Ethanol-induced cardiac hypertrophy: effects of peripheral sympathectomy

1987 ◽  
Vol 65 (12) ◽  
pp. 2363-2367
Author(s):  
M. Hirst ◽  
M. A. Adams
Keyword(s):  
Cardiac Hypertrophy ◽  
Sympathetic Nerve ◽  
Adrenal Glands ◽  
Rapid Development ◽  
Control Diet ◽  
Nerve Supply ◽  
Myocardial Oedema ◽  
Cardiac Sympathetic Nerve ◽  
6 Hydroxydopamine ◽  
And Control

The development of cardiac hypertrophy was examined in rats that had undergone sympathectomy with 6-hydroxydopamine. After 4 days, the rats were given severely intoxicating doses of ethanol or isocalorically paired quantities of maltose–dextrin by intubation at 8-h intervals up to 48 h. The ethanol and sugar intubations were applied in a nutritionally adequate, liquid diet mix. The extent of the peripheral sympathectomy was evident from the absence of detectable quantities of noradrenaline in hearts of animals injected with the neurotoxin and in the reduced levels of excreted noradrenaline. The adrenal medullary catecholamine contents of sympathectomized rats were unchanged in the absence of ethanol; there were reduced quantities of adrenaline in the medullae of rats given ethanol. The adrenal glands of rats given ethanol were larger than those from control animals. Urine samples from sympathectomized and control rats, given ethanol, displayed equivalent increases in excreted adrenaline and noradrenaline. Increases in relative cardiac weight were evident in hearts from sympathectomized animals after 4 days of sympathectomy, and this change reached significance in the hearts from 6-hydroxydopamine-treated rats after a further 2 days on the control diet. Hearts from animals exposed to ethanol showed a marked, rapid development of cardiomegaly; after 24 h there was an increased mass of some 17%, which was sustained over the remaining 24-h period. The proportion of cardiac protein did not differ in the large hearts from ethanol-treated animals and those from their controls, hence myocardial oedema could not account for the increase in weight. The results of the study indicate that ethanol-induced cardiomegaly can occur in the absence of an intact cardiac sympathetic nerve supply.

The influence of adrenal medollectomy on the development of ethanol-induced cardiac hypertrophy

1986 ◽  
Vol 64 (5) ◽  
pp. 592-596 ◽  
Author(s):  
Michael A. Adams ◽  
Maurice Hirst
Keyword(s):  
Cardiac Hypertrophy ◽  
Adrenal Glands ◽  
Rapid Development ◽  
Liquid Diet ◽  
Urine Samples ◽  
Ethanol Intoxication ◽  
Sham Control ◽  
And Control ◽  
Urinary Noradrenaline ◽  
Noradrenaline Levels

Cardiac hypertrophy was assessed in adrenal medullectomized and sham control rats given ethanol in a liquid diet mixture, intragastrically, in severely intoxicating doses at 8-h intervals for 48 and 96 h. The ethanol treatments produced increases of some 20% in wet and dry proportional heart weights in the control animals, but this rapid development of hypertrophy was less apparent in the medullectomized rats. Hearts of the medullectomized animals given ethanol were heavier than those of pair-matched controls given isocaloric maltose–dextrin in the diet mix. These increases were not statistically significant. The ethanol treatments produced, in addition, equivalent increases in the weight of the adrenal glands of both medullectomized and control animals. Medullectomy was evaluated by analysis of adrenal glands and urine samples for catecholamines. The majority of adrenals from the demedullated group had nondetectable amounts of catecholamines and minimal quantities were found in the remainder. Adrenaline was not detected generally in urine samples from this group. The adrenaline contents of adrenals from sham controls given ethanol were markedly reduced by the ethanol treatments, whereas the quantities in urine were many times greater than those from rats given maltose–dextrin. Urinary noradrenaline levels were increased in both control and medullectomized rats given ethanol. The results of this study identify that adrenal medullary catecholamines participate in the rapid development of cardiac hypertrophy that results from severe, continuing ethanol intoxication in the rat.

Long-term serial changes of cardiac sympathetic nerve dysfunction in acute decompensated heart failure patients with reduced, mid-range and preserved left ventricular ejection fraction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Seo ◽  
T Yamada ◽  
T Watanabe ◽  
T Morita ◽  
Y Furukawa ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sympathetic Nerve ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Left Ventricular Ejection ◽  
Mibg Imaging ◽  
Cardiac Sympathetic Nerve ◽  
Heart Failure Hospitalization ◽  
Nerve Dysfunction

Abstract Background Cardiac sympathetic nerve dysfunction, which is assessed by I-123 metaiodobenzylguanidine (MIBG) imaging, is associated with the poor outcomes in patients with chronic heart failure (CHF). Serial evaluation of cardiac MIBG imaging was shown to be useful for predicting adverse outcome in CHF. However, there was no information available on long-term serial changes of cardiac sympathetic nerve dysfunction after discharge of acute decompensated heart failure (ADHF) hospitalization. Purpose We aimed to clarify the serial change of cardiac MIBG imaging parameter in long-term after discharge of heart failure hospitalization, especially relating to HFrEF (LVEF<40%), HFmrEF (40%≤LVEF<50%) and HFpEF (LVEF≥50%). Methods We studied 112 patients (HFrEF; n=44, HFmrEF; n=23 and HFpEF; n=45) who were admitted for ADHF, discharged with survival and without heart failure hospitalization during follow-up period. All patients underwent cardiac MIBG imaging at the timing of discharge, in 6–12 months and in 18–24 months after discharge. The cardiac MIBG heart to mediastinum ratio (H/M) was calculated on the early image and the delayed image (late H/M). The cardiac MIBG washout rate (WR) was calculated from the early and delayed planar images after taking radioactive decay of I-123 into consideration. Results In HFrEF patients, late H/M was significantly improved from discharge to 6–12 months data (1.60±0.24 vs 1.75±0.31, p<0.0001). Late H/M of HFmrEF patients was also significantly improved from discharge to 18–24 months data (1.71±0.27 vs 1.84±0.29 p=0.043). On the other hand, late H/M of HFpEF patients was not significantly changed. As for WR, WR in HFrEF and HFmrEF patients was significantly improved from discharge to 18–24 months data, although WR of HFpEF was not significantly changed. Conclusion The improvement in cardiac sympathetic nerve dysfunction was observed in patients with HFrEF and HFmrEF, not in HFpEF, after the discharge of acute heart failure hospitalization. Funding Acknowledgement Type of funding source: None

The impact of maternal protein restriction during perinatal life on the response to a septic insult in adult rats

2020 ◽  
pp. 1-8
Author(s):  
Reza Khazaee ◽  
Anastasiya Vinokurtseva ◽  
Lynda A. McCaig ◽  
Cory Yamashita ◽  
Daniel B. Hardy ◽  
...  
Keyword(s):  
Control Diet ◽  
Protein Restriction ◽  
Saline Control ◽  
Female Adult ◽  
Adult Rats ◽  
Male And Female ◽  
Maternal Protein Restriction ◽  
And Control ◽  
The Impact ◽  
Septic Insult

Abstract Although abundant evidence exists that adverse events during pregnancy lead to chronic conditions, there is limited information on the impact of acute insults such as sepsis. This study tested the hypothesis that impaired fetal development leads to altered organ responses to a septic insult in both male and female adult offspring. Fetal growth restricted (FGR) rats were generated using a maternal protein-restricted diet. Male and female FGR and control diet rats were housed until 150–160 d of age when they were exposed either a saline (control) or a fecal slurry intraperitoneal (Sepsis) injection. After 6 h, livers and lungs were analyzed for inflammation and, additionally, the amounts and function of pulmonary surfactant were measured. The results showed increases in the steady-state mRNA levels of inflammatory cytokines in the liver in response to the septic insult in both males and females; these responses were not different between FGR and control diet groups. In the lungs, cytokines were not detectable in any of the experimental groups. A significant decrease in the relative amount of surfactant was observed in male FGR offspring, but this was not observed in control males or in female animals. Overall, it is concluded that FGR induced by maternal protein restriction does not impact liver and lung inflammatory response to sepsis in either male or female adult rats. An altered septic response in male FGR offspring with respect to surfactant may imply a contribution to lung dysfunction.

Remote Wireless Network Monitoring Application System

2012 ◽  
Vol 433-440 ◽  
pp. 7024-7028
Author(s):  
Hui Fu ◽  
Bin Jin ◽  
Lin Han ◽  
Zuo Tang Tao
Keyword(s):  
Wireless Network ◽  
Remote Monitoring ◽  
Rapid Development ◽  
Self Monitoring ◽  
Information Display ◽  
Remote Monitoring System ◽  
Encrypt Data ◽  
And Control ◽  
Embedded Applications ◽  
Monitoring Application

With computer technology, communication technology and the rapid development of electronic technology, remote monitoring technology will be more widely used for data transmission requirements and more stringent. GPRS-based remote monitoring system, which is based in communications equipment, through the server to PC, as the remote control platform, embedded applications, network programming and other technology, the remote information display and control. Throughout the system, users can allow each terminal in the case of permission to accept the data on the changes and settings. Wireless network communication is important that the network transmission of data security and consistency, to solve this problem this thesis, performance of network communications software technology to achieve self-monitoring and self-recovery, while use of end to end encryption to encrypt data on the transmission , which can guarantee data reliability, completeness, real time and security.

Effects of Ketamine on In Vivo Cardiac Sympathetic Nerve Endings

2001 ◽  
Vol 38 ◽  
pp. S39-S42 ◽  
Author(s):  
Hirotoshi Kitagawa ◽  
Toji Yamazaki ◽  
Tsuyoshi Akiyama ◽  
Hidezo Mori ◽  
Kenji Sunagawa
Keyword(s):  
Sympathetic Nerve ◽  
Nerve Endings ◽  
Cardiac Sympathetic Nerve

Menadione nicotinamide bisulphite as a source of vitamin K and niacin activities for the growing pig

2000 ◽  
Vol 71 (1) ◽  
pp. 111-117 ◽  
Author(s):  
M. Marchetti ◽  
M. Tassinari ◽  
S. Marchetti
Keyword(s):  
Vitamin K ◽  
Control Diet ◽  
Live Weight ◽  
Organic Salt ◽  
Free Form ◽  
Food Supplementation ◽  
Sodium Bisulphite ◽  
Chemical Factors ◽  
And Control ◽  
Physical And Chemical

AbstractWhen compared with other menadione derivatives such as menadione sodium bisulphite (MSB), menadione nicotinamide bisulphite (MNB), an organic salt combining menadione and nicotinamide, shows better stability towards physical and chemical factors once it is added to pre-mixes or foods. The present work evaluates the bioavailability of the two vitamins present in this compound and toxicity in the pig. To assess vitamin bioavailability, pigs were given small amounts of food containing MNB or equivalent amounts of MSB and nicotinamide in the free form. Menadione and nicotinamide concentrations in blood samples drawn at set times after the diets were given did not reveal any significant differences between the two modes of administration. Haematic levels of both vitamins in animals receiving MNB, or MSB and nicotinamide, were after 2, 4, 8 and 12 h higher (P < 0·001) than those of untreated animals. The tolerance level to MNB was evaluated in pigs given diets containing graded amounts of MNB (100, 500, 2500 mg/kg) for 28 days. No significant (P > 0·05) differences were recorded in live weight, food intake and gain/food ratio in pigs given these diets when compared with those given an unsupplemented diet. Haemoglobin and bilirubin levels did not differ between animals given various amounts of MNB and control animals. Plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities in pigs given 100 mg/kg of MNB did not show significant differences when compared with those observed in pigs given an unsupplemented control diet. In pigs on the diets supplemented with 500 and 2500 mg/kg of MNB there was a significant increase in the two enzymatic activities as compared with controls (P < 0·001 and P < 0·01). In the case of ALT this had disappeared by 28 weeks. MNB is a good source of vitamin K for the pig and does not appear to have any adverse effects, even when administered at levels higher than those normally used in pig food supplementation.

scholarly journals Alterations by Norepinephrine of Cardiac Sympathetic Nerve Terminal Function and Myocardial β-Adrenergic Receptor Sensitivity in the Ferret

Circulation ◽  
2000 ◽  
Vol 102 (1) ◽  
pp. 96-103 ◽  
Author(s):  
Chang-seng Liang ◽  
Naomi Kenmotsu Rounds ◽  
Erdan Dong ◽  
Suzanne Y. Stevens ◽  
Junya Shite ◽  
...  
Keyword(s):  
Nerve Terminal ◽  
Sympathetic Nerve ◽  
Adrenergic Receptor ◽  
Cardiac Sympathetic Nerve ◽  
Receptor Sensitivity ◽  
Sympathetic Nerve Terminal

Increased Renal Sensitivity to Aldosterone in the Potassium-Loaded Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 315s-317s
Author(s):  
W. R. Adam ◽  
J. W. Funder
Keyword(s):  
Sodium Intake ◽  
Control Diet ◽  
High Potassium ◽  
High Sodium ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
High K ◽  
And Control

1. The renal response to aldosterone (urinary sodium and potassium excretion) was determined in adrenalectomized rats previously fed either a high potassium diet or a control diet. High K+ rats showed an enhanced response to aldosterone at all doses tested. 2. This enhanced response to aldosterone required the presence of the adrenal glands during the induction period, could be suppressed by a high sodium intake, but could not be induced by a low sodium diet. 3. No difference between high K+ and control rats could be detected in renal mineralocorticoid receptors, assessed by both in vivo and in vitro binding of tritiated aldosterone. 4. The method of the induction, and the mechanism of the enhanced response, remain to be defined.

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