scholarly journals Hypertension and Cardiovascular Remodelling in Rats Exposed to Continuous Light: Protection by ACE-Inhibition and Melatonin

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Fedor Simko ◽  
Olga Pechanova ◽  
Kristina Repova Bednarova ◽  
Kristina Krajcirovicova ◽  
Peter Celec ◽  
...  
Keyword(s):  
Enzyme Inhibitor ◽  
Light Exposure ◽  
Hypertensive Heart Disease ◽  
Continuous Light ◽  
Ace Inhibition ◽  
Left Ventricular ◽  
Cross Sectional ◽  
Light Protection ◽  
Male Wistar Rats ◽  
Hypertension Development

Exposure of rats to continuous light attenuates melatonin production and results in hypertension development. This study investigated whether hypertension induced by continuous light (24 hours/day) exposure induces heart and aorta remodelling and if these alterations are prevented by melatonin or angiotensin converting enzyme inhibitor captopril. Four groups of 3-month-old male Wistar rats (10 per group) were treated as follows for six weeks: untreated controls, exposed to continuous light, light-exposed, and treated with either captopril (100 mg/kg/day) or melatonin (10 mg/kg/day). Exposure to continuous light led to hypertension, left ventricular (LV) hypertrophy and fibrosis, and enhancement of the oxidative load in the LV and aorta. Increase in systolic blood pressure by continuous light exposure was prevented completely by captopril and partially by melatonin. Both captopril and melatonin reduced the wall thickness and cross-sectional area of the aorta and reduced the level of oxidative stress. However, only captopril reduced LV hypertrophy development and only melatonin reduced LV hydroxyproline concentration in insoluble and total collagen in rats exposed to continuous light. In conclusion, captopril prevented LV hypertrophy development in the continuous light-induced hypertension model, while only melatonin significantly reduced fibrosis. This antifibrotic action of melatonin may be protective in hypertensive heart disease.

scholarly journals CONTINUOUS LIGHT EXPOSURE- AND L-NAME-INDUCED LEFT VENTRICULAR REMODELLING: INTERACTIONS WITH MELATONIN AND CAPTOPRIL: PP.29.155

2010 ◽  
Vol 28 ◽  
pp. e496 ◽  
Author(s):  
F Simko ◽  
O Pechanova ◽  
V Pelouch ◽  
K Krajcirovicova ◽  
K Bednarova ◽  
...  
Keyword(s):  
Light Exposure ◽  
Continuous Light ◽  
Left Ventricular ◽  
Ventricular Remodelling ◽  
Left Ventricular Remodelling

Cardiac interstitial bradykinin and mast cells modulate pattern of LV remodeling in volume overload in rats

2003 ◽  
Vol 285 (2) ◽  
pp. H784-H792 ◽  
Author(s):  
Chih-Chang Wei ◽  
Pamela A. Lucchesi ◽  
Jose Tallaj ◽  
Wayne E. Bradley ◽  
Pamela C. Powell ◽  
...  
Keyword(s):  
Mast Cells ◽  
Enzyme Inhibitor ◽  
Weight Ratio ◽  
Volume Overload ◽  
Left Ventricular ◽  
Ang Ii ◽  
Cross Sectional ◽  
Important Interaction ◽  
Lv Remodeling ◽  
Hoe 140

In the current study, interstitial fluid (ISF), bradykinin (BK), and angiotensin II (ANG II) levels were measured using cardiac microdialysis in conscious, nonsedated rats at baseline and at 48 h and 5 days after each of the following: sham surgery (sham, n = 6), sham + administration of ANG-converting enzyme inhibitor ramipril (R, n = 6), creation of aortocaval fistula (ACF, n = 6), ACF + R ( n = 6), and ACF + R + BK2 receptor antagonist (HOE-140) administration ( n = 6). At 5 days, both ISF ANG II and BK increased in ACF rats ( P < 0.05); however, in ACF + R rats, ISF ANG II did not differ from basal levels and ISF BK increased greater than threefold above baseline at 2 and 5 days ( P < 0.05). Five days after ACF, the left ventricular (LV) weight-to-body weight ratio increased 30% ( P < 0.05) in ACF but did not differ from sham in ACF + R and ACF + R + HOE-140 rats despite similar systemic arterial pressures across all ACF groups. However, ACF + R + HOE-140 rats had greater postmortem wall thickness-to-diameter ratio and smaller cross-sectional diameter compared with ACF + R rats. There was a significant increase in mast cell density in ACF and ACF + R rats that decreased below sham in ACF + R + HOE-140 rats. These results suggest a potentially important interaction of mast cells and BK in the cardiac interstitium that modulates the pattern of LV remodeling in the acute phase of volume overload.

scholarly journals Correlation between P-Wave Terminal Force V1 (PTFV1) from 12-Lead ECG and Left Ventricular Diastolic Dysfunction in Patients Diagnosed With Hypertension

2020 ◽  
Vol 6 (2) ◽  
pp. 97-103
Author(s):  
Bambang Arie Hidayat Dalimunthe ◽  
Nizam Akbar ◽  
Refli Hasan ◽  
Harris Hasan ◽  
Andika Sitepu ◽  
...  
Keyword(s):  
Diastolic Dysfunction ◽  
Systolic Dysfunction ◽  
Hypertensive Heart Disease ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
P Wave ◽  
P Value ◽  
Cross Sectional ◽  
Ventricular Diastolic Dysfunction ◽  
Grade Iii

Background: Patients diagnosed with hypertension will deteriorate into hypertensive heart disease which is characterized by diastolic dysfunction first followed by systolic dysfunction later in the course of the disease. Diastolic dysfunction of the left ventricle causes an increase in LVEDP as well as in the dimension of the left atrium. P-Wave Terminal Force V1 (PTFV1) which is derived from 12 lead ECG could help diagnose diastolic dysfunction in centers where echocardiography is not available. The purpose of this study was to determine the correlation of PTFV1 on the 12-lead Electrocardiography with diastolic dysfunction in patients diagnosed with hypertension in the outpatient clinic of Cardiac Center Adam Malik General Hospital in Medan. Methods: This is a cross-sectional study conducted from March 2019 until August 2019. Patients with hypertension who met the inclusion criteria were examined electrocardiographically to obtain PTFV1 value. Then echocardiography examination was then performed to assess the grades of diastolic dysfunction and other parameters. Analysis of correlation between PTFV1 values and diastolic dysfunction was then conducted. Results: From the clinical characteristics, there is no difference regarding age, sex , and risk factorsbetween the three diastolic dysfunction groups, while echocardiography characteristic shows more reduced EF in grade III diastolic dysfunction (36.5±7.7). Significant differences in PTFV1 are found among diastolic dysfunction groups. Grade I diastolic dysfunction has PTFV1 value of 23.8 mm.ms, grade II diastolic dysfunction has PTFV1 value of 34.1 mm.ms, and grade III diastolic dysfunction has PTFV1 value of 52.1 mm.ms, Significance of  p value is <0.001. There is a strong correlation between PTFV1 and diastolic dysfunction grade (r = 0.63 (P <0.001)). Cut off point of PTFV1 > 29.8 mm.ms can discriminate patients who have increased LAP with a sensitivity of 84% and specificity of 71%. Conclusions: PTFV1 is a simple screening tool which is widely available and correlate well with left ventricular diastolic dysfunction in patients with hypertension, which makes it a good alternative tool especially in areas where echocardiography is not readily available.

scholarly journals Prophylactic, single-drug cardioprotection in a comparative, experimental study of doxorubicin-induced cardiomyopathy

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Mária Lódi ◽  
Viktor Bánhegyi ◽  
Beáta Bódi ◽  
Alexandra Gyöngyösi ◽  
Árpád Kovács ◽  
...  
Keyword(s):  
Enzyme Inhibitor ◽  
Primary Prophylaxis ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Common Side Effect ◽  
Serum Samples ◽  
Ventricular Ejection Fraction ◽  
Oncological Patients ◽  
Male Wistar Rats

Abstract Background Cardiomyopathy is a common side effect of doxorubicin (DOX) chemotherapy. Despite intensive research efforts in the field, there is still no evidence available for routine cardioprotective prophylaxis to prevent cardiotoxicity in the majority of oncological patients at low risk of cardiovascular disease. We have recently demonstrated the advantages of a prophylactic, combined heart failure therapy in an experimental model of DOX-induced cardiomyopathy. In the current work, we focus on individually applied prophylactic medications studied in the same translational environment to clarify their distinct roles in the prevention of DOX cardiotoxicity. Methods Twelve-week-old male Wistar rats were divided into 5 subgroups. Prophylactic β-blocker (BB, bisoprolol), angiotensin-converting enzyme inhibitor (ACEI, perindopril) or aldosterone antagonist (AA, eplerenone) treatments were applied 1 week before DOX administration, then 6 cycles of intravenous DOX chemotherapy were administered. Rats receiving only intravenous DOX or saline served as positive and negative controls. Blood pressure, heart rate, body weight, and echocardiographic parameters were monitored in vivo. Two months after the last DOX administration, the animals were sacrificed, and their heart and serum samples were frozen in liquid nitrogen for histological, mechanical, and biochemical measurements. Results All prophylactic treatments increased the survival of DOX-receiving animals. The lowest mortality rates were seen in the BB and ACEI groups. The left ventricular ejection fraction was only preserved in the BB group. The DOX-induced increase in the isovolumetric relaxation time could not be prevented by any prophylactic treatment. A decreased number of apoptotic nuclei and a preserved myocardial ultrastructure were found in all groups receiving prophylactic cardioprotection, while the DOX-induced fibrotic remodelling and the increase in caspase-3 levels could only be substantially prevented by the BB and ACEI treatments. Conclusion Primary prophylaxis with cardioprotective agents like BB or ACEI has a key role in the prevention of DOX-induced cardiotoxicity in healthy rats. Future human studies are necessary to implement this finding in the clinical management of oncological patients free of cardiovascular risk factors.

scholarly journals Effect of Captopril and Melatonin on Fibrotic Rebuilding of the Aorta in 24 Hour Light-Induced Hypertension

2013 ◽  
pp. S135-S141 ◽  
Author(s):  
K. REPOVÁ-BEDNÁROVÁ ◽  
S. AZIRIOVÁ ◽  
J. HRENÁK ◽  
K. KRAJČÍROVIČOVÁ ◽  
M. ADAMCOVÁ ◽  
...  
Keyword(s):  
Enzyme Inhibitor ◽  
Light Exposure ◽  
Continuous Light ◽  
Collagen Type I ◽  
Collagen I ◽  
Aortic Tissue ◽  
Type I ◽  
Collagen Iii ◽  
Induced Hypertension ◽  
Aortic Media

Chronic continuous light exposure leads to melatonin deficiency along with complex neurohumoral activation resulting in hypertension development in rats. The aim of this study was to show, whether continuous light induces fibrotic rebuilding of the aorta and whether the treatment with melatonin or angiotensin converting enzyme inhibitor captopril can prevent these potential alterations. In a six-week experiment, 3-month-old Wistar rats were divided into 4 groups (ten per group): controls, rats exposed to continuous light, exposed to continuous light plus treated with captopril (100 mg/kg/24 h) and exposed to continuous light plus treated with melatonin (10 mg/kg/24 h). Systolic blood pressure (SBP) and collagen type I and III in the media of thoracic aorta were measured. Continuous light induced hypertension and fibrotic rebuilding of the aorta in terms of enhancement of collagen I and III concentration in the aortic media. Both captopril and melatonin prevented SBP rise and reduced collagen III concentration in the aorta. However, only melatonin reduced collagen I and the sum of collagen I and III in the aortic tissue. We conclude that in continuous light-induced hypertension, administration of melatonin, along with SBP reduction, decreases collagen I and III concentration in the aorta. It is suggested that antifibrotic effect of melatonin may reduce the stiffness of the aorta and small arteries and beneficially influence the nature of the pulse wave and peripheral vascular resistance.

Isoproterenol-induced cardiac hypertrophy: role of circulatory versus cardiac renin-angiotensin system

2001 ◽  
Vol 281 (6) ◽  
pp. H2410-H2416 ◽  
Author(s):  
Frans H. H. Leenen ◽  
Roselyn White ◽  
Baoxue Yuan
Keyword(s):  
Cardiac Hypertrophy ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Left Ventricular ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Male Wistar Rats ◽  
Β Receptor

To assess the possible contribution of the circulatory and cardiac renin-angiotensin system (RAS) to the cardiac hypertrophy induced by a β-agonist, the present study evaluated the effects of isoproterenol, alone or combined with an angiotensin I-converting enzyme inhibitor or AT1 receptor blocker, on plasma and LV renin activity, ANG I, and ANG II, as well as left ventricular (LV) and right ventricular (RV) weight. Male Wistar rats received isoproterenol by osmotic minipump subcutaneously and quinapril or losartan once daily by gavage. Plasma and LV ANGs were measured by radioimmunoassay after separation by HPLC. Isoproterenol alone decreased blood pressure, more markedly when combined with losartan or quinapril. Isoproterenol significantly increased LV and RV weight and total collagen. Neither losartan nor quinapril inhibited the increases in LV or RV weight. Losartan prevented the increase in RV collagen but enhanced the increase in LV collagen. Isoproterenol increased plasma renin, ANG I, and ANG II three- to fourfold. Isoproterenol combined with losartan or quinapril, caused marked further increases except for a significant decrease in plasma ANG II with quinapril. Isoproterenol alone did not increase LV ANG II and, combined with losartan or quinapril, actually decreased LV ANG II. These results indicate that isoproterenol-induced cardiac hypertrophy is associated with clear increases in plasma ANG II, but not in LV ANG II. Both losartan and quinapril lower LV ANG II below control levels, but do not prevent the isoproterenol-induced cardiac hypertrophy. These findings do not support a role for the circulatory or cardiac RAS in the cardiac trophic responses to β-receptor stimulation.

scholarly journals Basal Septal Hypertrophy as the Early Imaging Biomarker for Adaptive Phase of Remodeling Prior to Heart Failure

2021 ◽  
Vol 11 (1) ◽  
pp. 75
Author(s):  
Fatih Yalçin ◽  
Hulya Yalçin ◽  
Nagehan Küçükler ◽  
Serbay Arslan ◽  
Oguz Akkuş ◽  
...  
Keyword(s):  
Heart Failure ◽  
Dominant Role ◽  
Quantitative Imaging ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Imaging Biomarker ◽  
Cross Sectional ◽  
Lv Remodeling ◽  
Septal Hypertrophy ◽  
Early Imaging

Hypertension plays a dominant role in the development of left ventricular (LV) remodeling and heart failure, in addition to being the main risk factor for coronary artery disease. In this review, we focus on the focal geometric and functional tissue aspects of the LV septal base, since basal septal hypertrophy (BSH), as the early imaging biomarker of LV remodeling due to hypertensive heart disease, is detected in cross-sectional clinic studies. In addition, the validation of BSH by animal studies using third generation microimaging and relevant clinical observations are also discussed in the report. Finally, an evaluation of both human and animal quantitative imaging studies and the importance of combined cardiac imaging methods and stress-induction in the separation of adaptive and maladaptive phases of the LV remodeling are pointed out. As a result, BSH, as the early imaging biomarker and quantitative follow-up of functional analysis in hypertension, could possibly contribute to early treatment in a timely fashion in the prevention of hypertensive disease progression to heart failure. A variety of stress stimuli in etiopathogenesis and the difficulty of diagnosing pure hemodynamic overload mediated BSH lead to an absence of the certain prevalence of this particular finding in the population.

Does ACE inhibition enhance endurance performance and muscle energy metabolism in rats?

2004 ◽  
Vol 96 (1) ◽  
pp. 59-64 ◽  
Author(s):  
L. Bahi ◽  
N. Koulmann ◽  
H. Sanchez ◽  
I. Momken ◽  
V. Veksler ◽  
...  
Keyword(s):  
Mitochondrial Respiration ◽  
Endurance Performance ◽  
Ace Inhibition ◽  
Oxidative Capacity ◽  
Treated Group ◽  
Left Ventricular ◽  
Endurance Capacity ◽  
Endurance Time ◽  
Male Wistar Rats ◽  
Ace Activity

The renin-angiotensin-aldosterone system plays an important role in the hydroelectrolytic balance, blood pressure regulation, and cell growth. In some studies, the insertion (I) allele of the angiotensin-converting enzyme (ACE) gene, associated with a lower ACE activity, has been found in excess frequency in elite endurance athletes, suggesting that decreased ACE activity could be involved in endurance performance (Myerson S, Hemingway H, Budget R, Martin J, Humphries S, and Montgomery H. J Appl Physiol 87: 1313-1316 , 1999). To test this hypothesis, we evaluated whether ACE inhibition could be associated with improved endurance performance and muscle oxidative capacity in rats. Eight male Wistar rats were treated for 10-12 wk with an ACE inhibitor, perindopril (2 mg·kg-1·day-1), and compared with eight control rats. Endurance time was measured on a treadmill, and oxidative capacity and regulation of mitochondrial respiration by substrates were evaluated in saponin-permeabilized fibers of slow soleus and fast gastrocnemius muscles. Endurance time did not differ between groups (57 ± 5 min for perindopril vs. 55 ± 6 min for control). Absolute and relative (to body weight) left ventricular weight was 20% ( P < 0.01) and 12% ( P < 0.01) lower, respectively, in the treated group. No difference in oxidative capacity, mitochondrial enzyme activities, or mitochondrial regulation by ADP was observed in soleus or gastrocnemius. Mitochondrial respiration with glycerol 3-phosphate was 17% higher in gastrocnemius ( P < 0.03) and with octanoylcarnitine 14% greater in soleus ( P < 0.01) of treated rats. These results demonstrate that ACE inhibition was not associated with improved endurance time and maximal oxidative capacity of skeletal muscles. This suggests that ACE activity has no implication in endurance capacity and only minor effects on mitochondrial function in sedentary animals.

Use of tibial length to quantify cardiac hypertrophy: application in the aging rat

1982 ◽  
Vol 243 (6) ◽  
pp. H941-H947 ◽  
Author(s):  
F. C. Yin ◽  
H. A. Spurgeon ◽  
K. Rakusan ◽  
M. L. Weisfeldt ◽  
E. G. Lakatta
Keyword(s):  
Body Weight ◽  
Cardiac Hypertrophy ◽  
Left Ventricular ◽  
Heart Weight ◽  
Weight Changes ◽  
Cross Sectional ◽  
Tibial Length ◽  
Aging Study ◽  
Male Wistar Rats ◽  
The Right

Fluctuations in body weight as occur with aging make body weight an unreliable reference for normalizing heart weight. We compared heart weight normalized by tibial length, which remains constant after maturity, with that normalized by body weight in 5- to 28-mo-old male Wistar rats. When normalized by tibial length or body weight, relative to the 5-mo heart, the senescent left ventricle undergoes 17 vs. 38% hypertrophy, respectively, and the right ventricle undergoes 0 vs. 28% hypertrophy, respectively. Histological measurements in the 25- compared with the 5-mo-old left ventricles reveal 6% larger myocyte diameters and 12% larger cellular cross-sectional areas, indicating about 15% hypertrophy; this value agrees more closely with the estimates based on tibial length than with those based on body weight. To allow prediction of left ventricular weight in a living rat, a regression equation using body weight, age, and tibial length was derived. This enabled us to perform a longitudinal aging study that verified that the above results were not biased by selective survival. Thus, in conditions in which body weight changes, cardiac hypertrophy can be more accurately quantified by relating heart weight to tibial length than to body weight. This approach may have applicability for assessing relative sizes of other organs as well.

scholarly journals The effect of continuous light exposure of rats on cardiac response to ischemia-reperfusion and NO-synthase activity.

2007 ◽  
pp. S63-S69
Author(s):  
R Važan ◽  
P Janega ◽  
S Hojná ◽  
J Zicha ◽  
F Šimko ◽  
...  
Keyword(s):  
Light Exposure ◽  
Ischemia Reperfusion ◽  
Continuous Light ◽  
Left Ventricular ◽  
No Synthase ◽  
Cardiac Response ◽  
No Production ◽  
Male Adult ◽  
Functional Parameters ◽  
Isolated Hearts

Factors modulating cardiac susceptibility to ischemia-reperfusion (I/R) are permanently attracting the attention of experimental cardiology research. We investigated, whether continuous 24 h/day light exposure of rats can modify cardiac response to I/R, NO-synthase (NOS) activity and the level of oxidative load represented by conjugated dienes (CD) concentration. Two groups of male adult Wistar rats were studied: controls exposed to normal light/dark cycle (12 h/day light, 12 h/day dark) and rats exposed to continuous light for 4 weeks. Perfused isolated hearts (Langendorff technique) were exposed to 25 min global ischemia and subsequent 30 min reperfusion. The recovery of functional parameters (coronary flow, left ventricular developed pressure, contractility and relaxation index) during reperfusion as well as the incidence, severity and duration of arrhythmias during first 10 min of reperfusion were determined. The hearts from rats exposed to continuous light showed more rapid recovery of functional parameters but higher incidence, duration and severity of reperfusion arrhythmias compared to controls. In the left ventricle, the NOS activity was attenuated, but the CD concentration was not significantly changed. We conclude that the exposure of rats to continuous light modified cardiac response to I/R. This effect could be at least partially mediated by attenuated NO production.

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