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Effects of sea anemone toxin anthopleurin-Q on potassium currents in rats and guinea pig ventricular myocytes

Yan Huang,Yang Li,Hasimu Buaijiaer,Juan Sun,Ping Fan,Jianguo Song,Yuemei Hou,Mingjiang Li,Salim Mohamed,Emmy Okello,

老年心脏病学杂志(英文版) , 2008,
Abstract: To investigate the effect of sea anemone toxin anthopleurin-Q (AP-Q) on potassium currents in isolated rats and guinea pig ventricular myocytes.Methods The ventricular cells of guinea pigs and SD rats were obtained by enzymatic dissociation method.Whole cell patch clamp technique was used to record potassium currents (Ito,IK,and IK1).Results AP-Q 3-100 nmol/L increased Ito in a concentration-dependent manner,with an EC50 value of 12.7 nmol/L.At a potential of +50mV,AP-Q 10nmol/L increased Ito from (13.3±3.4) pA pF-1 to (19.46±4.3) pA pF-1.AP-Q 0.1-100 nmol/L increased IK and IK tail in a concentration-dependent manner with EC50 values of 4.7 nmol/L and 5.0 nmol/L,respectively.AP-Q 1 pmol/L-100 nmol/L increased IK1 in dose-dependent manner,with an EC50 of 0.2 nmol/L.Conclusions The effect of AP-Q on Ito,IK and IK1 may partly explain its mechanism in shortening APD and increasing RP.(J Geriatr Cardiol 2008;5:243-247)
Comparative Electropharmacological Actions of Some Constituents from Ginkgo biloba Extract in Guinea-pig Ventricular Cardiomyocytes  [PDF]
Hiroyasu Satoh
Evidence-Based Complementary and Alternative Medicine , 2004, DOI: 10.1093/ecam/neh044
Abstract: Effects of the constituents from Ginkgo biloba extract (GBE) on the action potentials and the ionic currents in guinea pig ventricular cardiomyocytes were investigated using whole-cell and current-clamp techniques. The constituents, ginkgolides A, B, C and quercetin, had depressant effects at 0.1–3μM on the action potential configuration. Ginkgolide A (1–3?μM) prolonged the action potential (action potential duration: APD) at 75% and 90% repolarizations (APD75 and APD90). However, ginkgolides B and C at low concentrations prolonged APD, but at higher concentrations (>1?μM) shortened APD. Quercetin at 3?μM prolonged the APD, but not at the lower concentrations. These constituents also inhibited the Vmax. The resting potential was unaffected. In voltage-clamp experiments, ginkgolides A and B (0.1–3?μM) markedly and concentration-dependently increased the Ca2
Resveratrol Attenuates the Na+-Dependent Intracellular Ca2+ Overload by Inhibiting H2O2-Induced Increase in Late Sodium Current in Ventricular Myocytes  [PDF]
Chunping Qian, Jihua Ma, Peihua Zhang, Antao Luo, Chao Wang, Zhiqiang Ren, Linghao Kong, Shuo Zhang, Xiaojing Wang, Ying Wu
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0051358
Abstract: Background/Aims Resveratrol has been demonstrated to be protective in the cardiovascular system. The aim of this study was to assess the effects of resveratrol on hydrogen peroxide (H2O2)-induced increase in late sodium current (INa.L) which augmented the reverse Na+-Ca2+ exchanger current (INCX), and the diastolic intracellular Ca2+ concentration in ventricular myocytes. Methods INa.L, INCX, L-type Ca2+ current (ICa.L) and intracellular Ca2+ properties were determined using whole-cell patch-clamp techniques and dual-excitation fluorescence photomultiplier system (IonOptix), respectively, in rabbit ventricular myocytes. Results Resveratrol (10, 20, 40 and 80 μM) decreased INa.L in myocytes both in the absence and presence of H2O2 (300 μM) in a concentration dependent manner. Ranolazine (3–9 μM) and tetrodotoxin (TTX, 4 μM), INa.L inhibitors, decreased INa.L in cardiomyocytes in the presence of 300 μM H2O2. H2O2 (300 μM) increased the reverse INCX and this increase was significantly attenuated by either 20 μM resveratrol or 4 μM ranolazine or 4 μM TTX. In addition, 10 μM resveratrol and 2 μM TTX significantly depressed the increase by 150 μM H2O2 of the diastolic intracellular Ca2+ fura-2 fluorescence intensity (FFI), fura-fluorescence intensity change (△FFI), maximal velocity of intracellular Ca2+ transient rise and decay. As expected, 2 μM TTX had no effect on ICa.L. Conclusion Resveratrol protects the cardiomyocytes by inhibiting the H2O2-induced augmentation of INa.L.and may contribute to the reduction of ischemia-induced lethal arrhythmias.
Causes of Abnormal Ca2+ Transients in Guinea Pig Pathophysiological Ventricular Muscle Revealed by Ca2+ and Action Potential Imaging at Cellular Level  [PDF]
Hiroto Nishizawa, Takeshi Suzuki, Takao Shioya, Yuji Nakazato, Hiroyuki Daida, Nagomi Kurebayashi
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0007069
Abstract: Background Abnormal Ca2+ transients are often observed in heart muscles under a variety of pathophysiological conditions including ventricular tachycardia. To clarify whether these abnormal Ca2+ transients can be attributed to abnormal action potential generation or abnormal Ca2+ handling/excitation-contraction (EC) coupling, we developed a procedure to determine Ca2+ and action potential signals at the cellular level in isolated heart tissues. Methodology/Principal Findings After loading ventricular papillary muscle with rhod-2 and di-4-ANEPPS, mono-wavelength fluorescence images from rhod-2 and ratiometric images of two wavelengths of emission from di-4-ANEPPS were sequentially obtained. To mimic the ventricular tachycardia, the ventricular muscles were field-stimulated in non-flowing Krebs solution which elicited abnormal Ca2+ transients. For the failed and alternating Ca2+ transient generation, there were two types of causes, i.e., failed or abnormal action potential generation and abnormal EC coupling. In cells showing delayed initiation of Ca2+ transients with field stimulation, action potential onset was delayed and the rate of rise was slower than in healthy cells. Similar delayed onset was also observed in the presence of heptanol, an inhibitor of gap junction channels but having a non-specific channel blocking effect. A Na+ channel blocker, on the other hand, reduced the rate of rise of the action potentials but did not result in desynchronization of the action potentials. The delayed onset of action potentials can be explained primarily by impaired gap junctions and partly by Na+ channel inactivation. Conclusions/Significance Our results indicate that there are multiple patterns for the causes of abnormal Ca2+ signals and that our methods are useful for investigating the physiology and pathophysiology of heart muscle.
Dynamic Changes in Sarcoplasmic Reticulum Structure in Ventricular Myocytes
Amanda L. Vega,Can Yuan,V. Scott Votaw,Luis F. Santana
Journal of Biomedicine and Biotechnology , 2011, DOI: 10.1155/2011/382586
Abstract: The fidelity of excitation-contraction (EC) coupling in ventricular myocytes is remarkable, with each action potential evoking a [Ca2
Severe allergic reactions to guinea pig
Michael C Zacharisen, Michael B Levy, Jeffrey L Shaw, Viswanath P Kurup
Clinical and Molecular Allergy , 2005, DOI: 10.1186/1476-7961-3-14
Abstract: We report two patients with severe allergic reactions following non-occupational exposure to guinea pigs. The first patient, an 11-year-old female, developed ocular, nasal, skin and laryngeal edema symptoms immediately after handling a guinea pig. The second patient, a 24-year-old female, developed symptoms of isolated laryngeal edema after cleaning a guinea pig cage. Percutaneous skin testing, RAST, ELISA and ELISA inhibition testing with guinea pig extract were performed.Both patients had IgE-mediated allergy to guinea pig confirmed by ELISA and either RAST or skin testing. ELISA inhibition studies confirmed the specificity of the IgE reactivity to guinea pig.Severe IgE-mediated reactions can occur following non-occupational guinea pig exposure. Physicians should be aware of this possibility.Guinea pigs are popular household pets and also used in laboratory research. Allergic symptoms including rhinitis, conjunctivitis, and asthma have been documented in laboratory animal workers exposed to guinea pigs [1-5]. An extensive review of the literature revealed no reports of severe allergic reactions resulting from guinea pig exposure. We report two patients with severe allergic reactions following direct exposure to guinea pigs in domestic settings.An 11-year-old female with a history of migraine headaches and exercise-induced asthma (EIA) was evaluated in the Allergy clinic two months after experiencing symptoms while holding a guinea pig at her hairdresser's home. This was the only episode of symptoms associated with guinea pig exposure; she had handled the pet previously without exhibiting symptoms. Within minutes of holding the guinea pig, she developed ocular itching, lacrimation, and periorbital angioedema. Symptoms rapidly progressed to facial urticaria and angioedema, rhinorrhea, throat tightness, and dyspnea. She had difficulty speaking, repeatedly attempted to clear her throat, and expressed feelings of impending doom. There was no coughing or audible wheezin
Increased Response to β2-Adrenoreceptor Stimulation Augments Inhibition of IKr in Heart Failure Ventricular Myocytes  [PDF]
Hegui Wang, Yanhong Chen, Hongjun Zhu, Sen Wang, Xiwen Zhang, Dongjie Xu, Kejiang Cao, Jiangang Zou
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0046186
Abstract: Background Increasing evidence indicates that the rapid component of delayed rectifier potassium current (IKr) is modulated by α- and β-adrenergic stimulation. However, the role and mechanism regulating IKr through β2-adrenoreceptor (β-AR) stimulation in heart failure (HF) are unclear. Methodology/Principal Findings In the present study, we investigated the effects of fenoterol, a highly selective β2-AR agonist, on IKr in left ventricular myocytes obtained from control and guinea pigs with HF induced by descending aortic banding. IKr was measured by using whole cell patch clamp technique. In control myocytes, superfusion of fenoterol (10 μM) caused a 17% decrease in IKr. In HF myocytes, the same concentration of fenoterol produced a significantly greater decrease (33%) in IKr. These effects were not modified by the incubation of myocytes with CGP-20712A, a β1-AR antagonist, but were abolished by pretreatment of myocytes with ICI-118551, a β2-AR antagonist. An inhibitory cAMP analog, Rp-cAMPS and PKA inhibitor significantly attenuated fenoterol-induced inhibition of IKr in HF myocytes. Moreover, fenoterol markedly prolonged action potential durations at 90% (APD90) repolarization in HF ventricular myocytes. Conclusions The results indicate that inhibition of IKr induced by β2-AR stimulation is increased in HF. The inhibitory effect is likely to be mediated through a cAMP/PKA pathway in HF ventricular myocytes.
Immunoglobulin Genomics in the Guinea Pig (Cavia porcellus)  [PDF]
Yongchen Guo, Yonghua Bao, Qingwen Meng, Xiaoxiang Hu, Qingyong Meng, Liming Ren, Ning Li, Yaofeng Zhao
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0039298
Abstract: In science, the guinea pig is known as one of the gold standards for modeling human disease. It is especially important as a molecular and cellular biology model for studying the human immune system, as its immunological genes are more similar to human genes than are those of mice. The utility of the guinea pig as a model organism can be further enhanced by further characterization of the genes encoding components of the immune system. Here, we report the genomic organization of the guinea pig immunoglobulin (Ig) heavy and light chain genes. The guinea pig IgH locus is located in genomic scaffolds 54 and 75, and spans approximately 6,480 kb. 507 VH segments (94 potentially functional genes and 413 pseudogenes), 41 DH segments, six JH segments, four constant region genes (μ, γ, ε, and α), and one reverse δ remnant fragment were identified within the two scaffolds. Many VH pseudogenes were found within the guinea pig, and likely constituted a potential donor pool for gene conversion during evolution. The Igκ locus mapped to a 4,029 kb region of scaffold 37 and 24 is composed of 349 Vκ (111 potentially functional genes and 238 pseudogenes), three Jκ and one Cκ genes. The Igλ locus spans 1,642 kb in scaffold 4 and consists of 142 Vλ (58 potentially functional genes and 84 pseudogenes) and 11 Jλ -Cλ clusters. Phylogenetic analysis suggested the guinea pig’s large germline VH gene segments appear to form limited gene families. Therefore, this species may generate antibody diversity via a gene conversion-like mechanism associated with its pseudogene reserves.
Characterization of the Receptors for Mycobacterial Cord Factor in Guinea Pig  [PDF]
Kenji Toyonaga, Yasunobu Miyake, Sho Yamasaki
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0088747
Abstract: Guinea pig is a widely used animal for research and development of tuberculosis vaccines, since its pathological disease process is similar to that present in humans. We have previously reported that two C-type lectin receptors, Mincle (macrophage inducible C-type lectin, also called Clec4e) and MCL (macrophage C-type lectin, also called Clec4d), recognize the mycobacterial cord factor, trehalose-6,6′-dimycolate (TDM). Here, we characterized the function of the guinea pig homologue of Mincle (gpMincle) and MCL (gpMCL). gpMincle directly bound to TDM and transduced an activating signal through ITAM-bearing adaptor molecule, FcRγ. Whereas, gpMCL lacked C-terminus and failed to bind to TDM. mRNA expression of gpMincle was detected in the spleen, lymph nodes and peritoneal macrophages and it was strongly up-regulated upon stimulation of zymosan and TDM. The surface expression of gpMincle was detected on activated macrophages by a newly established monoclonal antibody that also possesses a blocking activity. This antibody potently suppressed TNF production in BCG-infected macrophages. Collectively, gpMincle is the TDM receptor in the guinea pig and TDM-Mincle axis is involved in host immune responses against mycobacteria.
Helminths of the guinea pig, Cavia porcellus (Linnaeus), in Brazil
Pinto, Roberto Magalh?es;Gomes, Delir Corrêa;Muniz-Pereira, Luís C.;Noronha, Dely;
Revista Brasileira de Zoologia , 2002, DOI: 10.1590/S0101-81752002000500020
Abstract: worm burdens were evaluated and compared in two groups of the guinea pig, cavia poreellus (linnaeus, 1758): animals of the first group were conventionally maintained in an institutional animal house and those of the second group were openly kept in pet shops in brazil. animals from both sources were infected only with the nematode paraspidodera uncinata (rudolphi, 1819) travassos, 1914 (10% of prevalence in guinea pigs from lhe institutional facility and 40% in those animals from the pet shop). other helminth samples recovered from brazilian guinea pigs during 52 years and that are deposited in the helminthological collection of the oswaldo cruz institute (chioc) were also analyzed. paraspidodera uncinata and the cestode monoecocestus parcitesticulatus rêgo, 1960 were identified in these samples.
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