Adenosine mono-phosphate-activated protein kinase-mammalian target of rapamycin signaling participates in the protective effect of chronic intermittent hypobaric hypoxia on vascular endothelium of metabolic syndrome rats.

Our previous study demonstrated that chronic intermittent hypobaric hypoxia (CIHH) protects vascular endothelium function through ameliorating autophagy in mesenteric arteries of metabolic syndrome (MS) rats. This study aimed to investigate the role of adenosine mono-phosphate-activated protein kinase-mammalian target of rapamycin (AMPK-mTOR) signaling in CIHH effect. Six-week-old male Sprague-Dawley rats were divided into control (CON), MS model, CIHH treatment (CIHH), and MS + CIHH groups. Serum pro-inflammatory cytokines were measured. The endothelium dependent relaxation (EDR), endothelial ultrastructure and autophagosomes were observed in mesenteric arteries. The expression of phosphor (p)-AMPKα, p-mTOR, autophagy-related and endoplasmic reticulum stress-related proteins, p-endothelial nitric oxide synthase, and cathepsin D were assayed. In MS rats, pro-inflammatory cytokines were increased, EDR was attenuated, and endothelial integrity was impaired. In addition, the expression level of p-AMPKα and cathepsin D was down-regulated, but the level of p-mTOR was up-regulated. While in MS + CIHH rats, all aforementioned abnormalities were ameliorated, and the beneficial effect of CIHH was cancelled by AMPKα inhibitor. In conclusion, AMPK-mTOR signaling pathway participates in the protection of CIHH on vascular endothelium of MS rats.

The Kv12 voltage-gated K+ channels are expressed in the Phox2b-expressing neurons in the nucleus tractus solitarii in mice.

Accumulating evidence demonstrates that the nucleus tractus solitarii (NTS) neurons serve as central respiratory chemoreceptors, but the underlying molecular mechanisms remain undefined. The present study investigated the expression of acid-sensitive ether-à-go-go-gene-like (Elk, Kv12) channels in the NTS of mice. Immunofluorescence staining was used to observe the distribution and cellular localization of the Kv12 channels in NTS neurons. Western blot and quantitative real-time PCR (qPCR) were used to evaluate protein and mRNA expression levels of Kv12 channels. The results showed that all of the three members (Kv12.1, Kv12.2, Kv12.3) of the Kv12 channel family were expressed in NTS neurons, and their expressions were co-localized with paired-like homeobox 2b gene (Phox2b) expression. The expression of Kv12.1 mRNA was the largest, whereas the expression of Kv12.3 was the least in the NTS. The results suggest Kv12 channels are expressed in Phox2b-expressing neurons in the NTS of mice, which provides molecular evidence for pH sensitivity in Phox2b-expressing NTS neurons.

Amplified cardiorespiratory activity by hypoxia in conscious spontaneously hypertensive rats.

Activation of peripheral respiratory chemoreceptors provokes respiratory and cardiovascular reflexes, providing a novel understanding of pathogenic mechanism of hypertension. Here we hypothesize that activation of peripheral respiratory chemoreceptors by hypoxia causes enhanced cardiorespiratory activity in conscious spontaneously hypertensive rats (SHRs). Using whole body plethysmography in combination with radio telemetry, pulmonary ventilation, arterial blood pressure and heart rate were examined in SHRs and Wistar-Kyoto (WKY) rats. We found that exposure to hypoxia induced greater increases in tidal volume and minute ventilation volume in SHRs compared to WKY rats. In addition, hypoxia caused a robust increase in arterial blood pressure and heart rate in SHRs relative to WKY counterparts. After carotid body denervation, the hypoxic ventilatory response was significantly decreased in both SHRs and WKY rats, but without significant difference between the two strains; moreover, the differences of arterial blood pressure and heart rate changes during hypoxic exposure were statistically insignificant between SHRs and WKY rats. It is concluded that hypoxia remarkably potentiates cardiorespiratory activity in the SHRs, suggesting an enhanced sensitivity of carotid bodies to hypoxia.

Limb remote ischemia per-conditioning protects the heart against ischemia-reperfusion injury through the opioid system in rats.

Remote ischemia per-conditioning (RPerC) has been demonstrated to have cardiac protection, but the underlying mechanism remains unclear. This study aimed to investigate the mechanism underlying cardiac protection of RPerC. Adult male Sprague-Dawley rats were used in this study. Cardiac ischemia/reperfusion (I/R) was induced by 30 min of occlusion and 3 h of reperfusion of the left anterior descending coronary artery. RPerC were performed by 5 min of occlusion of the right femoral artery followed by 5 min of reperfusion for three times during cardiac ischemia. The hemodynamics, left ventricular function, arrhythmia, and infarct area were measured. Protein expression levels of endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), protein kinase C-ε (PKCε), and PKCδ in the myocardium were assayed. During I/R, systolic artery pressure and left ventricular function were decreased, infarct area was increased, and arrhythmia score was increased (P < 0.05). However, changes of the above parameters were significantly attenuated in RPerC-treated rats compared with control rats (P < 0.05). The cardiac protective effects of RPerC were prevented by naloxone or glibenclamide. Also, RPerC increased the protein expression levels of eNOS, iNOS, PKCε, and PKCδ in the myocardium compared with control rats. These effects were blocked by naloxone, an opioid receptor antagonist, and glibenclamide, an ATP-sensitive K+ channel blocker (KATP). In summary, this study suggests that RPerC protects the heart against I/R injury through activation of opioid receptors and the NO-PKC-KATP channel signaling pathways.

Beneficial Effects of Hypoxic Preconditioning on Human Umbilical Cord Mesenchymal Stem Cells.

As human umbilical cord mesenchymal stem cells (hUC-MSCs) transplanation may be promising in heart failure treatment, it is important to know whether hypoxic preconditioning (HP) promote hUC-MSCs proliferation and differentiation and protect them against chemical hypoxic damages. This study aimed to investigate the effects of HP on proliferation and differentiation of human umbilical cord mesenchymal stem cells (hUC-MSCs). The study also aimed to confirm our hypothesis that HP could promote hUC-MSCs proliferation and differentiation to cardiomyocyte-like cells as well as effectively protecting hUC-MSCs and cardiomyocyte-like cells against chemical hypoxic damages. Isolated hUC-MSCs were cultured in hypoxia at 1%, 3% and 5% O2 for 72 hours. 5-azacytidine (5-AZA) induced differentiation of hUC-MSCs to cardiomyocyte-like cells was determined by streptavidin-perosidase (SP) immunohistochemical staining and the content of troponin (TnI). Flow cytometry was used to measure cell cycle in hUC-MSCs and cardiomyocyte-like cells. The mitochondrial membrane potential (ΔΨ(m)) and mitochondrial Ca²âº concentration ([Ca²âº](m)), were measured in hUC-MSCs and cardiomyocyte-like cells during chemical hypoxia induced by cobalt chloride (100 µmol/L). HP optimally promoted the proliferation of hUC-MSCs at 3% O2 and enhanced the differentiation of hUC-MSCs to cardiomyocyte-like cells by 5-AZA in a concentration-dependent manner. The cell cycle distribution of cardiomyocyte-like cells, but not hUC-MSCs, was clearly changed by HP. Chemical hypoxic damage, decreased ΔΨ(m) and increased [Ca²âº](m), were alleviated significantly in HP-treated cells compared with the normaxia-treated cells. The results demonstrate that HP promoted hUC-MSCs proliferation and differentiation to cardiomyocyte-like cells, and protected both cell types against chemical hypoxic damage.

Clinical observation on removal of small foreign bodies touching the optic nerve in the deep orbital region: a case series.

PURPOSE: Five patients presented to our institution with deep intraorbital foreign bodies adjacent to the optic nerve. We removed all foreign bodies by lateral orbitotomy to evaluate the treatment and the benefits of their extraction. METHODS: The clinical outcomes of the five patients were retrospectively analyzed. RESULTS: Radiology in all five patients revealed small foreign bodies touching the optic nerve in the deep orbital region. All patients also suffered from significant secondary psychological disturbances, these including anxiety and altered sleep patterns. They had become preoccupied with a strong desire to remove the intraorbital foreign bodies [IFB]. In this cohort, two had no light perception before surgery, another two had light perception, and one had hand motion perception as well as vitreous hemorrhage that had been plugged with silicone oil in other hospital. All foreign bodies were removed via lateral orbitotomy. Visual acuity improved after the operation in only three cases. However, the psychological well-being of all five patients improved. CONCLUSIONS: Consideration should be given to removal of intraorbital foreign bodies adjacent to the optic nerve, even where a significant degree of vision has already been lost. Furthermore some patients can achieved vision improvement and such surgery can frequently address the significant psychological disturbance that can be associated with such orbital foreign bodies.

[Clinical analysis for the treatment of 63 cases of orbital tumors in Xinjiang].

OBJECTIVE: To analyse the clinical features, histopathological classifications, treatments and prognosis of orbital tumors in Xinjiang. METHODS: The authors retrospectively analyse 63 patients (64 eyes) with orbital tumors, including all nationalities which had been received and treated in ophthalmic department of the PLA 474th Hospital during 2005 to 2009. RESULTS: The nationality composition in our cases was 37 Han, 16 Uygur (16 eyes), 4 Hui, 3 Mongol, and 3 Kazak. Our data mainly consisted of benign tumor., in which, the majority were the vascular tumors, and then were cysts, inflammatory pseudotumor, neurogenic tumors, mixed tumors of lacrimal gland, lipoma and hydatid. The malignant tumors mainly consisted of rhabdomyosarcoma and adenocarcinoma of lacrimal gland, then was non-Hodgkin lymphoma. The operation methods we selected were approaching by orbital skin or anterior skin incision, lateral orbitotomy and approaching by outer canthus incision plus lower fornical conjunctiva incision. The severe postoperative complication was impaired vision, and 2 patients with inflammatory pseudotumor had recrudesced. CONCLUSIONS: There is no difference on the types and morbidity situation of orbital tumors between Xinjiang and other areas in general, in addition orbital hydatid which was closely related to regional characteristic of Xinjiang, Surgical excision is the main and effective treatment, the prognosis is related to the local tissue extension of tumor, comprehensive pre-operation preparations, careful operation, appropriate post-operative managements and rich clinic experience of doctor.

Suture clamping of intraocular lenses without a scleral flap: A new implantation method for patients with an aphakic capsule.

We aim to describe a technique for intraocular lens (IOL) implantation with suture clamping for aphakic capsules. This prospective, noncomparative, interventional case study included three eyes of three patients with an aphakic capsule after vitrectomy, in which the IOL was clamped by suturing. The suturing procedure was transconjunctival or subconjunctival performed without scleral flaps. The IOLs were implanted without difficulty, and visual acuity improved after IOL implantation. There were no severe complications, and the position of each IOL remained correct through 18 months of follow-up. The present technique is straightforward and effective in the treatment of eyes with an aphakic capsule.

Choroidal metastatic mucinous abscess caused by Pseudomonas aeruginosa: A case report.

BACKGROUND: Pseudomonas aeruginosa (P. aeruginosa) is considered a common pathogenic bacterium. Choroidal metastatic mucinous abscess caused by P. aeruginosa is rarely reported. CASE SUMMARY: We describe the diagnostic and treatment processes of a case involving a complex choroidal space-occupying lesion. Our analyses of early clinical manifestations revealed a high possibility of choroidal melanoma, as indicated by the choroidal space-occupying lesion and uveitis. Further magnetic resonance imaging results revealed no positive evidence for the diagnosis of choroidal melanoma. The exact properties of the space-occupying lesion could not be ascertained prior to surgery. However, the lesion was subsequently confirmed as a metastatic abscess by diagnostic vitrectomy. The occupying lesion was found to occupy 75% of the vitreous cavity in the surgery. The entire white viscous tissue was completely removed, and the necrotic retina was cleaned up. After surgery, microbiological culture revealed mucoid P. aeruginosa, which was sensitive to a variety of antibiotics. The bacterial infection grew and disseminated towards the outside of the eye. After the fifth injection, the left eye was successfully retained. CONCLUSION: This is a peculiar case because a huge, local, space-occupying lesion had formed due to the dissemination of low-toxic mucinous P. aeruginosa in the blood from the lungs to the choroid. After surgical removal, the bacteria were able to re-grow; thus, local infection re-spread following surgery. The patient lost vision, but we managed to retain the full structure of the eyeball and eliminated the focus of infection.

CIHH protects the heart against left ventricular remodelling and myocardial fibrosis by balancing the renin-angiotensin system in SHR.

AIM: The aim of our study was to clarify the cardioprotection of chronic intermittent hypobaric hypoxia (CIHH) and the underlying mechanism in spontaneously hypertensive rats (SHR). MAIN METHODS: Adult male rats were divided into normal blood pressure Wistar-Kyoto rats (WKY) control (WKY-CON), WKY rats with CIHH treatment (WKY-CIHH), SHR control (SHR-CON) and SHR with CIHH treatment (SHR-CIHH) groups. SHR-CIHH and WKY-CIHH rats were subjected to hypobaric hypoxia simulating 4000-m altitude for 35 days, 5 h per day. Arterial blood pressure and cardiac function parameters, including ejection fraction, fractional shortening and left ventricular (LV) wall thickness, were evaluated. Cardiac pathomorphology and myocardial fibrosis were determined. The expression of angiotensin-converting enzyme (ACE), ACE2, Ang II, Ang1-7, AT1 receptor, Mas receptor, IL-6, TNF-α，IL-10, SOD and MDA were assayed in myocardium. KEY FINDINGS: CIHH significantly decreased arterial blood pressure, alleviated LV hypertrophy, and improved cardiovascular function in SHR (P < 0.05-0.01). Also, CIHH protected SHR heart against morphological changes and fibrosis. In addition, CIHH significantly down-regulated the ACE/Ang II/AT1 receptor axis and up-regulated the ACE2/Ang1-7/Mas axis of renin-angiotensin system (RAS) in SHR (P < 0.05-0.01). CIHH significantly reduced IL-6, TNF-α, and MDA levels, but increased IL-10 and SOD in SHR myocardium (P < 0.05-0.01). SIGNIFICANCE: The CIHH treatment protected the heart of SHR against LV remodelling and myocardial fibrosis, which might be carried out through a balance in the ACE/Ang II/AT1 axis and the ACE2/Ang1-7/Mas axis of the RAS to reduce inflammation, and inhibit oxidative stress.

Elevated expression of the leptin receptor ob­R may contribute to inflammation in patients with ulcerative colitis.

The effect of leptin on ulcerative colitis (UC) has been controversial. The present study aimed to investigate the role of leptin and its receptor ob­R in UC and the underlying mechanism of this role. The level of serum leptin and the protein expression of the leptin receptor ob­R in the colonic mucosa were determined in patients with UC. Experimental colitis was induced through intrarectal administration of 2,4,6­trinitrobenzene sulfonic acid (TNBS) in leptin receptor­deficient Zucker rats (LR­D). The body weight, disease activity index, colon length, and macroscopic and histopathological appearance were evaluated. Furthermore, the myeloperoxidase (MPO) enzyme activity and cytokine levels in colon tissues were also determined. The expression of the signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3 (p­STAT3), nuclear factor (NF)­κB­p65, and Ras homolog gene family member A (RhoA) proteins in colon tissues was assessed. The results revealed that the expression of the leptin receptor ob­R was increased in the colonic mucosa but the serum leptin level was not altered in patients with UC compared with healthy volunteers. The severity of experimental colitis, represented by body weight loss, disease activity index, colon length, and macroscopic and histological changes, was ameliorated in LR­D rats compared with the wild­type (WT) rats. Moreover, the MPO activity; levels of cytokines including interleukin (IL)­1ß, IL­6, and tumor necrosis factor­α; and expression of p­STAT3, NF­κB, and RhoA proteins were reduced in colon tissues of LR­D rats compared with WT rats. In conclusion, activation of the leptin receptor ob­R is an important pathogenic mechanism of UC, and leptin receptor deficiency may provide resistance against TNBS­induced colitis by inhibiting the NF­κB and RhoA signaling pathways.

Chronic Intermittent Hypobaric Hypoxia Ameliorates Renal Vascular Hypertension Through Up-regulating NOS in Nucleus Tractus Solitarii.

Chronic intermittent hypobaric hypoxia (CIHH) is known to have an anti-hypertensive effect, which might be related to modulation of the baroreflex in rats with renal vascular hypertension (RVH). In this study, RVH was induced by the 2-kidney-1-clip method (2K1C) in adult male Sprague-Dawley rats. The rats were then treated with hypobaric hypoxia simulating 5000 m altitude for 6 h/day for 28 days. The arterial blood pressure (ABP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were measured before and after microinjection of L-arginine into the nucleus tractus solitarii (NTS) in anesthetized rats. Evoked excitatory postsynaptic currents (eEPSCs) and spontaneous EPSCs (sEPSCs) were recorded in anterogradely-labeled NTS neurons receiving baroreceptor afferents. We measured the protein expression of neuronal nitric oxide synthase (nNOS) and endothelial NOS (eNOS) in the NTS. The results showed that the ABP in RVH rats was significantly lower after CIHH treatment. The inhibition of ABP, HR, and RSNA induced by L-arginine was less in RVH rats than in sham rats, and greater in the CIHH-treated RVH rats than the untreated RVH rats. The eEPSC amplitude in NTS neurons receiving baroreceptor afferents was lower in the RVH rats than in the sham rats and recovered after CIHH. The protein expression of nNOS and eNOS in the NTS was lower in the RVH rats than in the sham rats and this decrease was reversed by CIHH. In short, CIHH treatment decreases ABP in RVH rats via up-regulating NOS expression in the NTS.

Chronic intermittent hypobaric hypoxia attenuates skeletal muscle ischemia-reperfusion injury in mice.

AIM: The aim of this study was to investigate the protective effect of chronic intermittent hypobaric hypoxia (CIHH) against skeletal muscle ischemia-reperfusion (IR) injury and to determine the underlying mechanism. MAIN METHODS: C57BL/6 mice were randomly divided into 3 groups: skeletal muscle IR injury group (IR), CIHH pretreatment following IR group (IR + CIHH), and sham operation group (Sham). The skeletal muscle IR injury model was induced by the unilateral application of a tourniquet on a hind limb for 3 h and then releasing it for 24 h. CIHH pretreatment simulating a 5000-m altitude was applied 6 h per day for 28 days. The functional and morphological performance of IR-injured gastrocnemius muscle was evaluated using contraction force, H&E staining, and transmission electron microscopy. IR injury-induced CD68+ macrophage infiltration was assessed by immunofluorescence. TNFα levels in serum and muscle were measured by ELISA and western blotting, respectively. Apoptosis was examined by TUNEL staining and Cleaved Caspase-3 protein expression. KEY FINDINGS: Acute IR injury resulted in reduced contraction tension, morphological destruction, macrophage infiltration, increased TNFα levels, and apoptosis in gastrocnemius muscle. CIHH pretreatment significantly ameliorated contraction function and morphological performance in IR-injured skeletal muscle. In addition, CIHH pretreatment resulted in marked decreases in CD68+ macrophage infiltration, TNFα levels, and apoptosis. SIGNIFICANCE: These data demonstrated that CIHH has a protective effect against acute IR injury in skeletal muscle via inhibition of inflammation and apoptosis.

Chronic intermittent hypobaric hypoxia protects vascular endothelium by ameliorating autophagy in metabolic syndrome rats.

AIMS: The study aimed to investigate the protective effect of chronic intermittent hypobaric hypoxia (CIHH) on endothelium function and relaxation of mesenteric artery in metabolism syndrome (MS) rats. MAIN METHODS: Male adult Sprague-Dawley rats were randomly divided into control (CON), CIHH (treated with 28-days hypobaric hypoxia simulating an altitude of 5000 m, 6 h daily), MS (induced by high fat diet and 10% fructose water feeding), and MS + CIHH groups. Body weight, systolic arterial pressure, blood biochemical and the endothelium dependent relaxation (EDR) of mesenteric arteries were measured. The expression of phosphor-endothelial nitric oxide synthase (p-eNOS), endoplasmic reticulum (ER) stress-related proteins and autophagy-related proteins in mesenteric arteries was assayed. KEY FINDINGS: The MS rats displayed hypertension, obesity, metabolic abnormity and insulin resistance, EDR was attenuated, p-eNOS expression was down-regulated, the expressions of ER stress-related proteins were up-regulated, and autophagy dysfunction occurred. All aforementioned abnormalities in MS rats were ameliorated in MS + CIHH rats. Furthermore, the improvement of CIHH on EDR and p-eNOS was cancelled by the ER stress inducer, and the autophagy inhibitor. SIGNIFICANCE: In conclusion CIHH protects endothelium function and enhances relaxation in mesenteric arteries of MS rats through improving autophagy function, reducing ER stress and up-regulating p-eNOS.

Chronic intermittent hypobaric hypoxia ameliorates diabetic nephropathy through enhancing HIF1 signaling in rats.

AIM: Our previous study demonstrated that chronic intermittent hypobaric hypoxia (CIHH) had anti-diabetes effect. The present study was to explore the renal protective effect of CIHH in diabetic rats. METHODS: Sprague-Dawley rats were randomly divided into three groups: diabetes mellitus group (DM, induced by high-fat diet combined with low-dose streptozotocin), diabetes plus CIHH treatment group (DM+CIHH, simulated 5000-m altitude, 6h per day for 28days, after diabetes model confirmed) and control group (CON). Systolic arterial blood pressure (SAP), blood biochemicals, urinary albumin, and histopathology of kidney were determined. The superoxide dismutase (SOD) activity, malondialdehyde (MDA) level, protein levels of hypoxia induced factors (HIFs) and transforming growth factor ß1 (TGF-ß1) in kidney were assayed. RESULTS: The increased SAP, urinary albumin, hyperplasia of glomerular, fibrosis in mesangial and glomerular, and abnormal lipid metabolism in diabetic rats were ameliorated by CIHH treatment. And decreased superoxide dismutase (SOD) activity and increased malondialdehyde (MDA) level in diabetic kidney were reversed in CIHH-treated DM rats. In addition up-regulated TGF-ß1 and down-regulated HIF1α in diabetic kidney returned back to normal level in CIHH-treated DM rats. CONCLUSIONS: These data demonstrated for the first time that CIHH had protective effects against the early stage damage of diabetic nephropathy through activating HIF1 signaling, improving anti-oxidation and inhibiting TGF-ß1 signaling in diabetic rats.

Anti-diabetes effect of chronic intermittent hypobaric hypoxia through improving liver insulin resistance in diabetic rats.

AIM: Cumulating evidence demonstrated that chronic intermittent hypobaric hypoxia (CIHH) had beneficial effects on the body. The present study was to investigate the anti-diabetes effect of CIHH in type-2 diabetic rats for the first time. MAIN METHODS: Sprague-Dawley rats were randomly divided into 4 groups: control group (CON), diabetes mellitus group (DM, induced by high-fat diet combined with low-dose streptozotocin), CIHH treatment group (CIHH, simulated 5000-m altitude, 6h per day for 28 days), and diabetes mellitus plus CIHH treatment group (DM+CIHH). Histopathology of liver, systolic arterial blood pressure (SAP), blood biochemicals, glucose and insulin tolerance were determined. The expression of proteins associated with insulin signaling pathway as well as hypoxia induced factors were assayed. KEY FINDINGS: Diabetic rats showed impaired glucose tolerance, dyslipidemia, hepatic steatosis and hepatic insulin resistance in addition to increased SAP. However, SAP, serum triglyceride and cholesterol were decreased, and hepatic steatosis and insulin resistance were improved in DM+CIHH rats. Furthermore, the protein expression of glucokinase (GCK), insulin receptor substrates (IRS-1 and IRS-2), and HIF1α were increased, while the expression of phosphoenolpyruvate carboxykinase (PEPCK), was markedly reduced in DM+CIHH rats. SIGNIFICANCE: We conclude that CIHH treatment has anti-diabetes effects through ameliorating insulin resistance via hepatic HIF-insulin signaling pathway in type-2 diabetic rats.

Chronic intermittent hypobaric hypoxia antagonizes renal vascular hypertension by enhancement of vasorelaxation via activating BKCa.

AIM: The purpose of the present study was to explore anti-hypertensive effect of chronic intermittent hypobaric hypoxia (CIHH) in renovascular hypertension (RVH) rats, as well as the role of large-conductance calcium-activated potassium channel (BKCa) in anti-hypertensive effect of CIHH. MAIN METHODS: Male adult age- and body weight-matched Sprague-Dawley rats were divided into SHAM, CIHH, RVH and RVH+CIHH groups. Hypertension was induced by two-kidney-1-clip method (2K1C) in RVH rats. CIHH rats were exposed to 28-days hypobaric hypoxia simulating 5000m altitude, 6h daily. SHAM rats got an operation without 2K1C, and RVH+CIHH rats received CIHH treatment after 2K1C. The endothelium-dependent vasorelaxation induced by acetylcholine (ACh), BKCa currents in smooth muscle cells (VSMCs) of mesenteric arteries and the protein expression of BKCa in mesenteric arteries was examined. KEY FINDINGS: The systolic arterial blood pressure (SAP) in RVH rats was higher than that in SHAM rats and CIHH treatment significantly decreased SAP in RVH rats. The enhanced vasorelaxation of mesenteric artery in CIHH-treated RVH rats was cancelled by BKCa blocker IBTX. The vasorelaxation induced by BKCa activator was reduced in RVH rats and the decreased vasorelaxation was improved by CIHH treatment. The ß1 subunit of BKCa in mesenteric artery was upregulated and BKCa current in VSMCs was increased in CIHH-treated RVH rats compared with RVH rats. SIGNIFICANCE: In conclusion, CIHH treatment enhances the relaxation of mesenteric artery through activation of BKCavia up-regulating ß1 subunit of BKCa, which might be one of mechanisms for anti-hypertensive effect of CIHH in RVH rats.

Adhesion of cavernous hemangioma in the orbit revealed by CT and MRI: analysis of 97 cases.

AIM: To assess features of cavernous hemangioma (CH) in the orbit revealed by CT and MRI and summarize prediction of preoperative CT and MRI for the adhesion degree of CH in the orbit. METHODS: A total of 97 patients with pathologically confirmed CH in the orbit were examined with axial and coronal CT scan, and axial, coronal, sagittal, and enhanced fat suppression MRI scan. CT and MRI findings and intraoperative adhesion degrees were retrospectively analyzed. RESULTS: There were 47 patients with slight adhesion, for whom CT and MRI showed round masses with well defined margins in the extraocular muscles; 14 patients with mild adhesion, for whom CT and MRI revealed irregular masses with unclear boundary between CH and the optic nerve in coronal images, and emissary veins in the posterior region of masses in contrast-enhanced images; 36 patients with severe adhesion, for whom CT and MRI exhibited an irregular or ovoid mass filling the orbital apex, or showed distorted and even spiky margins in the posterior region of masses in contrast enhanced images at the presence of a transparent triangle between the mass and the orbital apex. CONCLUSION: Preoperative CT and MRI aid in accurate diagnosis, selection of the surgical approach, and assessment of the adhesion degree and surgical risks for CH.