scholarly journals Effects of Lead and/or Cadmium on the Contractile Function of the Rat Myocardium Following Subchronic Exposure and Its Attenuation with a Complex of Bioprotectors

2021 ◽  
pp. 25-33
Author(s):  
SV Klinova ◽  
IA Minigalieva ◽  
MP Sutunkova ◽  
LI Privalova ◽  
OP Gerzen ◽  
...  
Keyword(s):  
Myocardial Contractility ◽  
Contractile Function ◽  
Copper Smelting ◽  
Rat Myocardium ◽  
Relaxation Cycle ◽  
Subchronic Exposure ◽  
Heavy Chains ◽  
Lead And Cadmium ◽  
The Right ◽  
Contraction And Relaxation

Background: As by-products of copper smelting, lead and cadmium pollute both workplace air at metallurgical plants and adjacent territories. Their increased levels in the human body pose a higher risk of cardiovascular diseases. The objective of our study was evaluate changes in the rat myocardium contractile function following moderate subchronic exposure to soluble lead and/or cadmium salts and its attenuation by means of a complex of bioprotectors. Materials and methods: The subchronic exposure of rats was modelled by intraperitoneal injections of 3-H2O lead acetate and/or 2.5-H2O cadmium chloride in single doses, 6.01 mg of Pb and 0.377 mg of Cd per kg of body weight, respectively, 3 times a week during 6 weeks. The myosin heavy chains isoform ratio was estimated by gel electrophoresis. Biomechanical measurements were performed on isolated multicellular preparations of the myocardium (trabeculae and papillary muscles) from the right ventricle. Results: The subchronic lead exposure slowed down the contraction and relaxation cycle and increased myosin expression towards slowly cycling V3 isomyosins. Cadmium intoxication, on the contrary, shortened the contraction and relaxation cycle and shifted the ratio of isomyosin forms towards rapidly cycling V1. Following the combined exposure to lead and cadmium, some contractile characteristics changed in the direction typical of the effect of lead while others – in that of cadmium. We observed that the metal combination either neutralized or enhanced the isolated damaging effect of each heavy metal. The use of a complex of bioprotectors normalized the myocardial contractility impaired by the exposure to lead and cadmium either partially or completely. Discussion: Despite the changes in myocardial contractility following the subchronic lead and cadmium exposure, the mechanisms of heterometric regulation were maintained. The adverse cardiotoxic effect of the combination of these industrial contaminants may be weakened by administering a complex of bioprotectors.

CONDITION OF HEMODYNAMICS IN THE PULMONARY CIRCULATION OF PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) CONCURRENT WITH METABOLIC SYNDROME WITH HYPERTROPHY AND ATROPHY OF THE MYOCARDIUM

2019 ◽  
Vol 72 (8) ◽  
pp. 1491-1493
Author(s):  
Viktor P. Boriak ◽  
Svitlana V. Shut’ ◽  
Tetiana A. Trybrat ◽  
Olena V. Filatova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Metabolic Syndrome ◽  
Right Ventricular ◽  
Pulmonary Disease ◽  
Pulmonary Circulation ◽  
Contractile Function ◽  
Ventricular Myocardium ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
The Right

Introduction: In recent years, COPD is observed as not an isolated, but an associated pathology, in particular, concurrent with metabolic syndrome. The aim of the research is to identify the differences in changes of the rheopulmonography parameters (RPG) depending on the presence of hypertrophy or atrophy of the right ventricular myocardium in patients with COPD concurrent with metabolic syndrome.. Materials and methods: We studied changes in rheopulmonography (RPG) in 145 patients with chronic obstructive pulmonary disease (COPD) concurrent with metabolic syndrome. Results: We detected precapillary hypertension of the pulmonary circulation in patients with right ventricular myocardial hypertrophy: anacrotism serration; flattened peak of the systolic wave; decreased Vcp; high placement of incisura; horizontal course of catacrotism; decreased amplitude of the systolic wave (in this case, due to a greater increase in the resistance of the blood flow in the pulmonary vessels than the decreased impact volume of the right ventricle); prolonged Q-a (in this group of patients, it depends more on hypertension of the pulmonary circulation than on the reduction of contractile function of the myocardium). In atrophy of the right ventricular myocardium, the following changes in the RPG were revealed: decreased systolic wave at its dramatic rise; prolonged Q-a (in this case, due to the weakened heart contraction); Vmax reduction (it reflects the reduction of myocardial contractility); in hypertrophy of the myocardium, Vcp., unlike RPG, does not decrease, which is explained by the decrease in the pressure of the pulmonary circulation. Conclusions: We believe that these changes in RPG allow differentiating hypertrophy and right ventricular myocardial atrophy along with established diagnostic criteria, and can be used as markers for the diagnosis and treatment of COPD concurrent with metabolic syndrome.

Viscerosomatic interaction induced by myocardial ischemia in conscious dogs

2007 ◽  
Vol 103 (2) ◽  
pp. 511-517 ◽  
Author(s):  
Patricia A. Gwirtz ◽  
Jerry Dickey ◽  
David Vick ◽  
Maurice A. Williams ◽  
Brian Foresman
Keyword(s):  
Myocardial Ischemia ◽  
Contractile Function ◽  
Muscle Tone ◽  
Muscle Tension ◽  
Left Ventricular ◽  
Diagnostic Potential ◽  
Myocardial Contractile ◽  
Muscle Groups ◽  
The Right ◽  
Somatic Response

Studies tested the hypothesis that myocardial ischemia induces increased paraspinal muscular tone localized to the T2–T5 region that can be detected by palpatory means. This is consistent with theories of manual medicine suggesting that disturbances in visceral organ physiology can cause increases in skeletal muscle tone in specific muscle groups. Clinical studies in manual and traditional medicine suggest this phenomenon occurs during episodes of myocardial ischemia and may have diagnostic potential. However, there is little direct evidence of a cardiac-somatic mechanism to explain these findings. Chronically instrumented dogs [12 neurally intact and 3 following selective left ventricular (LV) sympathectomy] were examined before, during, and after myocardial ischemia. Circumflex blood flow (CBF), left ventricular contractile function, electromyographic (EMG) analysis, and blinded manual palpatory assessments (MPA) of tissue over the transverse spinal processes at segments T2–T5 and T11–T12 (control) were performed. Myocardial ischemia was associated with a decrease in myocardial contractile function and an increase in heart rate. MPA revealed increases in muscle tension and texture/firmness during ischemia in the T2–T5 segments on the left, but not on the right or in control segments. EMG demonstrated increased amplitude for the T4–T5 segments. After LV sympathectomy, MPA and EMG evidence of increased muscle tone were absent. In conclusion, myocardial ischemia is associated with significant increased paraspinal muscle tone localized to the left side T4–T5 myotomes in neurally intact dogs. LV sympathectomy eliminates the somatic response, suggesting that sympathetic neural traffic between the heart and somatic musculature may function as the mechanism for the interaction.

scholarly journals Characterization of morphology and function of the ‘neo-atria’ after a modified Mustard operation

2021 ◽  
Vol 2021 (3) ◽  
Author(s):  
Mohamed Nagy ◽  
Hatem Hosny ◽  
Amr El Sawy ◽  
Ahmed Mahgoub ◽  
Magdi H Yacoub
Keyword(s):  
Contractile Function ◽  
Postoperative Recovery ◽  
Long Term Results ◽  
3D Segmentation ◽  
Mustard Operation ◽  
The Right ◽  
And Function ◽  
Atrial Systole

Background: There is a pressing need to improve early and long-term results of the Mustard operation. A modification of the operation was introduced at the Aswan Heart Centre for this purpose which relies on creating new functional atria rather than the two rigid channels in the classical Mustard operation.Objectives: To evaluate the morphology and function of the neo-atria, shortly after modified mustard operation for a ‘neglected’ patient with TGA, VSD and severe pulmonary hypertension.Methods: A 6-year-old with neglected TGA, VSD and pulmonary hypertension presented with severe cyanosis, clubbing and haemoconcentration (Hb 22 g/dL), underwent the modified Aswan-Mustard operation (MAM) with rapid smooth postoperative recovery. Repeated 2D echograms and multi-slice CT scans, followed by 3D segmentation, were performed after the operation. The size, shape, and morphology of the neo-atria were measured and measurements of the patterns of instantaneous filling and emptying of the right and left ventricles were quantified.Results: The neo-systemic venous atrium consisted of three components with a combined volume of 78 mL/m2, all of which contributed to the reservoir, conduit, and importantly contractile function of the neo-atrium. The pulmonary venous atrium consisted of two components with a combined volume of 66 mL/m2. These measurements were made at atrial end diastole. The volumes of the systemic venous and the pulmonary venous diminished to 51 and 54 mL/m2, respectively, at the end atrial systole - indicating relatively preserved contractile functions.

Effects of vagus nerve on heart rate and ventricular contractility in chicken

1989 ◽  
Vol 256 (5) ◽  
pp. H1295-H1302
Author(s):  
S. A. Lang ◽  
M. N. Levy
Keyword(s):  
Vagus Nerve ◽  
Cycle Length ◽  
Cardiac Cycle ◽  
Ventricular Contractility ◽  
Ventricular Contraction ◽  
Vagus Stimulation ◽  
Constant Frequency ◽  
The Right ◽  
Contraction And Relaxation ◽  
Left Vagus

We determined the effects of vagus nerve stimulation on cardiac cycle length and on ventricular contraction and relaxation in 18 chickens anesthetized with pentobarbital. Right vagus stimulation at a constant frequency of 35 Hz prolonged cycle length by 190%, whereas left vagus stimulation at the same frequency increased cycle length by 136%. When one burst of stimuli was delivered to the right vagus nerve each cardiac cycle, but the timing of the stimuli was changed within the cardiac cycle, the response of the avian pacemaker cells varied substantially with the timing of the stimuli. Right and left vagus stimulation at a constant frequency of 20 Hz depressed ventricular contraction by 62 +/- 6 and 52 +/- 6%, respectively, and depressed ventricular relaxation by 56 +/- 7 and 53 +/- 7%, respectively. These results indicate that in the chicken the chronotropic effects of right vagus stimulation are greater than those of left vagus stimulation, whereas right and left vagus stimulation are approximately equipotent on ventricular contraction and relaxation.

Activator calcium and myocardial contractility in fetal sheep exposed to long-term high-altitude hypoxia

1997 ◽  
Vol 272 (3) ◽  
pp. H1196-H1204 ◽  
Author(s):  
V. A. Browne ◽  
V. M. Stiffel ◽  
W. J. Pearce ◽  
L. D. Longo ◽  
R. D. Gilbert
Keyword(s):  
High Altitude ◽  
Myocardial Contractility ◽  
Active Tension ◽  
Fetal Sheep ◽  
Lower Maximum ◽  
Left And Right ◽  
Baseline Values ◽  
The Right ◽  
Maximum Rate Of Rise

We studied myocardial contractility in fetal sheep from ewes exposed to approximately 112 days of hypoxia at high altitude (3,820 m). We measured the inotropic response to extracellular Ca2+ concentration ([Ca2+]o, 0.2-10 mM) and ryanodine (10(-10) to 10(-4) M) in isometrically contracting papillary muscles and quantified dihydropyridine (DHPR) and ryanodine (RyR) receptors. In hypoxic fetuses, curves describing the force-[Ca2+]o relationship were shifted left, and the top plateaus were decreased by approximately 35% in both left and right ventricles. In normoxic and hypoxic fetuses, ryanodine (10(-4) M) reduced maximum active tension (Tmax) to approximately 25-40% of baseline values, indicating that the sarcoplasmic reticulum was the chief source of activator Ca2+ and that Ca2+ influx alone was not sufficient to activate a contraction of normal amplitude. Hypoxia resulted in a lower Tmax in the right ventricle and a lower maximum rate of rise in the left ventricle after treatment with ryanodine. DHPR number did not change, but RyR number and the RyR/DHPR in both ventricles were higher in hypoxic fetuses. We conclude that hypoxia decreases contractility, possibly by reducing the availability of activator Ca2+. Further studies are needed to directly measure the Ca2+ current and intracellular Ca2+ transient and to examine myofilament protein and adenosinetriphosphatase activity.

scholarly journals Changes in rat myocardium contractility under subchronic intoxication with lead and cadmium salts administered alone or in combination

2020 ◽  
Vol 7 ◽  
pp. 433-442 ◽  
Author(s):  
Yuri L. Protsenko ◽  
Svetlana V. Klinova ◽  
Oksana P. Gerzen ◽  
Larisa I. Privalova ◽  
Ilzira A. Minigalieva ◽  
...  
Keyword(s):  
Rat Myocardium ◽  
Lead And Cadmium

Altered myocardial Gs protein and adenylyl cyclase signaling in rats exposed to chronic hypoxia and normoxic recovery

2003 ◽  
Vol 94 (6) ◽  
pp. 2423-2432 ◽  
Author(s):  
Markéta Hrbasová ◽  
Jiri Novotny ◽  
Lucie Hejnová ◽  
František Kolář ◽  
Jan Neckář ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
G Protein ◽  
Contractile Function ◽  
Left Ventricular ◽  
Adaptation To Hypoxia ◽  
Adrenergic Stimulation ◽  
Α Subunit ◽  
Stimulatory G Protein ◽  
Membrane Bound ◽  
The Right

The present work has analyzed the consequences of chronic intermittent high-altitude hypoxia for functioning of the G protein-mediated adenylyl cyclase (AC) signaling system in the right (RV) and left ventricular (LV) myocardium in rats. Adaptation to hypoxia did not appreciably affect the number of β-adrenoceptors and the content of predominantly membrane-bound α-subunit (Gsα) of the stimulatory G protein, but it raised the amount of cytosolic Gsα in RV. The levels of myocardial inhibitory Gα protein were not altered. Activity of AC stimulated by GTP, fluoride, forskolin, or isoprotertenol was reduced by ∼50% in RV from chronically hypoxic rats, and a weaker depression was also found in LV. In addition, hypoxia significantly diminished a functional activity of membrane-bound Gsα in both RV and LV. The RV baseline contractile function was markedly increased in chronically hypoxic animals, and its sensitivity to β-adrenergic stimulation was decreased. Animals recovering from hypoxia for 5 wk still exhibited markedly elevated levels of cytosolic Gsα and significantly lower activity of AC in RV than did age-matched controls, but contractile responsiveness to β-agonists was normal.

scholarly journals Endothelin-Induced Contraction and Relaxation of Rat Isolated Basilar Artery: Effect of BQ-123

1994 ◽  
Vol 14 (5) ◽  
pp. 845-852 ◽  
Author(s):  
G. I. Feger ◽  
L. Schilling ◽  
H. Ehrenreich ◽  
M. Wahl
Keyword(s):  
Nitric Oxide ◽  
Basilar Artery ◽  
Competitive Inhibition ◽  
Regression Curve ◽  
Low Concentrations ◽  
Small Contraction ◽  
The Right ◽  
Contraction And Relaxation ◽  
Oxide Synthase ◽  
Concentration Response Curve

In ring segments from rat basilar artery (BA) the endothelin (ET) peptides ET-1, ET-2, and ET-3 induced concentration-related contractions. The order of potency was ET-1 = ET-2 > ET-3, while no differences occurred in the maximum contraction. The selective ETA receptor antagonist, BQ-123 (10−10-10−4 M) alone elicited a small contraction only at 10−4 M. In the presence of BQ-123 (10−7-10−5 M), the concentration-response curve for ET-1 was shifted to the right without any decrease in maximum contraction, indicating competitive inhibition of ET-1 binding to the ETA receptor by BQ-123. The pA2 value calculated for BQ-123 was 6.935; the slope of the regression curve was 0.734. In contrast to ET-1, the contractile action of ET-3 was abolished by 10−5 M BQ-123. In segments precontracted with 10−6 M serotonin, ET-3, but not ET-1, induced relaxation at low concentrations (10−11-10−8 M), with maximum relaxation amounting to 17.8 ± 14.7% of precontraction (mean ± SD; n = 16). The relaxant action of ET-3 was abolished in vessels incubated with NG-nitro-l-arginine (10−5 M), an inhibitor of nitric oxide synthase. These results indicate that the ET-induced contraction of the isolated rat BA involves activation of the ETA receptor. The ET-3-induced relaxation of precontracted rat BA is apparently mediated by release of nitric oxide from the endothelium.

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