Dietary fatty acid composition changes mitochondrial phospholipids and oxidative capacities in rainbow trout red muscle

Dietary conditioning of juvenile trout changed the acyl chain composition of mitochondrial phospholipids and the oxidative capacities of muscle mitochondria. Trout were fed three diets differing only in fatty acid (FA) composition. The highly unsaturated 22:6 n-3 (DHA) accounted for 0.4, 14, and 30% of fatty acids in Diets 1, 2 and 3. After 10 weeks of growth, the dietary groups differed markedly in FA composition of mitochondrial phospholipids, with significant dietary effects for virtually all FA. Mean mitochondrial DHA levels were 19, 40 and 33% in trout fed Diets 1, 2 and 3. Mitochondrial oxidative capacities changed with diet, while mitochondrial concentrations of cytochromes and of the adenylate nucleotide translocase (nmol mg¹ protein) did not. Mitochondria from fish fed Diet 1 had higher non-phosphorylating (state 4) rates at 5°C than those fed other diets. When phosphorylating (state 3) rates differed between dietary groups, rates at 5 and 15°C were higher for fish fed the more unsaturated diets. Stepwise multiple regressions indicated that FA composition could explain much (42–70%) of the variability of state 4 rates, particularly at 5°C. At 15°C, FA composition explained 16–42% of the variability of states 3 and 4 rates. Similar conclusions were obtained for the complete data set (trout fed diets 1, 2 and 3) and for the data from trout achieving similar growth rates (e.g. those fed Diets 1 and 2). Neither general characteristics of membrane FA, such as % saturates, unsaturation index, n-3, n-6 or n-3/n-6 nor levels of abundant unsaturated FA such as DHA or 18:1(n-9 + n-7), were systematically correlated with mitochondrial capacities even though they differed considerably between trout fed the different diets. Relatively minor FA (20:5n-3, 20:0, 18:2n-6, 18:3n-3, 18:0 and 15:0) showed better correlations with mitochondrial oxidative capacities. This supports the concept that acyl chain composition modulates mitochondrial capacities via interactions between membrane proteins and specific FA of particular phospholipid classes in their microenvironment.     

Dual chamber pacing in a patient of hypertrophic cardiomyopathy with failure to wean from mechanical ventilator

We discuss the case of a 63 years old female who required repeated intubation due to recurrent pulmonary edema. She was found to have hypertrophic cardiomyopathy with a gradient of 82 mmHg across the left ventricular outflow tract. Initially adequate rate control and treatment with negative inotropes did not help her condition. Finally a dual chamber pacemaker implantation and atrioventricular node modification lead to successful extubation.     

永久起搏器程控在心房颤动诊断中的临床应用及意义

摘要 目的：探究永久起搏器程控在心房颤动诊断中的临床应用及意义。方法：选择78例我院收治的心房颤动患者随机分为程控组和非程控组2组,其中观察组患者给与永久起搏器程控诊断,非程控组则仅给植入永久起搏器,但非程控。对比分析两组患者基本资料、房颤负荷、心房与心室起搏比、心房结构重构及左心功能、P波结果;比较永久起搏器程控诊断与临床诊断结果的差异,分析永久起搏器程控在心房颤动诊断敏感度。结果：程控组和非程控组患者的男女比例、年龄、心率失常的类型、存在的基础性疾病以及使用过的治疗药物比较,差异均无统计学意义（P>0.05）;程控组和非程控组患者的房颤负荷、VP值和P波最小时限均显著小于非程控组,AP值、P波最大时限和P波离散度则显著大于非程控组（P<0.05）;程控组和非程控组患者的LAD、RAD、LVEDD和LVEF值在植入前和植入后均不存在显著性差异（P>0.05）。与临床诊断结果比较可以发现,永久起搏器程控对心房颤动检出率为97.44 %,且永久起搏器程控应用于诊断心房颤动敏感度高达98.72 %。结论：对心房颤动患者采用永久起搏器程控进行诊断,可以在心电图检查的各项指标结果上对患者的心房颤动给与准确的判断,具有较高的临床应用价值,值得临床推广使用。     

“缺血”心肌起搏离子流If的观察研究

本文观察“缺血”及肾上腺素能激动剂对绵羊心室浦肯野纤维起搏离子流Ｉｆ的影响。用模拟缺血溶液灌流１５,３０和６０ｍｉｎ后,在Ｅｃ—６０ｍＶ—１２０ｍＶ之间的各不同指令电位水平Ｉｆ离子流幅值均降低（ｎ＝７,Ｐ＜０．０５）,激活达稳态时间及半激活时间延长（ｎ＝７,Ｐ＜Ｏ．０５）,激活曲线向超极化方向移位。１×１０－６ｍｏｌ／Ｌ异丙基肾上腺素能使Ｉｆ离子流幅值增加（ｎ＝１０,Ｐ＞０．０５）,激活达稳态时间及半激活时间缩短（ｎ＝１０,Ｐ＜０．０５）,激活曲线向除极化方向移位,但不能完全逆转“缺血”对Ｉｆ离子流的抑制作用。在５×１０－７ｍｏｌ／Ｌ普萘洛尔存在条件下,５×１０－５ｍｏｌ／Ｌ新福林对正常绵羊心室浦肯野纤维Ｉｆ离子流影响不一致,但可加剧“缺血”对Ｉｆ离子流的抑制作用。上述结果表明：急性心肌缺血时,心室浦肯野纤维正常起搏活动不是增强,而是减弱。提示急性缺血性室性心律失常不是由于心室正常自律活动异常增强引起。     

Combined effects of octopamine and filling pressure on the isolated heart of the lobster,Panulirus japonicus

Summary The effects of octopamine (OA) on the isolated and pumping heart of Panulirus japonicus were investigated. Under low filling pressure, OA (10^-7-10^-5 M) decreased the heart rate and enhanced the first systolic contraction (FSC) while reducing the second systolic contraction (SSC). The decrease in heart rate was transient whereas the enhancement of the FSC continued for 10 min or more after washout of OA. Pressure and OA synergistically intensified the FSC and reduced the SSC. The effect of OA on heart rate changed from a deceleration to an acceleration as the pressure was raised. Octopamine decreased both the firing frequency and the burst rate of the small cardiac neurons in a dose-dependent manner. In contrast, the amine often induced a slow ramp potential in the large cardiac neurons and increased their burst rate. Octopamine had no effect on the excitatory junction potentials evoked in cardiac muscle cells. Contraction and closure of the posterior cardioarterial valve were induced by OA, resulting in rebound internal heart pressure and stretching of the heart. The stretch augmented the heart rate and the FSC. The inhibition of small cardiac neurons by OA was related to the reduction of the heart rate and the SSC. The activation of large cardiac neurons and of cardiac and valve muscles by OA augmented the heart rate and the FSC. These multiple actions on the perfused heart lead to abolition of the SSC. After abolition of the SSC, increases of pressure can rapidly raise the heart rate.Abbreviations EJP excitatory junction potential - FLP first large potential - FSC first systolic contraction - OA octopamine - SLP second large potential - SSC second systolic contraction     

Leadless pacing in a young patient with cardioinhibitory vasovagal syncope

Vasovagal syncope is characterized by vasodilatation and/or bradycardia and thereby a fall in arterial BP and global cerebral perfusion in response to a trigger. Although it is a benign condition, patients with frequent and traumatic episodes need treatment in order to improve quality of life. We describe the case of a 17-years-old boy suffering from cardioinhibitory syncope. At the end of a complete negative cardiac and neurological examination, a loop recorder was implanted. During the subsequent follow-up the ILR documented a 9-s pause. To improve the patient's compliance, and considering cardioinhibitory syncope as a temporary condition, a leadless pacemaker was eventually implanted.     

溶血磷脂酰胆碱对缺血条件下羊浦肯野纤维If电流的影响

本文用双微电极电压箝制术观察“缺血”及毒性代谢产物溶血磷脂酸胆碱（LPC）对绵羊心室浦肯野纤维起搏离子流If的影响。用模拟缺血溶液灌流15,30和60min后,在一60mV～120mV之间的各不同指令电位水平If离子流幅值均降低（n=5,P＜0．05）,激活达稳态时间及半激活时间延长（n=5,P＜0．05）,稳态激活曲线向超极化方向移位。在正常台氏液中加入2×10-5mol/LIPC,灌流后,各个膜电位水平的浦氏纤维起搏离子流If的幅值显著降低（n=10,P＜0.05）,稳态激活曲线向超极化方向移位,但If激活达稳态时间及半激活时间均无明显改变。在模拟缺血溶液灌流30min基础上,再加2×10－5mol／LLPC灌流,15min后测得If幅值进一步减小（n=10,P＜0．05）,加剧了“缺血”对If离子流的抑制作用。上述结果表明：缺血代谢产物溶血磷脂酸胆碱对心室的正常自律活动具有抑制作用,在模拟缺血条件下,它能使已受抑制的自律活动抑制进一步加深。因此它的存在不会异常增强心室自律性活动而发生快速性室性心律失常。     

Implication of the nucleus in excitation contraction coupling of heart cells

In the present study, Fluo-3 Ca²⁺ measurement and confocal microscopy techniques were used in order to localize cytosolic [ ]_c and nuclear [ ]_n free Ca²⁺ distribution in resting and spontaneously contracting single heart cells from 10-day-old chick embryos. In resting single cells, the concentration of Ca²⁺ in the cytoplasm was lower than that in the nucleus. Increasing cytosolic free Ca²⁺ from 100–1600 nM gradually increased [Ca²⁺]_n with a maximum capacity near 1200 nM. Results from Fura-2 microfluorometry and Fluo-3 confocal microscopy suggest a potential cross talk between the increase of cytosolic free Ca²⁺ and the uptake and release of Ca²⁺ by the nucleus during spontaneous contraction of single myocytes. Calcium waves in spontaneously contracting cells were found to spread from one cell to the next with the nucleus acting as a fluorescent beacon in which Ca²⁺ levels remained elevated for several milliseconds even after cytosolic Ca²⁺ had returned to near basal values. These results strongly suggest that the nucleus plays a negative and positive feedback role in controlling cytosolic free Ca²⁺ concentration during excitation-contraction coupling in heart cells.     

Comparison of steady-state electrophysiological properties of isolated cells from bullfrog atrium and sinus venous

Summary Single electrode whole cell voltage-clamp experiments and frequency domain analyses have been used to study and compare the K⁺ currents in enzymatically dispersed single cells from the atrium and the sinus venosus (pacemaker region) of the bullfrog heart. Admittance measurements made near the resting or zero-current potential yield data from which the equivalent circuit of each cell type may be obtained. Data from both atrial and pacemaker cells are well-fitted by a model consisting only of parallel resistance-capacitative elements, as predicted from their micro-anatomy. Neither of these amphibian cardiac cells contain a transverse tubule system (TT) and both have very little sarcoplasmic reticulum (SR). These results complement and extend two earlier investigations: (i) Moore, Schmid and Isenberg (J. Membrane Biol. 81:29–40, 1984) have reported that in guinea pig ventricle cells (whichdo contain an internal membrane system consisting of transverse tubules and a substantial SR) the SR may be electrically coupled to the sarcolemma; (ii) Shibata and Giles (Biophys. J. 45:136a, 1984) have shown that although bullfrog atrial cells have an inwardly rectifying back-ground K⁺ current, , pacemaker cells from the immediately adjacent sinus venosus do not. Data from admittance measurements also provide evidence that a TTX-insensitive inward Ca²⁺ current is activated in the pacemaker range of potentials.     

Membrane and calcium clock mechanisms contribute variably as a function of temperature to setting cardiac pacemaker rate in zebrafish Danio rerio

Here, we show that heart rate in zebrafish Danio rerio is dependent upon two pacemaking mechanisms and it possesses a limited ability to reset the cardiac pacemaker with temperature acclimation. Electrocardiogram recordings, taken from individual, anaesthetised zebrafish that had been acclimated to 18, 23 or 28°C were used to follow the response of maximum heart rate (f_Hmax) to acute warming from 18°C until signs of cardiac failure appeared (up to c. 40°C). Because f_Hmax was similar across the acclimation groups at almost all equivalent test temperatures, warm acclimation was limited to one significant effect, the 23°C acclimated zebrafish had a significantly higher (21%) peak f_Hmax and reached a higher (3°C) test temperature than the 18°C acclimated zebrafish. Using zatebradine to block the membrane hyperpolarisation-activated cyclic nucleotide–gated channels (HCN) and examine the contribution of the membrane clock mechanisms to cardiac pacemaking, f _Hmax was significantly reduced (by at least 40%) at all acute test temperatures and significantly more so at most test temperatures for zebrafish acclimated to 28°C vs. 23°C. Thus, HCN channels and the membrane clock were not only important, but could be modified by thermal acclimation. Using a combination of ryanodine (to block sarcoplasmic calcium release) and thapsigargin (to block sarcoplasmic calcium reuptake) to examine the contribution of sarcoplasmic reticular handling of calcium and the calcium clock, f _Hmax was again consistently reduced independent of the test temperature and acclimation temperature, but to a significantly lesser degree than zatebradine for zebrafish acclimated to both 28 and 18°C. Thus, the calcium clock mechanism plays an additional role in setting pacemaker activity that was independent of temperature. In conclusion, the zebrafish cardiac pacemaker has a limited temperature acclimation ability compared with known effects for other fishes and involves two pacemaking mechanisms, one of which was independent of temperature.