Inhaled nitric oxide prevents left ventricular impairment during endotoxemia

1998 ◽  
Vol 85 (6) ◽  
pp. 2018-2024 ◽  
Author(s):  
Satoshi Ishihara ◽  
John A. Ward ◽  
Osamu Tasaki ◽  
Basil A. Pruitt ◽  
Cleon W. Goodwin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Left Ventricle ◽  
Cardiac Contractility ◽  
Ringer Solution ◽  
Left Ventricular ◽  
Control Group ◽  
Baseline Levels ◽  
Lv Volume

We evaluated the effect of long-term inhalation of nitric oxide (NO) on cardiac contractility after endotoxemia by using the end-systolic elastance of the left ventricle (LV) as a load-independent contractility index. Chronic instrumentation in 12 pigs included implantation of two pairs of endocardial dimension transducers to measure LV volume and a micromanometer to measure LV pressure. One week later, the animals were divided into a control group ( n = 6) or a NO group ( n = 6). All animals received intravenous Escherichia coliendotoxin (10 μg ⋅ kg−1 ⋅ h−1) and equivalent lactated Ringer solution. NO inhalation (20 parts/million) was begun 30 min after the initiation of endotoxemia and was continued for 24 h. In both groups, tachycardia, pulmonary hypertension, and systemic hyperdynamic changes were noted. The end-systolic elastance in the control group was significantly decreased beyond 7 h. NO inhalation maintained the end-systolic elastance at baseline levels and prevented its impairment. These findings indicate that NO exerts a protective effect on LV contractility in this model of endotoxemia.

Nitric oxide modulates cardiac contractility and oxygen consumption without changing contractile efficiency

1998 ◽  
Vol 275 (1) ◽  
pp. H41-H49 ◽  
Author(s):  
Naoyuki Suto ◽  
Atsushi Mikuniya ◽  
Tomoyuki Okubo ◽  
Hiroyuki Hanada ◽  
Nobuyo Shinozaki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Oxygen Metabolism ◽  
Left Ventricular ◽  
Before And After ◽  
Lv Volume ◽  
Synthase Inhibitor

Nitric oxide (NO) affects myocardial contractility and myocardial oxygen consumption (MV˙o 2) in vitro. In α-chloralose-anesthetized dogs instrumented for the measurements of left ventricular (LV) pressure, LV volume using a conductance catheter, coronary blood flow, and coronary venous oxygen saturation (S[Formula: see text]) using a fiber-optic catheter, LV end-systolic pressure-volume relationships (ESPVR) and the relationship between MV˙o 2 and LV pressure-volume area (PVA) were analyzed before and after intravenous infusions of the NO synthase inhibitor N G-monomethyl-l-arginine acetate (l-NMMA; 5 mg/kg, 8 dogs) and the NO substrate l-arginine (600 mg/kg, 7 dogs). l-NMMA increased the slope of the ESPVR ( E max) ( P < 0.05) without changing contractile efficiency indicated by the inverse of the slope of the MV˙o 2-PVA line.l-NMMA also increased unloaded MV˙o 2, indicated by the y-axis intercept of the MV˙o 2-PVA line ( P < 0.05). In contrast,l-arginine decreased E max( P < 0.05) while decreasing MV˙o 2( P < 0.05), and without changing contractile efficiency. The basal oxygen metabolism was not affected byl-NMMA andl-arginine. These data imply that endogenous NO spares MV˙o 2 by reducing oxygen use in excitation-contraction coupling and attenuates cardiac contractility without changing contractile efficiency.

scholarly journals Synthetic Pyridoindole and Rutin Affect Upregulation of Endothelial Nitric Oxide Synthase and Heart Function in Rats Fed a High-Fat-Fructose Diet

2021 ◽  
pp. 851-863
Author(s):  
L. Salvaras ◽  
T. Kovacic ◽  
P. Janega ◽  
B. Liptak ◽  
M. Sasvariova ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Left Ventricle ◽  
Endothelial Nitric Oxide Synthase ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Control Group ◽  
High Fat ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Metabolic syndrome (MetS) belongs to the serious health complications expanding in cardiovascular diseases, obesity, insulin resistance, and hyperglycemia. In this study, hypertriacylglycerolemic rats fed a high-fat-fructose diet (HFFD) were used as an experimental model of MetS to explore the effect of tested compounds. Effects of a new prospective pyridoindole derivative coded SMe1EC2 and the natural polyphenol rutin were tested. Endothelial nitric oxide synthase (NOS3) and nuclear factor kappa B (NF-κB) expression were assessed in the left ventricle immunohistochemically and left ventricle activity was monitored in isolated perfused rat hearts. NOS3 activity in the left ventricle decreased markedly as a result of a HFFD. NOS3 expression was upregulated by both substances. NF-κB expression was increased in the MetS group in comparison to control rats and the expression further increased in the SMe1EC2 treatment. This compound significantly improved the coronary flow in comparison to the control group during reperfusion of the heart followed after ischemia. Further, it tended to increase left ventricular systolic pressure, heart product, rate of maximal contraction and relaxation, and coronary flow during baseline assessment. Moreover, the compound SMe1EC2 decreased the sensitivity of hearts to electrically induced ventricular fibrillation. Contrary to this rutin decreased coronary flow in reperfusion. Present results suggest that despite upregulation of NOS3 by both substances tested, pyridoindole SMe1EC2 rather than rutin could be suitable in treatment strategies of cardiovascular disorders in MetS-like conditions.

Persistent Pulmonary Hypertension of the Newborn: Role of Nitric Oxide

1995 ◽  
Vol 10 (6) ◽  
pp. 270-282
Author(s):  
Stella Kourembanas
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Structural Changes ◽  
Critical Role ◽  
Persistent Pulmonary Hypertension ◽  
Cell Contractility ◽  
Vasoactive Mediators ◽  
Nitric Oxide Therapy

Persistent pulmonary hypertension of the newborn (PPHN) is a common cause of respiratory failure in the full-term neonate. Molecular and cellular studies in vascular biology have revealed that endothelial-derived mediators play a critical role in the pathogenesis and treatment of PPHN. Endothelial-derived vasoconstrictors, like endothelin, may increase smooth muscle cell contractility and growth, leading to the physiologic and structural changes observed in the pulmonary arterioles of infants with this disease. On the other hand, decreased production of the endothelial-derived relaxing factor, nitric oxide, may exacerbate pulmonary vasoreactivity and lead to more severe pulmonary hypertension. Exogenous (inhaled) nitric oxide therapy reduces pulmonary vascular resistance and improves oxygenation. The safety and efficacy of this therapy in reducing the need for extracorporeal membrane oxygenation and decreasing long-term morbidity is being tested in several trials nationally and abroad. Understanding the basic mechanisms that regulate the gene expression and production of these vasoactive mediators will lead to improved preventive and therapeutic strategies for PPHN.

scholarly journals Effects of Long-term Nonylphenol Exposure on Myocardial Fibrosis and Cardiac Function in Rats

2021 ◽  
Author(s):  
Chao Liu ◽  
Chengyu Ni ◽  
Weichu Liu ◽  
Xiaolian Yang ◽  
Renyi Zhang ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Myocardial Fibrosis ◽  
Posterior Wall ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Environmental Estrogens ◽  
Control Group ◽  
Cardiac Structure ◽  
Collagen Iii

Abstract Background: Myocardial fibrosis is a critical pathological basis for the poor prognosis of cardiovascular diseases. Studies have found that myocardial fibrosis is closely associated with exposure to environmental estrogens such as nonylphenol (NP), as a representative of environmental estrogens. The aim of this study was to examine the effects of NP chronic exposure on myocardial fibrosis as well as cardiac structure and function. Forty Sprague Dawley rats were randomly divided into four groups (n = 10): control group (C), low NP dose (0.4 mg/kg, L), medium NP dose (4 mg/kg, M), and high NP dose (40 mg/kg, H) groups. The NP dose groups were gavaged with NP for 180 days. Results: The NP level in the heart of the NP groups was significantly higher than those in the control group (F = 43.658, P < 0.001). Serum aspartate aminotransferase (AST), creatine kinase (CK), creatine kinase isozyme (CK-MB), lactate dehydrogenase (LDH) and α-hydroxybutyrate dehydrogenase (α-HBDH) significantly increased in the NP groups compared with the control group (). Histopathological examination of the heart biopsy illustrates that in the medium and high NP groups, the fibrous connective tissue had a disordered and loose gridding shape, muscle fibers had fractured, and muscle fibers were loose with a widened gap. Extensive inflammatory cell infiltration and fibroblast proliferation in the myocardial interstitium were also found. With increasing NP dose, the degree of muscle fiber loosing and disorder became more significant in the NP treatment groups, and the collagen volume fraction (CVF) was higher than that in the control group (P < 0.01). Compared with the control group, the expression of collagen I and collagen III increased significantly in the medium and high NP groups (P < 0.05). The values of the systolic thickness of the left ventricular anterior wall (LVAWs), the diastolic thickness of the left ventricular posterior wall (LVPWd), the systolic thickness of the left ventricular posterior wall (LVPWs), and the left ventricular anterior wall (LVAWd) in the NP groups are were slightly lower than those in of the control group. The values of left ventricular end systolic dimensions (LVIDs) in the NP groups increased compared with the control group. Conclusions: Long-term NP exposure could lead to fibrosis in the rat myocardium, which is characterized by increased expressions of myocardial collagen I and collagen III, as well as elevated cardiac enzymes. In addition, the cardiac structure was affected and changes were observed in the thinner ventricular wall and as an enlarged ventricular cavity.

scholarly journals Features of structural and functional remodeling of the left ventricle in patients suffering from arterial hypertension with concomitant hypothyroidism

2019 ◽  
Vol 26 (5) ◽  
pp. 43-52
Author(s):  
V. I. Tseluyko ◽  
L. M. Yakovleva ◽  
D. A. Korchagina
Keyword(s):  
Body Mass Index ◽  
Left Ventricle ◽  
Arterial Hypertension ◽  
Diastolic Dysfunction ◽  
Body Mass ◽  
Mean Value ◽  
Left Ventricular ◽  
Control Group ◽  
Functional Remodeling ◽  
The Mean

The aim – to study the features of structural and functional remodeling of the left ventricle in patients suffering from arterial hypertension with concomitant hypothyroidism and to determine clinical and past medical history and laboratory factors associated with their development. Materials and methods. 50 patients suffering from hypertension with concomitant hypothyroidism were enrolled into the study. Depending on the level of thyroid stimulating hormone in the serum the examined patients were distributed into two groups of 25 patients with the compensated and 25 with decompensated course of hypothyroidism. The control group consisted of 30 patients with hypertension in which the pathology of the thyroid gland was excluded. The comparison of the main parameters of the echocardiography study of the myocardium has been performed depending on hypothyroidism compensation. Assessment of parameters of transmitral diastolic blood flow has been performed. A regression analysis has been conducted to detect the relation of clinical and past medical history factors and echocardiographic parameters with the development of diastolic dysfunction by E/A ratio. The values of central hemodynamics have been studied for evaluation of the contractile function of the myocardium. Results and discussion. According to the results of the echocardiography of both examined groups it has been found that the final systolic and stroke volume exceeded the parameters of the control group. The mean value of the left ventricle ejection fraction was statistically significantly lower than in the control group (p=0.004). The left ventricle myocardial mass in patients with hypothyroidism was statistically significantly greater than in the control group. It was proved that in patients, who were diagnosed with decompensated hypothyroidism, the mean value of the left atrium size to growth by the degree of 2.7 was statistically significantly higher than in the control group (p=0.01), whereas the average value of the ratio of the size of the left atrium to the surface area of the body had no statistically significant differences between the groups. It has been found that in both groups the proportion of patients with diastolic dysfunction in which the E/A ratio was less than 1.0 was higher than in the control group (р=0.01 and p=0.03, respectively). The independent factors of diastolic dysfunction of the left ventricle in patients with hypertension in the presence of hypothyroidism have been found. Conclusions. In the presence of decompensated hypothyroidism in patients with arterial hypertension, both with obesity and with normal body mass index, left ventricular mass indexes were significantly higher in comparison with a control group. Regardless of the compensation of the thyroid state in patients with arterial hypertension, the ejection fraction was significantly lower. According to regression analysis, independent factors for the development of diastolic dysfunction in patients with arterial hypertension and hypothyroidism with a body mass index ≥ 30 kg/m2 is the index of mass of the left ventricular myocardium, determined by the degree of 2.7, the level of total cholesterol to statistical significance – the level of office systolic blood pressure and the duration of hormone replacement therapy for hypothyroidism; with body mass index < 30 kg/m2 – age and left atrial index, determined by body surface area. For patients with arterial hypertension and reduced thyroid gland function, violation of the left ventricular myocardial relaxation is typical as evidenced by a higher proportion of patients with a decrease in E/A to less than 0.8 in these patients.

Isolated left ventricular apical hypoplasia in a young child

2021 ◽  
Vol 14 (1) ◽  
pp. e239297
Author(s):  
H Ravi Ramamurthy ◽  
Onkar Auti ◽  
Vimal Raj ◽  
Kiran Viralam
Keyword(s):  
Left Ventricle ◽  
Left Ventricular ◽  
Long Term Outcomes ◽  
Wave Inversion ◽  
St Segment ◽  
Cardiac Apex ◽  
The Right ◽  
First Time ◽  
Left Lead

A 16-month-old, healthy, asymptomatic male child presented with a diagnosis of dilated cardiomyopathy. Cardiovascular examination and chest radiograph were normal. ECG revealed sinus rhythm, and the augmented vector left lead showed raised ST segment, T wave inversion and q waves. Echocardiography showed a globular left ventricle with notched cardiac apex, abnormal echogenicity in the left ventricular apical myocardium, single papillary muscle and normal biventricular function. Cardiac MRI scan revealed a globular left ventricle with fibrofatty changes and retraction of the apex, the papillary muscles closely approximated, and the right ventricle wrapping around the apex of the left ventricle. This is described as isolated left ventricular apical hypoplasia. Diagnosis of this rare entity can be made by MRI, and it has been diagnosed largely in adults. The pathophysiology and long-term outcomes are unknown. We characterise the echocardiography findings of this rare anomaly in a child for the first time in the literature.

Stentless Pericarbon Freedom Versus Stented Perimount Aortic Bioprosthesis: Propensity-Matched Long-Term Follow-Up

2020 ◽  
Vol 15 (5) ◽  
pp. 440-448
Author(s):  
Guglielmo Stefanelli ◽  
Fabrizio Pirro ◽  
Vincenzo Smorto ◽  
Alessandro Bellisario ◽  
Emilio Chiurlia ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Clinical Outcomes ◽  
Large Body ◽  
Left Ventricular ◽  
Control Group ◽  
Late Mortality ◽  
Small Aortic Root ◽  
Hemodynamic Performance

Objective Stentless aortic valves have shown superior hemodynamic performance and faster left ventricular mass regression compared to stented bioprostheses. Yet, controversies exist concerning the durability of stentless valves. This case-matched study compared short- and long-term clinical outcomes of stentless LivaNova-Sorin Pericarbon Freedom™ (SPF) and stented Carpentier-Edwards Perimount (CEP) aortic prostheses. Methods From 2003 through 2006, 134 consecutive patients received aortic valve replacement with SPF at our institution. This cohort was matched, according to 20 preoperative clinical parameters, with a control group of 390 patients who received CEP prosthesis during the same time. The resulting 55 + 55 matched patients were analyzed for perioperative results and long-term clinical outcomes. Results Early mortality was 0% for both groups. Lower transvalvular gradients were found in the SPF group (10.6 ± 2.9 versus 15.7 ± 3.1 mmHg, P < 0.001). Overall late mortality (mean follow-up: 10.03 years) was similar for both groups (50.1% versus 42.8%, P = 0.96). Freedom from structural valve degeneration (SVD) at 13 years was similar for both groups (SPF = 92.3%, CEP = 73.9%, P = 0.06). Freedom from aortic valve reinterventions did not differ (SPF = 92.3%, CEP = 93.5%, P = 0.55). Gradients at 13-year follow-up remained significantly lower in SPF group (10.0 ± 4.5 versus 16.2 ± 9.5 mmHg, P < 0.001). Incidence of acute bacterial endocarditis (ABE) and major adverse cardiovascular and cerebrovascular events (MACCE) was similar. Conclusions SPF and CEP demonstrated comparable long-term outcomes related to late mortality, SVD, aortic valve reinterventions, and incidence of ABE and MACCE. Superior hemodynamic performance of SPF over time can make this valve a suitable choice in patients with small aortic root and large body surface area.

Effects of chronic inhibition of inducible nitric oxide synthase in hyperthyroid rats

2005 ◽  
Vol 288 (6) ◽  
pp. E1252-E1257 ◽  
Author(s):  
Isabel Rodríguez-Gómez ◽  
Rosemary Wangensteen ◽  
Juan Manuel Moreno ◽  
Virginia Chamorro ◽  
Antonio Osuna ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Control Group ◽  
Hemodynamic Variable ◽  
Male Wistar Rats ◽  
Oxide Synthase ◽  
Inos Inhibition ◽  
Inducible Nitric Oxide

We hypothesized that nitric oxide generated by inducible nitric oxide synthase (iNOS) may contribute to the homeostatic role of this agent in hyperthyroidism and may, therefore, participate in long-term control of blood pressure (BP). The effects of chronic iNOS inhibition by oral aminoguanidine (AG) administration on BP and morphological and renal variables in hyperthyroid rats were analyzed. The following four groups ( n = 8 each) of male Wistar rats were used: control group and groups treated with AG (50 mg·kg−1·day−1, via drinking water), thyroxine (T4, 50 μg·rat−1·day−1), or AG + T4. All treatments were maintained for 3 wk. Tail systolic BP and heart rate (HR) were recorded weekly. Finally, we measured BP (mmHg) and HR in conscious rats and morphological, plasma, and renal variables. T4 administration produced a small BP (125 ± 2, P < 0.05) increase vs. control (115 ± 2) rats. AG administration to normal rats did not modify BP (109 ± 3) or any other hemodynamic variable. However, coadministration of T4 and AG produced a marked increase in BP (140 ± 3, P < 0.01 vs. T4). Pulse pressure and HR were increased in both T4- and T4 + AG -treated groups without differences between them. Plasma NOx (μmol/l) were increased in the T4 group (10.02 ± 0.15, P < 0.05 vs. controls 6.1 ± 0.10), and AG reduced this variable in T4-treated rats (6.81 ± 0.14, P < 0.05 vs. T4) but not in normal rats (5.78 ± 0.20). Renal and ventricular hypertrophy and proteinuria of hyperthyroid rats were unaffected by AG treatment. In conclusion, the results of the present paper indicate that iNOS activity may counterbalance the prohypertensive effects of T4.

The nitric oxide synthase inhibitor, N-monomethyl-L-arginine blocks induction of a long-term potentiation-like phenomenon in rat medial frontal cortical neurons in vitro

1993 ◽  
Vol 70 (3) ◽  
pp. 1255-1259 ◽  
Author(s):  
A. V. Nowicky ◽  
L. J. Bindman
Keyword(s):  
Nitric Oxide ◽  
Cortical Neurons ◽  
Long Term Potentiation ◽  
Control Group ◽  
Term Potentiation ◽  
The Mean ◽  
Synthase Inhibitor ◽  
Stimulation Of

1. Nitric oxide has been implicated in the production of long-term depression (LTD) in the cerebellum and in the production of long-term potentiation (LTP) and LTD in the hippocampus. We now provide evidence of its involvement in the induction of long-term synaptic potentiation in in vitro slices in the cerebral cortex of the rat. 2. Intracellular recordings were made from layer V neurons in the medial frontal cortex, and excitatory synaptic potentials (EPSPs) were evoked by electrical stimulation of layers II/III. Tetanic stimulation of this pathway may induce LTD or LTP or no change at these synapses. First we established experimental conditions under which a long lasting potentiation could be induced with a high incidence (> 60%), namely perfusion of slices with 1 microM bicuculline methiodide, second the use of increased shock duration in the tetanic conditioning stimuli, third and most important the addition of QX-314 to the microelectrode to reduce potassium conductances. Because the potentiation of the mean EPSP slope was significantly greater than the control at 40-min postconditioning, but was declining throughout this period, we refer to it for brevity as LTP, but strictly class it as an LTP-like phenomenon. 3. The nitric oxide (NO) synthase inhibitor interfered with the production of LTP. In the control group of neurons (n = 13) the mean depolarizing slope of the EPSP at 30-min post-conditioning was 142.7 +/- 2% (mean +/- SE) of the prestimulation control.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Insulin Preconditioning Elevates p-Akt and Cardiac Contractility after Reperfusion in the Isolated Ischemic Rat Heart

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Tamaki Sato ◽  
Hiroaki Sato ◽  
Takeshi Oguchi ◽  
Hisashi Fukushima ◽  
George Carvalho ◽  
...  
Keyword(s):  
Myocardial Dysfunction ◽  
Cardiac Contractility ◽  
Left Ventricular ◽  
Control Group ◽  
Optimal Timing ◽  
Insulin Administration ◽  
Rat Hearts ◽  
Reperfusion Period ◽  
Pressure Development ◽  
And Control

Insulin induces cardioprotection partly via an antiapoptotic effect. However, the optimal timing of insulin administration for the best quality cardioprotection remains unclear. We tested the hypothesis that insulin administered prior to ischemia provides better cardioprotection than insulin administration after ischemia. Isolated rat hearts were prepared using Langendorff method and divided into three groups. The Pre-Ins group (Pre-Ins) received 0.5 U/L insulin prior to 15 min no-flow ischemia for 20 min followed by 20 min of reperfusion. The Post-Ins group (Post-Ins) received 0.5 U/L insulin during the reperfusion period only. The control group (Control) was perfused with KH buffer throughout. The maximum of left ventricular derivative of pressure development (dP/dt(max)) was recorded continuously. Measurements of TNF-αand p-Akt in each time point were assayed by ELISA. After reperfusion, dP/dt(max) in Pre-Ins was elevated, compared with Post-Ins at 10 minutes after reperfusion and Control at all-time points. TNF-αlevels at 5 minutes after reperfusion in the Pre-Ins were lower than the others. After 5 minutes of reperfusion, p-Akt was elevated in Pre-Ins compared with the other groups. Insulin administration prior to ischemia provides better cardioprotection than insulin administration only at reperfusion. TNF-αsuppression is possibly mediated via p-Akt leading to a reduction in contractile myocardial dysfunction.

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