Since it has been suggested that atrial receptor may be involved in the mechanism of extracellular volume regulation, it was shown that the granularity of atrial cardiocytes can be changed by water and salt depletion, and that an extract of cardiac atrial tissue, when injected intravenously into anesthetized rats, was shown to cause a large and rapid increase in renal excretion of sodium. Various natriuretic peptides were isolated and synthetized, and the effects were investigated by many workers. Most studies, however, have been carried out under anesthesia and there have teen some controversies over direct effect of the factor on the renal function. Therefore, it was attempted in this study to access the effects of an atrial extract and a synthetic natriuretic factor in unanesthetized rabbits. Intrarenal arterial infusion of atrial extract caused a rapid increase of urinary volume and excretion of sodium. Glomerular filtration rate and renal plasma flow were both increased with no change in filtration fraction. The ventricular extract produced no change in urinary excretion of electrolytes, nor in renal hemodynamics. Intrarenal infusion of synthetic atrial natriuretic factor caused increases of renal excretory rate of sodium, chloride and potassium, and $FE_{Na}$. Glomerular filtration rate, renal plasma flow increased. And free water clearance also increased. Accentuated excretory function correlated well with increased glomerular filtration rate and renal plasma flow during infusion and for 10 minutes following the cessation of the infusion. Renin secretion rate decreased during constant infusion of atrial natriuretic factor. However, no correlation was found with the changes in glomerular filtration rate, renal plasma flow, or urinary excretion of sodium. These results suggest that atrial extract or atrial natriuretic factor induces changes in renal hemodynamics, as in excretion of electrolytes either indirectly through hemodynamic changes or directly by inhibiting tubular reabsorption. At the same time, renin secretory function is affected by the factor possibly through an unknown mechanism.
Effects of synthetic atrial natriuretic peptide and furosemide on the cardiovascular and renal functions were examined in the freshwater turtle, Amyda japonica. Both atria and ventricle of turtle contained an immunoreactive atrial natriuretic peptide. Synthetic rat atrial natriuretic peptide (atriopeptin III) and turtle atrial extract caused a decrease in mean arterial blood pressure and the vasodepressor effect was dose-dependent. In hydrated turtles received either atriopeptin III or turtle atrial extract, no significant change in renal function was observed until 100 min except a slight natriuresis at 60 or 100 min after injection of 30 ug/kg atriopeptin III or atrial extract, respectively. However, furosemide, 2 mg/kg, caused marked diuresis, natriuresis and kaliuresis. In non-hydrated turtles, no significant change in renal function was observed until 6 hrs following injection of 30 ug/kg atriopeptin III. Plasma aldosterone decreased at 2 hr and increased at 24 hr after injection of atriopeptin III although plasma renin concentration did not change. But, furosemide caused persistent diuresis, natriuresis and kaliuresis. Additionally, plasma aldosterone and renin concentrations were significantly increased at 24 hrs after injection of furosemide. In conclusion, we suggest that the freshwater turtle may have an atrial natriuretic peptide in heart and vascular receptors for atrial natriuretic peptide, and that atrial natriuretic peptide is more important in the regulation of blood pressure rather than that of renal function in freshwater turtles. We also suggest that an increased plasma renin concentration caused by furosemide may not be due to the sodium concentration delivered to macula densa, but due to the dehydration caused by persistent diuresis and natriuresis.
Atrial fibrillation is the most common of all cardiac arrhythmias. It is associated with significant morbidity and mortality and is frequently resistant to medical therapy. On the experimental and clinical study, the presence of macroreentrant circuits and the absence of either microreentrant circuits or evidence of atrial automaticity suggests that atrial fibrillation should be amenable to surgical ablation. The results of the maze III procedure are associated with a higher incidence of postoperative sinus rhythm, improved long-term sinus node function, fewer pacemaker requirements, less arrhythmia recurrence, and improved long-term atrial transport function. We had experienced 4 patients with chronic atrial fibrillation. For the first time, Hioki procedure had been performed in the first patient with ASD and atrial fibrillation, regular sinus rhythm showed on postoperative EKG, but junctional rhythm and bradycardia developed postoperative 3 years. The maze III procedure for the rest with mitral valvular disease and atrial fibrillation had been done, followed by regular sinus rhythm for 2 patients and atrial fibrillation for 1 patient, managed with amiodarone, on immediate postoperative state. Echocardiogram documented good contraction of right atrium and hardly contraction of left atrium for 2 patients with regular sinus rhythm postoperative 3 months.
The aim of this study was to explore the role of IL-6-miR-210 in the regulation of Tregs function and atrial fibrosis in atrial fibrillation (AF). The levels of interleukin (IL)-6 and IL-10 in AF patients were detected by using ELISA. Proportions of Treg cells were detected by fluorescence activated cell sorting analysis in AF patients. The expression of Foxp3, α-SMA, collagen I and collagen III were determined by western blot. The atrial mechanocytes were authenticated by vimentin immunostaining. The expression of miR-210 was performed by quantitative real-time polymerase chain reaction (qRT-PCR). TargetScan was used to predict potential targets of miR-210. The cardiomyocyte transverse sections in AF model group were observed by H&E staining. The myocardial filaments were observed by masson staining. The level of IL-6 was highly increased while the level of IL-10 (Tregs) was significantly decreased in AF patients as compared to normal control subjects, and IL-6 suppressed Tregs function and promoted the expression of α-SMA, collagen I and collagen III. Furthermore, miR-210 regulated Tregs function by targeting Foxp3, and IL-6 promoted expression of miR-210 via regulating hypoxia inducible factor-1α (HIF-1α). IL-6-miR-210 suppresses regulatory T cell function and promotes atrial fibrosis by targeting Foxp3.
Since the atrial receptor was suggested to be involved in the control of extracellular fluid volume, it has been shown that the granularity of atrial cardiocytes can be changed by water and salt depletion, and that an extract of atrial tissue, when injected intravenously into anesthetized rats, causes a large and rapid increase in renal excretions of sodium and water. The immunoreactive atrial natriuretic peptide (ANP) has been found in the plasma of patients suffering from various cardiovascular diseases. A high level of ANP in the plasma has been reported in essential hypertension. Several studies on the effects of ANP on renal function and arterial blood pressure have presented contradictory results showing attenuated or accentuated responses. Thus, involvement of the ANP in the development of hypertension remains unresolved. Present study was undertaken to investigate whether the ANP is involved in the development of hypertension in two-kidney one-clip Goldblatt hypertensive rats. The plasma concentration of immunoreactive ANP appeared to be significantly elevated in hypertensive rats as compared with normotensive Goldblatt operated and sham-operated rats. Plasma renin concentration was higher in hypertensive rats than in normotensive rats, as observed in earlier experiments. Intravenous infusions of ANP resulted in increases of urine flow and urinary excretions of sodium and potassium in both hypertensive and normotensive rats. The renal response to ANP was markedly accentuated in Goldblatt hypertensive rats. The plasma concentration of ANP showed a linear relationship with the arterial blood pressure. Infusions of ANP reduced blood pressure both in hypertensive and normotensive rats. These results suggest that in Goldblatt hypertensive rats an elevation of ANP level in the plasma may not be a cause, but instead a consequence of hypertension, and that the renal responsiveness to the ANP is accentuated by some unknown mechanisms.
It is well known that the atrial natriuretic peptide (ANP) has a prepro-hormone of 151 amino-acids which loses their hydrophobic signal peptide to form 126 amino acid prohormone. The whole prohormone is released and then cleaved by proteases into more than one circulating forms. Recently, Winters et al. (1988a, b) reported that high concentrations of N-terminal fragments of prepro-ANP $(26{\sim}55),\;(56{\sim}92)\;and\;(104{\sim}123)$ were detected in human plasma. However, their physiological roles have not been established. The present study was conducted to determine whether the N-terminal fragments of pro-ANP have any effect on the renal function and to compare the effect with those of G-terminal fragments of pro-ANP The results indicate that intrarenal arterial infusions of prepro-ANP $(26{\sim}41),\;(26{\sim}55),\;(56{\sim}92)\;and\;(104{\sim}123)$ induced no significant changes in renal function. Whereas ${\alpha}-human$ ANP $(prepro-ANP,\;124{\sim}151)$ and pro-ANP caused a significant increase in urine volume, renal plasma flow, glomerular filtration rate, urinary excretions of sodium, chloride and potassium, and fractional excretion of sodium. These results suggest that the N-terminal fragments of pro-ANP are ineffective, while the C-terminal fragments retain the natriuretic and diuretic activities.
Background: The current study was undertaken to investigate the results of a modification in the conventional Maze III Procedure devised by the authors. The aim of the technical modification was in improving the left atrial contractility. Material and Method: Between July 1997 and December 1998, 34 patients with chronic atrial fibrillation for more than 1 year duration underwent a modified Maze III procedure. The assessment of the left atrial function was made by various echocardiographic measurements and SA nodal recovery was evaluated by HRV Holter monitoring. Result: All 34 patients were in sinus rhythm. On echocardiography, right atrial contraction was detected in 32 patients(94.1%) and left atrial contraction in 33 patients(97.1%). The echocardiographic A wave at 1, 6, and 12 months or more were 50.5$\pm$31.5, 62.1$\pm$25.1, 66$\pm$20.6 cm/sec, respectively, and the E wave measurements at the same time points were 152$\pm$31.1, 134.4$\pm$35.2, 133$\pm$27.5 cm/sec. The corresponding A/E ratios were 0.32$\pm$0.13, 0.48$\pm$0.18, 0.5$\pm$0.15, showing a rising trend. Treadmill evaluation at 6 months showed a mean 82% increase in heart rate after excising, and the SDNN and SDANN upon HRV Holter at 1 and 3 months postoperatively were 65.3$\pm$28.1/87.8$\pm$27.2 ms, and 60.0$\pm$24.1/83.4$\pm$25.7 ms, respectively, showing a predoinant autonomic recovery in the parasympathetic system(PSDNN = 0.01, PSDANN =0.015). Conclusion: The results of our data suggest that the current modification in the conventional Maze III Procedure was efective in enhancing the postoperative left atrial contractility.
Quan, He Xiu;Kim, Sun-Young;Jin, Xuan-Shun;Park, Jong-Kwan;Kim, Sung-Zoo;Cho, Kyung-Woo
The Korean Journal of Physiology and Pharmacology
/
v.10
no.3
/
pp.149-154
/
2006
Selective inhibition of phosphodiesterase (PDE) 5 opened a new therapeutic approach for cardiovascular disorders. Therefore, the effect of PDE5 inhibition on the cardiac function should thoroughly be defined. The purpose of the present study was to define the effects of sildenafil, a selective inhibitor of PDE5, on the atrial cGMP efflux, atrial dynamics, and the release of atrial natriuretic peptide (ANP). By perfusing rabbit left atria to allow atrial pacing, changes in atrial stroke volume and pulse pressure, transmural extracellular fluid translocation, cGMP efflux, and ANP secretion were measured. SIN-I, an NO donor and soluble (s) guanylyl cyclase (GC) activator, and C-type natriuretic peptide (CNP), an activator of particulate (p) GC activator, were used. Sildenafil increased basal levels of cGMP efflux slightly but not significantly. Sildenafil in a therapeutic dose increased atrial dynamics (for atrial stroke volume, $2.84{\pm}1.71%$, n=12, vs $-0.71{\pm}0.86%$, n=21; p<0.05) and decreased ANP release ($-9.02{\pm}3.36%$, n=14, vs $1.35{\pm}3.25%$, n=23; p < 0.05), however, it had no effect on the SIN-1- or CNP-induced increase of cGMP levels. Furthermore, sildenafil in a therapeutic dose accentuated SIN-1-induced, but not CNP-induced, decrease of atrial pulse pressure and ANP release. These data indicate that PDE5 inhibition with sildenafil has a minor effect on cGMP levels, but has a distinct effect on pGC-cGMP- and sGC-cGMP-induced contractile and secretory function.
To understand the factors influencing Atrial fibrillation and embolism in mitral valve surgery and prevent their risk, we have reviewed our 324 patients who underwent mitral valve surgery from Fev. 1982 to May 1992. Age, disease duration, lesion type, left ventricular function and left atrial dimension were chosen as preoperative factors influencing the incidence of atrial fibrillation and embolism and their postoperative course, The number and type of replaced valve, site of atriotmy, LA obliteration, ACT and use of Defibrillator were chaser. as operative factors influencing postoperative rhythm change and postop emb-olization. The results of analyses were as follows 1. The incidence of preoperative atrial fibrillation, systemic embolism and LA throbmus was 63. 6%, 10.56% and 19.8% relatively. 2. The preoperative factors of atrial fibrillation onset was old age, prolonged symptom duration, stenotic lesion, lager LAD and lower ejection fraction. In the preoperative systemic embolism preoperative factors were old age, female, stenotic lesion. The left atrial thrombus found more commonly in patients with atrial fibrillation, old age, prolonged symptom duration, stenotic lesion and low ejection fraction. 3. The preoperative atrial fibriation persisted postoperatively in 165[50.9%] and converted to normal sinus rhythm in 50[15.4%]. The preoperative normal sinus rhythm per-eisted in 100[31%] and atrial fibrillation was occured postoperatively in 9[2.7%]. The prolonged symptom duration was the preoperative factor of persist atrial fibrillation. 4. Among 95 long term follow-up patients, atiral fibrillation was continued in 59[60%]. Conversion to normal sinus rhythm was more common significantly in left atriotomy and bileaflet valve replacement. 5. There were 12 patients who had postoperative embolism. Female, persist atrial fibrillation, no LA olbiteration and tilting disc monocusp valve were considered as possible factors influencing postoperative embolism but was impossible to analyse their statistical significance due to small sample size. So we have concluded that the patients with above risk factors need anticoagulant and early surgical intervention. Left atriotomy with minimal atrial injury, left auricular obliteration and bileaflet valve replacement may be needed to reduce postoperative atrial fibrillation persist and embolism.
Kim, Hwan-Wook;Lee, Jae-Won;Cho, Won-Chul;Jung, Sung-Ho;Choo, Suk-Jung;Song, Hyun;Chung, Cheol-Hyun
Journal of Chest Surgery
/
v.42
no.3
/
pp.317-323
/
2009
Background: Although high efficiency of conversion into sinus rhythm has been demonstrated after performing the Cox-Maze procedure in patients with atrial fibrillation associated with mitral valve disease, the changes in the mechanical function and size of the left atrium have not been determined. The aim of the study was to evaluate the effect of the Maze procedure on the left atrial size and contractile transport function. Material and Method: From July 1997 to July 2008, 647 consecutive patients were operated on for chronic atrial fibrillation associated with mitral valve disease. Among these, 211 patients that (1) were able to be followed up for 2 years after surgery, (2) had sustained normal sinus rhythm, regardless of whether they were taking anti-arrhythmic medications and (3) did not have valvular regurgitation greater than grade III or they did not have moderate grade valvular stenosis were selected for evaluation. The left atrial size and contractile transport function were assessed by transthoracic echocardiography at the postoperative base line (1 year) and at regular follow-up periods (2 years, 3 years, 4 years and 6 year). Result: The left atrial dimension was increased and the contractile transport function was decreased during the follow-up period. The longer the follow-up period, the greater was the statistical significance of the left atrial size increase and contractile transport function decrease. Conclusion: In patients who sustain normal sinus rhythm conversion after a Maze III procedure with a mitral valve operation, there is a gradual increase of the left atrial dimensions and a decrease of contractile transport function during the follow-up period. Therefore, scrupulous follow-up is needed for these patients.
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