共查询到20条相似文献,搜索用时 31 毫秒
1.
P. Hakim N. Brice R. Thresher J. Lawrence Y. Zhang A. P. Jackson A. A. Grace C. L.-H. Huang 《Acta physiologica (Oxford, England)》2010,198(1):47-59
Aim: In contrast to extensive reports on the roles of Nav1.5 α-subunits, there have been few studies associating the β-subunits with cardiac arrhythmogenesis. We investigated the sino-atrial and conduction properties in the hearts of Scn3b−/− mice. Methods: The following properties were compared in the hearts of wild-type (WT) and Scn3b−/− mice: (1) mRNA expression levels of Scn3b, Scn1b and Scn5a in atrial tissue. (2) Expression of the β3 protein in isolated cardiac myocytes. (3) Electrocardiographic recordings in intact anaesthetized preparations. (4) Bipolar electrogram recordings from the atria of spontaneously beating and electrically stimulated Langendorff-perfused hearts. Results: Scn3b mRNA was expressed in the atria of WT but not Scn3b−/− hearts. This was in contrast to similar expression levels of Scn1b and Scn5a mRNA. Immunofluorescence experiments confirmed that the β3 protein was expressed in WT and absent in Scn3b−/− cardiac myocytes. Lead I electrocardiograms from Scn3b−/− mice showed slower heart rates, longer P wave durations and prolonged PR intervals than WT hearts. Spontaneously beating Langendorff-perfused Scn3b−/− hearts demonstrated both abnormal atrial electrophysiological properties and evidence of partial or complete dissociation of atrial and ventricular activity. Atrial burst pacing protocols induced atrial tachycardia and fibrillation in all Scn3b−/− but hardly any WT hearts. Scn3b−/− hearts also demonstrated significantly longer sinus node recovery times than WT hearts. Conclusion: These findings demonstrate, for the first time, that a deficiency in Scn3b results in significant atrial electrophysiological and intracardiac conduction abnormalities, complementing the changes in ventricular electrophysiology reported on an earlier occasion. 相似文献
2.
Elizabeth Nance Siva P. Kambhampati Elizabeth S. Smith Zhi Zhang Fan Zhang Sarabdeep Singh Michael V. Johnston Rangaramanujam M. Kannan Sujatha Kannan 《Journal of neuroinflammation》2017,14(1):252
Background
Rett syndrome (RTT) is a pervasive developmental disorder that is progressive and has no effective cure. Immune dysregulation, oxidative stress, and excess glutamate in the brain mediated by glial dysfunction have been implicated in the pathogenesis and worsening of symptoms of RTT. In this study, we investigated a new nanotherapeutic approach to target glia for attenuation of brain inflammation/injury both in vitro and in vivo using a Mecp2-null mouse model of Rett syndrome.Methods
To determine whether inflammation and immune dysregulation were potential targets for dendrimer-based therapeutics in RTT, we assessed the immune response of primary glial cells from Mecp2-null and wild-type (WT) mice to LPS. Using dendrimers that intrinsically target activated microglia and astrocytes, we studied N-acetyl cysteine (NAC) and dendrimer-conjugated N-acetyl cysteine (D-NAC) effects on inflammatory cytokines by PCR and multiplex assay in WT vs Mecp2-null glia. Since the cysteine-glutamate antiporter (Xc?) is upregulated in Mecp2-null glia when compared to WT, the role of Xc? in the uptake of NAC and l-cysteine into the cell was compared to that of D-NAC using BV2 cells in vitro. We then assessed the ability of D-NAC given systemically twice weekly to Mecp2-null mice to improve behavioral phenotype and lifespan.Results
We demonstrated that the mixed glia derived from Mecp2-null mice have an exaggerated inflammatory and oxidative stress response to LPS stimulation when compared to WT glia. Expression of Xc? was significantly upregulated in the Mecp2-null glia when compared to WT and was further increased in the presence of LPS stimulation. Unlike NAC, D-NAC bypasses the Xc? for cell uptake, increasing intracellular GSH levels while preventing extracellular glutamate release and excitotoxicity. Systemically administered dendrimers were localized in microglia in Mecp2-null mice, but not in age-matched WT littermates. Treatment with D-NAC significantly improved behavioral outcomes in Mecp2-null mice, but not survival.Conclusions
These results suggest that delivery of drugs using dendrimer nanodevices offers a potential strategy for targeting glia and modulating oxidative stress and immune responses in RTT.3.
A. Schmiedl P. A. Schnabel K. Marten H. Kausch Blecken von Schmeling J. Richter 《Medical Electron Microscopy》1999,32(3):151-160
4.
Purpose
Despite the fact that desflurane prolongs the QTC interval in humans, little is known about the mechanisms that underlie these actions. We investigated the effects of desflurane on action potential (AP) duration and underlying electrophysiological mechanisms in rat ventricular myocytes.Materials and Methods
Rat ventricular myocytes were enzymatically isolated and studied at room temperature. AP was measured using a current clamp technique. The effects of 6% (0.78 mM) and 12% (1.23 mM) desflurane on transient outward K+ current (Ito), sustained outward current (Isus), inward rectifier K+ current (IKI), and L-type Ca2+ current were determined using a whole cell voltage clamp.Results
Desflurane prolonged AP duration, while the amplitude and resting membrane potential remained unchanged. Desflurane at 0.78 mM and 1.23 mM significantly reduced the peak Ito by 20±8% and 32±7%, respectively, at +60 mV. Desflurane (1.23 mM) shifted the steady-state inactivation curve in a hyperpolarizing direction and accelerated inactivation of the current. While desflurane (1.23 mM) had no effects on Isus and IKI, it reduced the L-type Ca2+ current by 40±6% (p<0.05).Conclusion
Clinically relevant concentrations of desflurane appear to prolong AP duration by suppressing Ito in rat ventricular myocytes. 相似文献5.
Aims
The effects of T helper (Th) cells on alcoholic cardiomyopathy have not been extensively investigated. Strain of mice with Th1 or Th2 immunological background were utilized in this study in order to explore the role of Th1/Th2 in chronic alcohol-induced cardiac fibrosis.Methods and results
C57BL/6 WT or Balb/c mice were treated with alcohol for 90 days. Then cardiac structure and function were analyzed via echocardiography. Spleen CD4 + CD25 + Foxp3+ Tregs were determined by flow cytometry. The hearts were stained using haematoxylin and eosin (HE) and Masson's trichome. Myocardial ultrastructure was observed by electron microscopy. Expression of T-bet, GATA-3, IL-4 and IFN-gamma were determined by real-time RT-PCR. The heart was dilated significantly in the C57BL/6 WT + alcohol group and Balb/c + alcohol group compared with the controls. CD4 + CD25 + Foxp3+ Tregs were not statistically different. Masson's trichome staining revealed that fibrosis was more pronounced in the alcohol treated groups than the controls. Fibrosis was more evident in the Balb/c + alcohol group compared to the C57BL/6 WT + alcohol group. Alcohol consumption caused a decrease in the Th1 poalrization and an increase in the Th2 response.Conclusions
Chronic alcohol consumption induced a Th2 response within the Th1/Th2 balance. Th2 response is one of the underlying mechanism involved in alcohol-induced cardiac fibrosis. 相似文献6.
Jake Thompson Fabian Mendoza Ethan Tan Jessica Wildgrube Bertol Arju S Gaggar Goo Jun Claudia Biguetti Walid D. Fakhouri 《Developmental dynamics》2019,248(3):221-232
Background: Interferon regulatory factor 6 (IRF6) plays a critical role in embryonic tissue development, including differentiation of epithelial cells. Besides orofacial clefting due to haploinsufficiency of IRF6, recent human genetic studies indicated that mutations in IRF6 are linked to small mandible and digit abnormalities. The function of IRF6 has been well studied in oral epithelium; however, its role in craniofacial skeletal formation remains unknown. In this study, we investigated the role of Irf6 in craniofacial bone development using comparative analyses between wild-type (WT) and Irf6-null littermate mice. Results: Immunostaining revealed the expression of IRF6 in hypertrophic chondrocytes, osteocytes, and bone matrix of craniofacial tissues. Histological analysis of Irf6-null mice showed a remarkable reduction in the number of lacunae, embedded osteocytes in matrices, and a reduction in mineralization during bone formation. These abnormalities may explain the decreased craniofacial bone density detected by micro-CT, loss of incisors, and mandibular bone abnormality of Irf6-null mice. To validate the autonomous role of IRF6 in bone, extracted primary osteoblasts from calvarial bone of WT and Irf6-null pups showed no effect on osteoblastic viability and proliferation. However, a reduction in mineralization was detected in Irf6-null cells. Conclusions: Altogether, these findings suggest an autonomous role of Irf6 in regulating bone differentiation and mineralization. Developmental Dynamics 248:221-232, 2019. © 2019 Wiley Periodicals, Inc. 相似文献
7.
Marina Miletic Kovacevic Nada Pejnovic Slobodanka Mitrovic Nemanja Jovicic Ivica Petrovic Nebojsa Arsenijevic Miodrag L. Lukic Biljana Ljujic 《Immunologic research》2018,66(4):491-502
Experimental autoimmune myocarditis (EAM) is a mouse model of immune-mediated myocarditis and cardiomyopathy. The role of Galectin-3 (Gal-3), a β-galactoside-binding lectin, in autoimmune myocarditis has not been studied. Therefore, the aim of this study was to delineate the role of Gal-3 in myosin peptide-induced autoimmune myocarditis in mice. EAM was induced in relatively resistant C57BL/6J mice (wild type, WT) and in mice with a targeted deletion of Gal-3 gene (Gal-3KO) by immunization with myosin peptide MyHCα334–352. Gal-3KO mice developed more severe myocarditis and more pronounced heart hypertrophy than WT mice. Increased infiltration of CD45+ leucocytes, CD3+ T cells, F4/80+ macrophages, and eosinophils was observed in hearts of Gal-3KO mice compared to WT mice on day 21 after EAM induction. Moreover, hearts of Gal-3KO mice had more T helper type 2 (Th2) cells, alternatively activated M2 macrophages, higher amounts of IgG deposits, and higher serum levels of IL-4 and IL-33 than WT mice. Ablation of Gal-3 in Th1-dominant C57BL/6J mice that are relatively resistant to EAM resulted in more severe disease characterized by type 2 cardiac inflammation. The complex effects of Gal-3 on EAM progression might be important in the consideration of therapeutic options for the treatment of EAM. 相似文献
8.
Heart sensitivity to electrolyte composition of perfusion solution of rats after severe brain injury
The in vitro model of isovolumic beating heart revealed enhanced sensitivity of the hearts from rats survived severe brain injury to concentration
of Ca2+, Na+, and H+ ions in the perfusion solution. Inhibition of myocardial contractile function after trauma was accompanied by destruction
signs in cardiomyocyte sarcolemma and mitochondrial dysfunction.
__________
Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 141, No. 6, pp. 639–642, June, 2006 相似文献
9.
Laila Guzadhur Sarah M. Pearcey Rudolf M. Duehmke Kamalan Jeevaratnam Anja F. Hohmann Yanmin Zhang Andrew A. Grace Ming Lei Christopher L.-H. Huang 《Pflügers Archiv : European journal of physiology》2010,460(3):593-601
Recent studies have reported that human mutations in Nav1.5 predispose to early age onset atrial arrhythmia. The present experiments accordingly assess atrial arrhythmogenicity in aging Scn5a+/?KPQ mice modeling long QT3 syndrome in relationship to cardiac Na+ channel, Nav1.5, expression. Atrial electrophysiological properties in isolated Langendorff-perfused hearts from 3- and 12-month-old wild type (WT), and Scn5a+/?KPQ mice were assessed using programmed electrical stimulation and their Nav1.5 expression assessed by Western blot. Cardiac conduction properties were assessed electrocardiographically in intact anesthetized animals. Monophasic action potential recordings demonstrated increased atrial arrhythmogenicity specifically in aged Scn5a+/ΔKPQ hearts. These showed greater action potential duration/refractory period ratios but lower atrial Nav1.5 expression levels than aged WT mice. Atrial Nav1.5 levels were higher in young Scn5a+/ΔKPQ than young WT. These levels increased with age in WT but not Scn5a+/ΔKPQ. Both young and aged Scn5a+/ΔKPQ mice showed lower heart rates and longer PR intervals than their WT counterparts. Young Scn5a+/ΔKPQ mice showed longer QT and QTc intervals than young WT. Aged Scn5a+/ΔKPQ showed longer QRS durations than aged WT. PR intervals were prolonged and QT intervals were shortened in young relative to aged WT. In contrast, ECG parameters were similar between young and aged Scn5a+/ΔKPQ. Aged murine Scn5a+/ΔKPQ hearts thus exhibit an increased atrial arrhythmogenicity. The differing Nav1.5 expression and electrocardiographic indicators of slowed cardiac conduction between Scn5a+/ΔKPQ and WT, which show further variations associated with aging, may contribute toward atrial arrhythmia in aged Scn5a+/ΔKPQ hearts. 相似文献
10.
Increased Ca2+ sensitivity and protein expression of SERCA 2a in situations of chronic β3-adrenoceptor deficiency 总被引:1,自引:1,他引:0
Ziskoven C Grafweg S Bölck B Wiesner RJ Jimenez M Giacobino JP Bloch W Schwinger RH Brixius K 《Pflügers Archiv : European journal of physiology》2007,453(4):443-453
This study investigated the influence of chronic β3-adrenoceptor deficiency on myocardial function. Therefore, we investigated Ca2+-regulatory proteins, SERCA 2a activity, and myofibrillar and mitochondrial function in hearts of wild-type (WT, n=7) and β3-adrenoceptor knockout mice (β3-KNO, n=7). Morphometric heart analysis showed no difference between WT and β3-KNO. No alterations were observed for the protein expression of the ryanodine receptor or phospholamban. However, in β3-KNO mice, protein expression of SERCA 2a and phospholamban phosphorylation were significantly increased. These changes were
accompanied by an increased SERCA 2a activity in β3-KNO. Alterations in phospholamban phosphorylation were independent of alterations in β1/β2-adrenoceptor distribution and protein expression of G proteins in β3-KNO. Measurement of myofibrillar Ca2+ sensitivity showed no difference in the Ca2+/force relation for WT and β3-KNO. The same seems to hold true for mitochondrial function since the protein expressions of cytochrome c, uncoupling protein 3 and cytochrome c oxidase subunit IV were similar in WT and β3-KNO. The conclusion is that depression of β3-adrenergic stimulation may modulate the protein expression of SERCA 2a and phospholamban phosphorylation, thereby improving
sarcoplasmic reticulum Ca2+ uptake. Thus, β3-adrenergic depression may be a therapeutic aim in situations of impaired SERCA 2a activity, e.g. for the treatment of heart
failure. 相似文献
11.
12.
Recruitment of macrophages and polymorphonuclear leukocytes in L:yme carditis 总被引:1,自引:0,他引:1
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Montgomery RR Booth CJ Wang X Blaho VA Malawista SE Brown CR 《Infection and immunity》2007,75(2):613-620
Lyme arthritis, caused by the spirochete Borrelia burgdorferi, can be recurrent or prolonged, whereas Lyme carditis is mostly nonrecurring. A prominent difference between arthritis and carditis is the differential representation of phagocytes in these lesions: polymorphonuclear leukocytes (PMN) are more prevalent in the joint, and macrophages predominate in the heart lesion. We have previously shown differential efficiency of B. burgdorferi clearance by PMN and macrophages, and we now investigate whether these functional differences at the cellular level may contribute to the observed differences in organ-specific pathogenesis. When we infected mice lacking the neutrophil chemokine receptor (CXCR2−/− mice) with spirochetes, we detected fewer PMN in joints and less-severe arthritis. Here we have investigated the effects of the absence of the macrophage chemokine receptor CCR2 on the development and resolution of Lyme carditis in resistant (C57BL/6J [B6]) and sensitive (C3H/HeJ [C3H]) strains of mice. In B6 CCR2−/− mice, although inflammation in hearts is mild, we detected an increased burden of B. burgdorferi compared to that in wild-type (WT) mice, suggesting reduced clearance in the absence of macrophages. In contrast, C3H CCR2−/− mice have severe inflammation but a decreased B. burgdorferi burden compared to that in WT C3H mice both at peak disease and during resolution. Histopathologic examination of infected hearts revealed that infected C3H CCR2−/− animals have an increased presence of PMN, suggesting compensatory mechanisms of B. burgdorferi clearance in the hearts of infected C3H CCR2−/− mice. The more efficient clearance of B. burgdorferi from hearts by CCR2−/− versus WT C3H mice suggests a natural defect in the recruitment or function of macrophages in C3H mice, which may contribute to the sensitivity of this strain to B. burgdorferi infection. 相似文献
13.
14.
To test the hypothesis that ablation of transient receptor potential vanilloid type 1 (TRPV1) channels leads to exacerbated inflammatory responses and organ damage during endotoxic shock, lipopolysaccharide (LPS; 5 million endotoxin units/kg of body weight) was injected intraperitoneally (i.p.) into wild-type (WT) and TRPV1-null mutant (TRPV1−/−) mice. Mean arterial pressure and heart rate, determined by radiotelemetry, were severely depressed after LPS injection into WT and TRPV1−/− mice, with no distinction between the two strains. At 24 h after LPS injection, renal glomerular hypercellularity and hepatocellular injury were observed in both strains, accompanying further elevated serum levels of creatinine and alanine aminotransferase in TRPV1−/− mice compared to those in WT mice. At 6 or 24 h after LPS injection, neutrophil recruitment into kidneys and livers, serum cytokine (tumor necrosis factor alpha [TNF-α], interleukin 1β [IL-1β], IL-6) and renal chemokine (KC, macrophage inflammatory protein 2 [MIP-2]) levels, and renal VCAM-1 and ICAM-1 expression were greater in TRPV1−/− mice than WT mice. In addition, increased plasma calcitonin gene-related peptide (CGRP) levels observed in WT mice 6 h after LPS injection were absent in TRPV1−/− mice. Thus, TRPV1 ablation aggravates inflammatory responses, including neutrophil infiltration, proinflammatory cytokine production, and adhesion molecule expression, leading to intensified organ damage during endotoxic shock in the absence of worsened circulatory failure. The data indicate that TRPV1 activation may attenuate endotoxin-induced organ damage, possibly via its anti-inflammatory action rather than alteration of hemodynamics. 相似文献
15.
Howarth FC Qureshi MA Hassan Z Al Kury LT Isaev D Parekh K Yammahi SR Oz M Adrian TE Adeghate E 《Experimental physiology》2011,96(3):325-337
The association between type 2 diabetes and obesity is very strong, and cardiovascular complications are the major cause of morbidity and mortality in diabetic patients. The aim of this study was to investigate early changes in the pattern of genes encoding cardiac muscle regulatory proteins and associated changes in ventricular myocyte contraction and Ca(2+) transport in young (9- to 13-week-old) type 2 Zucker diabetic fatty (ZDF) rats. The amplitude of myocyte shortening was unaltered; however, time-to-peak shortening and time to half-relaxation of shortening were prolonged in ZDF myocytes (163 ± 5 and 127 ± 7 ms, respectively) compared with age-matched control rats (136 ± 5 and 103 ± 4 ms, respectively). The amplitude of the Ca(2+) transient was unaltered; however, time-to-peak Ca(2+) transient was prolonged in ZDF myocytes (66.9 ± 2.6 ms) compared with control myocytes (57.6 ± 2.3 ms). The L-type Ca(2+) current was reduced, and inactivation was prolonged over a range of test potentials in ZDF myocytes. At 0 mV, the density of L-type Ca(2+) current was 1.19 ± 0.28 pA pF(-1) in ZDF myocytes compared with 2.42 ± 0.40 pA pF(-1) in control myocytes. Sarcoplasmic reticulum Ca(2+) content, release and uptake and myofilament sensitivity to Ca(2+) were unaltered in ZDF myocytes compared with control myocytes. Expression of genes encoding various L-type Ca(2+) channel proteins (Cacna1c, Cacna1g, Cacna1h and Cacna2d1) and cardiac muscle proteins (Myh7) were upregulated, and genes encoding intracellular Ca(2+) transport regulatory proteins (Atp2a2 and Calm1) and some cardiac muscle proteins (Myh6, Myl2, Actc1, Tnni3, Tnn2, and Tnnc1) were downregulated in ZDF heart compared with control heart. A change in the expression of genes encoding myosin heavy chain and L-type Ca(2+) channel proteins might partly underlie alterations in the time course of contraction and Ca(2+) transients in ventricular myocytes from ZDF rats. 相似文献
16.
Hiroki Shimizu Yasushi Obase Shigeki Katoh Keiji Mouri Yoshihiro Kobashi Mikio Oka 《Inflammation research》2013,62(10):911-917
Objective and design
Asthma is associated with eosinophilic airway inflammation and characterized by enhanced airway sensitivity. Interleukin (IL)-5 plays an important role in the pathogenesis of asthma. The involvement of IL-5 receptor-mediated cellular signals in the pathogenesis of a mite antigen-induced chronic asthma model was investigated.Subjects
In this study, 48 female C57BL/6J (WT) mice and IL-5 receptor-deficient (IL-5RKO) mice were used.Treatment
Mite antigen (50 μl) was intranasally administered 13 times to WT and IL-5RKO mice.Methods
Airway hypersensitivity (Mch PC200) and specific antigen exposure tests were performed, and lung tissue, bronchoalveolar lavage fluid (BALF), and blood were collected to investigate the asthma pathology and differences in the local pulmonary levels of cytokines and chemokines.Results
Airway sensitivity was enhanced and antigen-specific airway resistance was increased in WT mice. In addition, the number of eosinophils and Th2 cytokine levels in the BALF were increased. In contrast, IL-5RKO mice did not acquire the asthma pathology, such as antigen-specific airway resistance and eosinophilic airway inflammation. Mch PC200 was significantly correlated with cysteinyl leukotriene levels in WT mice.Conclusion
These findings suggested that both IL-5 induced eosinophils and cysteinyl leukotrienes are involved in the pathology of this mite antigen-induced chronic asthma model. 相似文献17.
Komai-Koma M Brombacher F Pushparaj PN Arendse B McSharry C Alexander J Chaudhuri R Thomson NC McKenzie AN McInnes I Liew FY Xu D 《Allergy》2012,67(9):1118-1126
Background
The regulation and function of IgE in healthy individuals and in antigen‐naïve animals is not well understood. IL‐33 administration increases serum IgE in mice with unknown mechanism. We tested the hypothesis that IL‐33 provides an antigen‐independent stimulus for IgE production and mast cell degranulation.Methods
IL‐33 was administered to naïve wild‐type (WT), nude and ST2?/?, IL‐4?/?, IL4Rα?/? and T‐or B‐cell‐specific IL‐4Rα?/? mice. IgEand cytokines were quantified by ELISA. T‐ and B‐lymphocyte numbers and CD40L expression were determined by flow cytometry. Anaphylaxis was measured by temperature, mast cell degranulation and histamine release.Results
IL‐33 enhanced IgE production in naïve WT, T‐IL‐4Rα?/? but not in ST2?/?, IL‐4?/?, IL‐4Rα?/? or B‐cell‐specific IL‐4Rα?/? mice, demonstrating IL‐33 specificity and IL‐4 dependency. Moreover, IL‐4 was required for IL‐33‐induced B‐cell proliferation and T‐cell CD40L expression, which promotes IgE production. IL‐33‐induced IL‐4 production was mainly from innate cells including mast cells and eosinophils. IL‐33 increased mast cell surface IgE and triggered degranulation and systemic anaphylaxis in allergen‐naïve WT but not in IL‐4Rα?/? mice.Conclusion
IL‐33 amplifies IgE synthesis and triggers anaphylaxis in naïve mice via IL‐4, independent of allergen. IL‐33 may play an important role in nonatopic allergy and idiopathic anaphylaxis.18.
Jiqing Guo Tamotsu Mitsuiye A. Noma 《Pflügers Archiv : European journal of physiology》1997,433(4):390-396
Single myocytes were dissociated from the sino-atrial (SA) node of guinea-pig hearts. Only a quite small fraction of the
cell population showed spontaneous action potentials and these cells were characterized by the presence of the hyperpolarization-activated
cation current I
f , the delayed rectifier K+ current I
K and the L-type Ca2+ current I
Ca,L as well as by the absence of both the transient outward current I
to and the inward rectifier K+ current I
K,1. After blocking I
f and I
K, depolarizing pulses from –80 mV revealed a large nicardipine-sensitive late current (NSLC). The NSLC was scarcely affected
by decreasing extracellular [Ca2+] ([Ca2+]o) from 1.8 to 0.1 mM, while it was decreased significantly by depleting [Na+]o, differently from I
Ca,L. NSLC was blocked by nicardipine and was increased by Bay K 8644. NSLC was increased by isoprenaline and the additional application
of acetylcholine reversed the increase of this current. We conclude that NSLC is largely composed of I
st described in the rabbit SA node pacemaker cells, and that I
st is unique for the pacemaker cells in mammalian SA node cells. Most of the quiescent cells showed neither I
f nor I
st.
Received: 22 July 1996 / Received after revision: 30 September 1996 / Accepted: 9 October 1996 相似文献
19.
Alireza Garjani Arash Afrooziyan Hossein Nazemiyeh Moslem Najafi Ali Kharazmkia Nasrin Maleki-Dizaji 《BMC complementary and alternative medicine》2009,9(1):28
Background
The rhizomes of Cynodon dactylon are used for the treatment of heart failure in folk medicine. In the present study, we investigated the effects of hydroalcoholic extract of C. dactylon rhizomes on cardiac contractility in normal hearts and on cardiac functions in right-heart failure in rats. 相似文献20.
Xiaoli Zhang Eridan Rocha-Ferreira Tao Li Regina Vontell Darakhshan Jabin Sha Hua Kai Zhou Arshed Nazmi Anna-Maj Albertsson Kristina Sobotka Joakim Ek Claire Thornton Henrik Hagberg Carina Mallard Jianmei W. Leavenworth Changlian Zhu Xiaoyang Wang 《Journal of neuroinflammation》2017,14(1):255