Right ventricular pressure load in pigs: Progressive loss of contractility W/O ischemia and downregulation of Ca2+ handling proteins
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Contractility
Ventricular pressure
Abstract Background To understand the relationship between myocardial contractility and external stimuli, detecting ex vivo myocardial contractility is necessary. Methods We elaborated a method for contractility detection of isolated C57 mouse papillary muscle using Myostation‐Intact system under different frequencies, voltages, and calcium concentrations. Results The results indicated that the basal contractility of the papillary muscle was 0.27 ± 0.03 mN at 10 V, 500‐ms pulse duration, and 1 Hz. From 0.1 to 1.0 Hz, contractility decreased with an increase in frequency (0.45 ± 0.11–0.10 ± 0.02 mN). The voltage‐initiated muscle contractility varied from 3 to 6 V, and the contractility gradually increased as the voltage increased from 6 to 10 V (0.14 ± 0.02–0.28 ± 0.03 mN). Moreover, the muscle contractility increased when the calcium concentration was increased from 1.5 to 3 mM (0.45 ± 0.17–1.11 ± 0.05 mN); however, the contractility stopped increasing even when the concentration was increased to 7.5 mM (1.02 ± 0.23 mN). Conclusions Our method guaranteed the survivability of papillary muscle ex vivo and provided instructions for Myostation‐Intact users for isolated muscle contractility investigations.
Contractility
Papillary muscle
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The mechanical and metabolic effects of 3 min of complete global ischemia and 25 min of reperfusion were studied in the isolated rat heart. The decrease in contracile function was biphasic; a rapid 50% decline occurred in the first 10 s of ischemia, after which contractile function transiently stabilized and then fell at a slower rate. During reperfusion, recovery of relaxation was impaired relative to recovery of contractile function. A second period of ischemia and reflow produced changes in contractility, relaxation, and lactate production virtually identical to the initial one. In the absence of glycolytic blockade, tissue lactate accumulation developed, no contracture occurred, the pacing threshold did not increase, and reperfusion after 3 min of ischemia resulted in complete recovery of contractile function. Glycolytic blockade with 0.1 mM iodoacetate (IAA) prevented ischemic lactate production, accelerated the fall in contractility, caused irreversible contracture after 30 s of ischemia, an irreversible increase in pacing threshold within 3 min of ischemia, and poor recovery of contractile function with reperfusion. Thus during the first 3 min of severe ischemia, glycolysis exerted a net beneficial effect on myocardial function despite significant tissue lactate accumulation.
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This is a report on ventricular contractility and electrogenesis disorders in rabbits, following intravenous injection of E. coli endotoxin at a dose of 2 mg.kg-1. At the 30th min, the right ventricular contractility indices (dP/dtmax)/P and [(dP/dt)/P]max had lower values, whereas end diastolic pressure (EDP), right ventricular systolic pressure (RVSP) and P(dP/dtmax) showed higher values compared to the initial ones. Most of the left ventricular contractility indices tested showed significantly lower values at the 30th and 60th min of the registration. In the scalar orthogonal ECG leads, at the 5th min an increased Qz amplitude, and at the 60th min an increased Rz amplitude, a decreased Ry amplitude, and QRS complex widening and bradicardia, were registered. In the spatial magnitude curve an increased amplitude of the main vectors of ventricular depolarization was documented. The changes in electrogenesis are interpreted first and foremost by the presence of hemodynamic disorders. The inference is reached that both left and right ventricular dysfunction have been already formed during the initial stage of endotoxin shock.
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Maternal viral infection is known to increase the risk for schizophrenia and autism in their offspring (Brown et al, 2004). C57BL/6 mice were infected with human influenza virus on day E18 of pregnancy and brains were collected at PN days 0, 14, or 56, from virally-exposed (N=3) or sham-infected control's (N=3) offspring. Microarray analysis of virally-exposed mouse brains showed significant (p<0.05) upregulation of 15 genes and downregulation of 3 genes in cerebellum, upregulation of 42 genes and downregulation of 9 genes in hippocampus, and upregulation of 4 genes and downregulation of 5 genes in prefrontal cortex vs. controls in day 0 mice. At day 14, there was a significant upregulation of 2 genes and downregulation of 0 genes in cerebellum, upregulation of 1 gene and downregulation of 1 gene in hippocampus, and upregulation of 3 genes and downregulation of 3 genes in prefrontal cortex vs. controls. At day 56, there was a significant upregulation of 13 genes and downregulation of 2 genes in cerebellum, upregulation of 4 genes and downregulation of 3 genes in hippocampus, and upregulation of 4 genes and downregulation of 1 gene in prefrontal cortex vs. controls. Implications of changes in brain genes for development of abnormal brain structure and function will be discussed. The generous support by the National Institute for Child Health and Human Development (1-R01-HD046589-01A2) to S.H.F. is greatly appreciated.
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Aim This study aims to observe the protective effect of Yixinyin on myocardial ischemia-reperfusion injuries in isolated working hearts of tats.Method 36 rats were randomly divided into three groups:Yixinyin group 1 (K-H fluid contain 0.01g·ml~(-1) Yixinyin ),Yixinyin group 2 (K-H fluid contain 0.1g·ml~(-1) Yixinyin) and control group.Myocardial founction was investigated by left ventricular systolic pressure (LVSP),rising and descending rate of left ventricular pressure (±dp/dt(max)),left ventricular end diastolic pressure (LVEDP),heart rate;tissue levels of malondialdehyde(MDA)as well as activity of super oxide demitasse(SOD) were measured in order to evaluate the changes of oxygen free radical metabolism; electron microscope and light microscope were performed to investigate the impairment of myocardial structure and Ca~(2+) distribution.Results Myocardial dynamics and homodynamic indexes LVSP and ±dp/dt(max) were improved siganificantly in Yixinyin group2;the content of MDA in Yixinyin group 2 was obviously lower than that in control group(P0.05). Yixinyin reduced abnormal of Myocardial structure and Ca~(2+) distribution by comparison with other groups.Conclusion Yixinyin have protective effects against the injury of myocardial ischemia-reperfusion.The effects increase when concentration of Yixinyin increased.
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Malondialdehyde
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Pressure overload
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Peak values of the normalized first and second derivatives of left ventricular pressure, which are measured during the isovolumic contraction period, have been shown to be useful measures for assessing myocardial contractility. These indices were readily obtained from high speed pressure tracings by means of a fiberoptic pressure catheter which has an unusually high frequency response and low noise level.
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Ventricular pressure
Isovolumetric contraction
Aortic pressure
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Cancer cells differ from normal cells in both gain of functions (i.e., upregulation) and loss of functions (i.e., downregulation). While it is common to suppress gain of function for chemotherapy, it remains challenging to target downregulation in cancer cells. Here we show the combination of enzyme-instructed assembly and disassembly to target downregulation in cancer cells by designing peptidic precursors as the substrates of both carboxylesterases (CESs) and alkaline phosphatases (ALPs). The precursors turn into self-assembling molecules to form nanofibrils upon dephosphorylation by ALP, but CES-catalyzed cleavage of the ester bond on the molecules results in disassembly of the nanofibrils. The precursors selectively inhibit the cancer cells that downregulate CES (e.g., OVSAHO) but are innocuous to a hepatocyte that overexpresses CES (HepG2), while the two cell lines exhibit comparable ALP activities. This work illustrates a potential approach for the development of chemotherapy via targeting downregulation (or loss of functions) in cancer cells.
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To study the correlation between quantity of the connexin43 express and ischemia time in rabbit.Left coronary arteries were ligated to create early myocardial ischemia during distinct time, HBFP staining was used in the ischemia spot and SP method was used to show the expression of connexin43 and the ischemia are were measured by the computer image analysis.Negative correlation was observed between the connexin43 quantity and the ischemia time. The significant was difference.With ischemia time raised, expression of connexin43 was descented.
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