time and fluoroscopic exposure time were significantly shorter in RST group. Two patients experienced cardiac tamponade in the RCT group, while no complications were observed in RST group (p = .498). The success rate was significantly higher in RST group compared to RCT group (81.9% vs. 100%, p = .029). Three patients in RCT group failed to ablate during the operation but were successfully ablated using the novel method. During regular follow-up, no patients in the RST group had a recurrence, while three patients in the RCT group did (p = .274). CONCLUSIONS: It suggests that the reserved S-curve technique, supported by a steerable sheath, is a feasible and effective method for ablating PVC originating from the free wall of TV.

The effectiveness and safety of temporary transvenous cardiac pacing leads placement into coronary sinus vein in patients with sick sinus syndrome.

BACKGROUND: The temporary pacing lead routinely is placed into right ventricular (RV), which pose a risk of dislocation and cardiac perforation. OBJECTIVE: We aim to evaluate the effectiveness and safety of temporary transvenous cardiac pacing (TTCP) leads placement into the coronary sinus vein (CSV) in patients with sick sinus syndrome (SSS). METHODS: We investigated patients with SSS who underwent TTCP lead placement into the CSV under the guidance of X-ray between January 2013 and May 2023. Patients were randomly divided into two groups: RV group (n = 33) and CSV group (n = 22). The ordinary passive bipolar electrodes were applied in both groups. In RV groups, electrodes were placed into RV. In CSV group, electrodes were placed into CSV. We evaluated the operation duration, fluoroscopic exposure, first-attempt success rate of leads placement, pacing threshold, success rate of leads placement, rate of leads displacement, and complications. RESULTS: Compared with that in RV group, the procedure time, fluoroscopic exposure was significantly prolonged, while the first-attempt success rate of lead placement was obviously increased in CSV group (both p < .05). Compared with that in RV group, the rate of leads displacement is lower in CSV group (both p < .05). There were three patients occurred cardiac perforation in RV group, but no cardiac perforation was reported in CSV group (p > .05). CONCLUSION: TTCP leads placement into the CSV is an effective and safe strategy in patients with SSS. It indicates a high rate of pacing effectiveness with low device replacement and complication rates.

Low-intensity focused ultrasound modulation of the paraventricular nucleus to prevent myocardial infarction-induced ventricular arrhythmia.

BACKGROUND: Our previous study showed that light-emitting diode modulation of the hypothalamic paraventricular nucleus (PVN), which is the control center of the sympathetic nervous system, might attenuate neuroinflammation in the PVN and prevent ventricular arrhythmias (VAs) after myocardial infarction (MI). Low-intensity focused ultrasound (LIFU) has deeper penetration than does light-emitting diode, while its effect on the PVN has not been reported. OBJECTIVE: This study aimed to explore the effect of LIFU modulation of the PVN on the inducibility of post-MI VAs. METHODS: Fifty-four Sprague-Dawley rats were randomly divided into acute control (n = 12, 22.22%), acute MI (AMI, n = 12, 22.22%), AMI + LIFU (n = 12, 22.22%), chronic control (n = 6, 11.11%), chronic MI (CMI, n = 6, 11.11%), and CMI + LIFU (n = 6, 11.11%) groups. MI was induced by left anterior artery ligation, and electrocardiographic recording for 0.5 hours after MI and programmed electrophysiological stimulation were used to test the vulnerability of VAs. Peripheral sympathetic neural activity was assessed by measuring left stellate ganglion neural activity. Finally, hearts and brains were extracted for Western blotting and histopathological analysis, respectively. RESULTS: Compared with the AMI group, AMI-induced VAs (P < .05) and left stellate ganglion neural activity (P < .05) were significantly attenuated in the AMI + LIFU group. In addition, LIFU resulted in a significant reduction of microglial activation in the PVN and expression of inflammatory cytokines in the peri-ischemic myocardium. In the CMI + LIFU group, there was no obvious tissue damage in the brain. CONCLUSION: LIFU modulation of the PVN may prevent the incidence of post-MI VAs by attenuating MI-induced sympathetic neural activation and inflammatory response.

Comparison between conventional approach and three-dimensional mapping system in the catheter ablation of accessory pathway associated with coronary sinus diverticulum: A single-center experience.

BACKGROUND: Posteroseptal accessory pathways (APs) associated with coronary sinus (CS) diverticulum present a rare and challenge for ablation. This study aimed to compare the safety and efficacy of conventional approach and three-dimensional (3D) mapping system in the catheter ablation. METHODS AND RESULTS: This was a retrospective study of all patients (from January 2013 to July 2022) who underwent catheter ablation of posteroseptal AP associated with CS diverticula in our center. Patients who underwent catheter ablation using the traditional fluoroscopy method were included in the conventional method group (n = 13). Patients who underwent catheter ablation using the 3D mapping method were included in the 3D mapping group (n = 11). Clinical characteristics, ablation procedure, and outcomes were recorded and analyzed between the two groups. Out of 669 patients with posteroseptal APs, 24 of them (3.6%) were associated with CS diverticula. All patients in both groups successfully completed the electrophysiological study. In the conventional method group, two patients experienced complications (one patient with pericardial effusion and the other patient with femoral arterial hematoma), and two patients had recurrence. However, no patients suffered from complications or recurrence during follow-up. The procedure time and fluoroscopy time in the conventional method group were significantly longer than those in the 3D mapping method group. CONCLUSIONS: The utilization of 3D mapping led to reduced fluoroscopy time, shorter procedure duration, enhanced acute success rates, and decreased incidence of complications.

Screening of an FDA-approved compound library identifies apigenin for the treatment of myocardial injury.

Apigenin is the active ingredient in Ludangshen. Although previous studies reported the cardioprotective actions of apigenin against doxorubicin (Dox)-induced cardiomyopathy, the underlying mechanisms remain incompletely understood. Since apigenin beneficially regulates various aspects of mitochondrial function and dynamics, we asked whether apigenin improves heart function in mice with Dox-induced cardiomyopathy by regulating the mitochondrial unfolded protein response (UPRmt). Co-administration of apigenin significantly restored heart function, reduced myocardial swelling, inhibited cardiac inflammation, increased cardiac transcription of UPRmt-related genes, and promoted cardiomyocyte survival in Dox-treated mice. In turn, blockade of UPRmt abolished the mito- and cytoprotective effects of apigenin, evidenced by decreased ATP production, suppressed mitochondrial antioxidant capacity, and increased apoptosis, in Dox-treated, cultured HL-1 cardiomyocytes. Furthermore, apigenin treatment prevented Dox-induced downregulation of Sirt1 and Atf5 expression, and the beneficial effects of apigenin were completely nullified in Sirt1 knockout (KO) mice or after siRNA-mediated Sirt1 knockdown in vitro. We thus provide novel evidence for a promotive effect of apigenin on UPRmt via regulation of the Sirt1/Atf5 pathway. Our findings uncover that apigenin seems to be an effective therapeutic agent to alleviate Dox-mediated cardiotoxicity.

The association between walking pace and hand grip strength with the risk of chronic obstructive pulmonary disease: a bidirectional Mendelian randomization study.

BACKGROUND: Chronic Obstructive Pulmonary Disease (COPD) currently ranks as the third leading cause of mortality worldwide, imposing substantial burdens on societal and individual health. Amongst health research tools, walking pace (WP) and hand grip strength (HGS) are cornerstones, extensively associated with diverse health conditions. However, the intricate interplay between these factors and COPD risk remains ambiguous. This study aims to elucidate the causal association of WP, HGS, with COPD risk through a bidirectional Mendelian randomization (MR) approach. METHODS: Bidirectional MR analysis was performed using Genome-wide association study (GWAS) data of European individuals for WP, HGS, and COPD. Inverse Variance Weighted (IVW) served as the primary MR analysis approach. To supplement the IVW findings, four additional MR methods [MR-Egger, weighted median, maximum likelihood, simple median] were used. To assess heterogeneity and pleiotropy, sensitivity analyses were performed. In addition, multivariate MR (MVMR) analysis was used to assess causality after adjustment for potential confounders. RESULTS: IVW method results show a significant negative association between WP and COPD risk in both initial (genome-wide threshold, odds ratio (OR) = 0.21, 95% confidence interval (CI) 0.09-0.51, P = 5.06 × 10- 4) and secondary (locus-wide threshold, OR = 0.27, 95%CI: 0.18-0.41, P = 4.88 × 10- 10) MR analysis. The reverse MR analysis suggested that COPD also diminishes WP. Additionally, a causal risk reduction for COPD with right HGS (OR = 0.74, 95% CI: 0.58-0.94, P = 1.44 × 10- 2) was only found in secondary MR analysis. The outcomes of the four additional MR methods also suggested similar causal relationships, and sensitivity analyses endorsed their robustness. Lastly, the MVMR analysis demonstrated that the WP's effect on reducing COPD risk persisted independently of potential confounding variables. CONCLUSION: A bidirectional causal relationship exists between typical WP and COPD risk. Conversely, a decrease in right HGS is unidirectionally associated with an increased risk of COPD. The study suggests that WP may serve as a predictive factor for COPD or as a simple evaluative indicator for prognosis.

[Expert consensus for diagnosis and treatment of post-cardiac arrest syndrome in adults by combining traditional Chinese and Western medicine in China (2023)].

Reperfusion injury occurs after return of spontaneous circulation (ROSC) in patients with cardiac arrest (CA), which leads to multiple organ dysfunction, called post-cardiac arrest syndrome (PCAS). PCAS is closely related to the prognosis of CA patients, and is an independent risk factor of survival. Integrated traditional Chinese and Western medicine diagnosis and treatment is critical for improving prognosis of PCAS. In order to guide and standardize integrated traditional Chinese and Western medicine diagnosis and treatment in PCAS among clinicians, nurses and research personnel in China, the Emergency Medicine Professional Committee of the Chinese Society of Integrated Chinese and Western Medicine has established an expert group to determine 14 clinical issues related to the diagnosis and treatment of PCAS with integrated traditional Chinese and Western medicine through clinical survey. The working group formulates a search strategy for each clinical issue according to the PICO principle. Chinese and English literature were searched from CNKI, Wanfang, VIP, SinoMed, PubMed, Embase, and Cochrane Library. The grade of recommendations assessment, development and evaluation (GRADE) were used to form the level of evidence and recommendation. When the literature evidence was insufficient, the recommendations and level of recommendation were formed after expert discussion. Combined with the aspects of generalizability, suitability, and resource utilization, the expert consensus developed 28 recommendations around the 14 aspects of three stages of PCAS, including early circulation, respiratory support and reversible cause relief, mid-term neuroprotection, improvement of coagulation, prevention and treatment of infection, kidney and gastrointestinal protection and blood sugar control, post rehabilitation treatment, providing references for the integrated traditional Chinese and Western medicine of the diagnosis and treatment for PCAS.

Causal effects of walking pace on osteoarthritis: a two-sample mendelian randomization study.

Background: Osteoarthritis (OA) is one of the most common joint diseases worldwide, imposing a substantial burden on individuals and society. Numerous pieces of evidence suggest that walking pace (WP) can serve as a predictive indicator for the risk of various diseases, and observational studies have also found a potential link between WP and the risk of OA. However, the causal relationship between WP and the risk of OA remains unclear. Methods: We conducted a mendelian randomization (MR) study using data from the European Genome-wide Association Study, which included WP (including 459,915 participants), OA (including 10,083 cases and 40,425 controls), knee OA (including 24,955 cases and 378,169 controls), and hip OA (including 15,704 cases and 378,169 controls). Single nucleotide polymorphisms (SNPs) associated with WP were utilized to infer causal associations with OA and its subtypes. The Inverse Variance Weighted (IVW) technique served as the primary causal analysis method. Three auxiliary MR methods - MR-Egger, weighted median, and maximum likelihood - were used to substantiate the IVW results. Sensitivity analyses were performed to examine heterogeneity and pleiotropy. In addition, multivariate MR (MVMR) analysis was used to assess causality after adjustment for three potential confounders. Results: According to the results of the IVW method, every 1 standard deviation increased in genetic WP corresponds to an 89% reduction in the risk of OA (odds ratio (OR) = 0.11; 95% confidence interval (CI), 0. 06-0.19; p = 1.57 × 10-13), an 83% reduction in the risk of knee OA (OR = 0.17; 95% CI, 0.11-0.28; p = 2.78 × 10-13), and a 76% reduction in the risk of hip OA (OR = 0.24; 95% CI, 0.14-0.43; p = 1.51 × 10-6). These results were confirmed by the three additional MR methods and validated by the sensitivity analysis. Ultimately, the MVMR analysis confirmed that the role of WP in reducing the risk of OA and its subtypes remains consistent regardless of potential confounders. Conclusion: The results of our MR study highlight a significant causal association between WP and the susceptibility to OA, including its knee and hip subtypes. These findings propose that WP could be utilized as a potential prognostic factor for OA risk.

Association between Serum Ferritin and Prognosis in Patients with Ischemic Heart Disease in Intensive Care Units.

PURPOSE: Recent years have seen a clear link established between elevated ferritin levels and COVID-19 prognosis. However, the impact of heightened ferritin levels on the prognosis of individuals with severe ischemic heart disease remains uncertain. METHODS: We utilized the MIMIC IV database to identify a cohort of ischemic heart disease patients who underwent serum ferritin testing. We conducted regression analyses, employed the overlap propensity score weighting model, and utilized the restricted cubic splines model to comprehensively investigate the associations between serum ferritin levels and clinical outcomes. RESULTS: Our cohort included 1173 patients with diagnosed ischemic heart disease, categorized into high and low serum ferritin groups. After meticulous adjustment for confounding factors in a fully adjusted model, the hazard ratios (HRs) for 90-day and 1-year mortality were 1.63 (95% CI: 1.27-2.09) and 1.49 (95% CI: 1.19-1.86), respectively, in the high-ferritin group compared to the low-ferritin group. Subsequent analyses with propensity score weighting confirmed these results. Remarkably, restricted cubic spline analysis revealed an almost linear relationship between log-transformed serum ferritin levels and the risk of both 90-day and 1-year all-cause mortality. Moreover, incorporating ferritin into conventional severity of illness scores significantly improved the area under the curve for both 90-day and 1-year mortality. CONCLUSIONS: This study provides compelling evidence regarding the prognostic significance of serum ferritin in predicting 90-day and one-year mortality rates among patients diagnosed with ischemic heart disease.

Chronic vagus nerve stimulation in patients with heart failure: challenge or failed translation?

Autonomic imbalance between the sympathetic and parasympathetic nervous systems contributes to the progression of chronic heart failure (HF). Preclinical studies have demonstrated that various neuromodulation strategies may exert beneficial cardioprotective effects in preclinical models of HF. Based on these encouraging experimental data, vagus nerve stimulation (VNS) has been assessed in patients with HF with a reduced ejection fraction. Nevertheless, the main trials conducted thus far have yielded conflicting findings, questioning the clinical efficacy of VNS in this context. This review will therefore focus on the role of the autonomic nervous system in HF pathophysiology and VNS therapy, highlighting the potential reasons behind the discrepancy between preclinical and clinical studies.

Transient cardiac electrophysiological changes in a rat model of subarachnoid haemorrhage: a brain-heart interaction.

AIMS: Subarachnoid haemorrhage (SAH) is one of the causes of sudden cardiac death (SCD). However, the time course of ventricular arrhythmias and potential mechanisms responsible for this effect after SAH remain unknown. OBJECTIVE: This study aims to investigate the effect of SAH on ventricular electrophysiological changes and its potential mechanisms in long-term phase. METHODS AND RESULTS: We examined the ventricular electrophysiological remodelling and potential mechanisms in a Sprague Dawley rat model of SAH at six time points (baseline, and Days 1, 3, 7, 14 and 28) and explored the potential mechanisms. We measured the ventricular effective refractory period (ERP), ventricular fibrillation threshold (VFT) and left stellate ganglion (LSG) activity at different time points before and after SAH. We also detected neuropeptide Y (NPY) levels in plasma and myocardial tissues by enzyme-linked immunosorbent assay, and quantified NPY 1 receptor (NPY1R) protein and mRNA expression levels by western blotting and quantitative real-time reverse transcription-polymerase chain reaction, respectively. Subarachnoid haemorrhage gradually prolonged QTc intervals, shortened ventricular ERP and reduced VFT during the acute phase, peaking at Day 3. However, no significant changes were observed from Days 14 to 28 compared to Day 0. Subarachnoid haemorrhage gradually increased LSG activity, increased NPY concentrations and up-regulated NPY1R expression in the acute phase of SAH, peaking at Day 3. However, no significant variations were found from Days 14 to 28 compared to Day 0. CONCLUSION: Subarachnoid haemorrhage increases the transient susceptibility of VAs in the acute phase, and the underlying mechanisms for this response included increased sympathetic activity and up-regulated NPY1R expression.