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Biomedicines
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Animal Models for the Study of Cardiovascular Physiology
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Animal Models for the Study of Cardiovascular Physiology

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 11154

Special Issue Editor

Dr. Sandra Lia Amaral

E-Mail Website
Guest Editor
1. Department of Physical Education, São Paulo State University-UNESP, Campus of Bauru, SP, Brazil
2. Joint Graduate Program in Physiological Sciences (PIPGCF), Federal University of Sao Carlos and São Paulo State University, UFSCar/UNESP, São Carlos, Brazil
Interests: hypertension; skeletal muscle; arterial stiffness; exercise training

Special Issue Information

Dear Colleagues,

Cardiovascular diseases, which include coronary heart disease, cerebrovascular disease, rheumatic heart disease, peripheral vascular disease, and other conditions, represent the leading cause of death worldwide. Among the top 10 diseases that lead the mortality rate worldwide, stroke and ischemic diseases are included here and are also consequences of hypertension. Since there are several behavioral risk factors for cardiovascular diseases, such as unhealthy diet, physical inactivity, tobacco consumption, and harmful use of alcohol, associated with hypertension, diabetes, and excess weight, the treatment for these pathologies can be very complex. Therefore, a deeper understanding of the disease mechanisms could significantly contribute to more effective treatment and to a reduction in premature deaths from cardiovascular diseases. Animal models are useful as they represent the main strategy for exploring the different mechanisms involved in cardiovascular diseases. Overall, this Special Issue invites you and your colleagues to share your expertise and knowledge by submitting original research articles, systematic reviews, and review articles that report new ideas and recent advances on this topic.

Dr. Sandra Lia Amaral
Guest Editor

Manuscript Submission Information

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Keywords

  • hypertension
  • stroke
  • myocardium infarction
  • arterial stiffness
  • supravalvular aortic stenosis
  • cardiac remodeling
  • capillary angiogenesis
  • exercise training
  • vascular diseases
  • non-pharmacological treatment

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Published Papers (10 papers)

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Research

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11 pages, 1313 KiB  
Article
Pharmacokinetics of Hydrogen During Hydrogen-Saturated Saline Infusion in Pigs
by Masaki Shibuya, Masafumi Fujinaka, Mako Yonezawa, Natsumi Nishimura, Hitoshi Uchinoumi, Hiroshi Sunahara, Kenji Tani, Eiji Kobayashi and Motoaki Sano
Biomedicines 2025, 13(1), 234; https://doi.org/10.3390/biomedicines13010234 - 19 Jan 2025
Viewed by 571
Abstract
Background: Hydrogen gas (H2) has been shown to be effective in the treatment of various clinical conditions, from acute illnesses to chronic illnesses. However, its clinical indications and the corresponding appropriate hydrogen delivery methods have yet to be determined. This [...] Read more.
Background: Hydrogen gas (H2) has been shown to be effective in the treatment of various clinical conditions, from acute illnesses to chronic illnesses. However, its clinical indications and the corresponding appropriate hydrogen delivery methods have yet to be determined. This is due to the fact that the pharmacokinetics and pharmacodynamics of hydrogen in each delivery method have not been experimentally proven. Here, we verified the pharmacokinetics of hydrogen after the infusion of hydrogen-saturated saline. Methods: Hydrogen-saturated saline was prepared and checked for sterility and component specifications. Hydrogen-saturated saline was administered intravenously (125 mL/h) through the left internal jugular vein of pigs, and the blood hydrogen concentration was measured over time. Results: It was confirmed that hydrogen can be safely mixed under pressure into intravenous solutions (pharmaceutical products) without the contamination of foreign substances by using a needle-less vial access cannula. No change in the PH or composition of the solution was observed due to hydrogen filling. The hydrogen concentrations of blood samples collected from the left internal jugular vein 3 cm to the heart from the tip of the infusion line were 6.4 (30 min), 4.7 (60 min), 4.9 (90 min), and 5.3 (120 min) ppb w/w, respectively. The hydrogen concentrations of blood samples collected from the right atrium were 0.7 (30 min), 0.5 (60 min), 0.7 (90 min), and 0.7 (120 min) ppb, respectively. The hydrogen concentration of blood samples collected from the right internal carotid artery were 0.1 (pre), 0.2 (30 min), 0.3 (60 min), 0.0 (90 min), and 0.0 (120 min) ppb w/w, respectively. Conclusions: We confirmed that hydrogen could be safely pressurized and filled into intravenous (pharmaceutical) solution without contamination by foreign objects using a needle-free vial access cannula. When saturated hydrogen saline was dripped intravenously, almost all of the hydrogen was expelled during its passage through the lungs and could not be supplied to the arterial side. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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12 pages, 2504 KiB  
Article
Normothermic Crystalloid Polarizing Cardioplegia Improves Systolic and Diastolic Function in a Porcine Model of Cardiopulmonary Bypass
by David Santer, Stefan Heber, Anne-Margarethe Kramer, Judith Radloff, Katharina Heissl, Attila Kiss, David J. Chambers, Seth Hallström and Bruno K. Podesser
Biomedicines 2025, 13(1), 70; https://doi.org/10.3390/biomedicines13010070 - 31 Dec 2024
Viewed by 525
Abstract
Background/Objectives: Previously, we showed that blood-based polarizing cardioplegia exerted beneficial cardioprotection during hypothermic ischemia; however, these positive effects of blood-based polarizing cardioplegia were reduced during normothermic ischemia compared to blood-based hyperkalemic (depolarizing) cardioplegia. This study compares crystalloid polarizing cardioplegia to crystalloid depolarizing cardioplegia [...] Read more.
Background/Objectives: Previously, we showed that blood-based polarizing cardioplegia exerted beneficial cardioprotection during hypothermic ischemia; however, these positive effects of blood-based polarizing cardioplegia were reduced during normothermic ischemia compared to blood-based hyperkalemic (depolarizing) cardioplegia. This study compares crystalloid polarizing cardioplegia to crystalloid depolarizing cardioplegia in a normothermic porcine model of cardiopulmonary bypass; Methods: Twelve pigs were randomized to receive either normothermic polarizing (n = 7) or depolarizing (n = 5) crystalloid cardioplegia. After the initiation of cardiopulmonary bypass, normothermic arrest (34 °C, 60 min) was followed by 60 min of on-pump and 90 min of off-pump reperfusion. Myocardial injury (arterial CK-MB), hemodynamic function, and the energy status of the hearts were measured; Results: The arterial release of CK-MB was comparable between groups (p = 0.78) during reperfusion. During 150 min of reperfusion, systolic left ventricular pressure (p = 0.01) and coronary flow (p = 0.009) were increased, and wedge pressure (p = 0.04) was decreased in the polarized group. Further hemodynamic parameters (cardiac output, stroke volume) and high-energy phosphate levels were similar between groups. The requirement for noradrenaline administration during reperfusion was significantly higher (p = 0.013) in the polarized group; Conclusions: Under normothermic conditions and despite a similar increase in levels of cardiac CK-MB, crystalloid polarizing cardioplegia protected systolic and diastolic cardiac function after 60 min of cardiac arrest. These results suggest beneficial effects for polarizing cardioplegia; clinical studies are required to confirm these effects. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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14 pages, 1242 KiB  
Article
Effects of Hydrogen Sulfide at Normal Body Temperature and in the Cold on Isolated Tail and Carotid Arteries from Rats and TRPA1 Knockout and Wild-Type Mice
by Leonardo Kelava, Eszter Pakai, Kazushi Ogasawara, Kata Fekete, Gabor Pozsgai, Erika Pinter and Andras Garami
Biomedicines 2024, 12(12), 2874; https://doi.org/10.3390/biomedicines12122874 - 18 Dec 2024
Viewed by 598
Abstract
Background: Hydrogen sulfide (H2S) is a gasotransmitter that modulates vascular tone, causing either vasodilation or vasoconstriction depending on the vascular bed, species, and experimental conditions. The cold-sensitive transient receptor potential ankyrin-1 (TRPA1) channel mediates H2S-induced effects; however, its contribution [...] Read more.
Background: Hydrogen sulfide (H2S) is a gasotransmitter that modulates vascular tone, causing either vasodilation or vasoconstriction depending on the vascular bed, species, and experimental conditions. The cold-sensitive transient receptor potential ankyrin-1 (TRPA1) channel mediates H2S-induced effects; however, its contribution to the vasomotor responses of different arteries at different temperatures has remained unclear. Here, we aimed to fill this gap by comparing the effects of sodium sulfide (Na2S), which is a fast-releasing H2S donor, on the isolated carotid and tail skin arteries of rats and mice at cold and normal body temperature with wire myography. Under the same circumstances, we also aimed to compare the effects of the canonical endothelium-dependent and -independent vasodilators, acetylcholine and sodium nitroprusside, respectively. Methods: We isolated the carotid and tail arteries from 32 adult Wistar rats and 64 TRPA1 knockout and wild-type mice, and then we studied their vasomotor responses to increasing doses (10−6–10−3 M) of Na2S as well as to acetylcholine and sodium nitroprusside (10−5 M for both) at 37 °C and in cold (17 or 20 °C). Results: In rat vessels, Na2S caused constriction of the carotids and relaxation of the tail arteries, which were not influenced by temperature. In mouse carotids, Na2S caused vasorelaxation, which was more pronounced in the cold at a lower dose (10−4 M). At a higher dose (10−3 M), the dilation was markedly attenuated in the absence of the TRPA1 channel. In the mouse tail arteries, Na2S caused vasorelaxation at 37 °C and vasocontraction in the cold. The genetic blockade of TRPA1 channels did not influence the vasomotor responses of the mouse tail arteries. Sodium nitroprusside-induced vasorelaxation was not influenced by any of the investigated factors, while acetylcholine-induced dilation decreased in the cold in all vessel types. Conclusions: Our results reveal the function of TRPA1 in the H2S-induced dilation of carotid arteries in mice. We also highlight interspecies differences in the vasomotor responses between rats and mice, as well as the importance of the effect of temperature on vascular responses. The implementation of the identified variables in future research can advance our understanding of cardiovascular physiology, especially in conditions with hypothermia (either accidental or therapeutic). Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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11 pages, 248 KiB  
Article
The Expression of Genes CYP1A1, CYP1B1, and CYP2J3 in Distinct Regions of the Heart and Its Possible Contribution to the Development of Hypertension
by Maria L. Perepechaeva, Natalia A. Stefanova, Alevtina Y. Grishanova and Nataliya G. Kolosova
Biomedicines 2024, 12(10), 2374; https://doi.org/10.3390/biomedicines12102374 - 17 Oct 2024
Viewed by 1046
Abstract
Background: It is believed that alterations in the functioning of the cytochrome P450 (CYP), which participates in metabolic transformations of endogenous polyunsaturated fatty acids (PUFAs) (with the formation of cardioprotective or cardiotoxic products), affects the development of age-related cardiovascular diseases and reduces the [...] Read more.
Background: It is believed that alterations in the functioning of the cytochrome P450 (CYP), which participates in metabolic transformations of endogenous polyunsaturated fatty acids (PUFAs) (with the formation of cardioprotective or cardiotoxic products), affects the development of age-related cardiovascular diseases and reduces the effectiveness of some cardioselective drugs. For example, CYP2J2 activation or CYP1B1 inhibition protects against the cardiovascular toxicity of anticancer drugs. It is currently unclear whether CYPs capable of metabolizing arachidonic acid and ω-3 PUFAs to vasodilatory and vasoconstrictive derivatives are expressed in all heart regions. Methods: The work was performed on senescence-accelerated OXYS rats featuring elevated blood pressure, OXYSb rats (an OXYS substrain with normal blood pressure), and Wistar rats as a “healthy” control. The mRNA level was determined in the right and left ventricles, the right and left atria, and the aorta of 1-, 3-, and 12-month-old rats. Results: We showed that all heart regions express CYPs capable of metabolizing arachidonic acid and ω-3 PUFAs and revealed significant differences between heart regions both in the mRNA level of genes CYP1B1, CYP2J3, and CYP1A1 and in the time course of expression changes with age. Conclusions: We noticed that expression levels of these CYPs in the heart regions and aorta differ between hypertensive OXYS rats, normotensive OXYSb rats, and healthy Wistar rats but could not detect any clear-cut patterns associated with the hypertensive status of OXYS rats. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
15 pages, 663 KiB  
Article
Beta-Blockers of Different Generations: Features of Influence on the Disturbances of Myocardial Energy Metabolism in Doxorubicin-Induced Chronic Heart Failure in Rats
by Igor Belenichev, Olexiy Goncharov, Nina Bukhtiyarova, Oleh Kuchkovskyi, Victor Ryzhenko, Lyudmyla Makyeyeva, Valentyn Oksenych and Oleksandr Kamyshnyi
Biomedicines 2024, 12(9), 1957; https://doi.org/10.3390/biomedicines12091957 - 28 Aug 2024
Viewed by 1500
Abstract
Beta-blockers are first-line drugs in the treatment of chronic heart failure (CHF). However, there is no consensus on the specific effects of the beta-blockers of the I-III generation on energy metabolism in CHF. The aim of this study is to conduct a study [...] Read more.
Beta-blockers are first-line drugs in the treatment of chronic heart failure (CHF). However, there is no consensus on the specific effects of the beta-blockers of the I-III generation on energy metabolism in CHF. The aim of this study is to conduct a study of beta-blockers of different generations on myocardial energy metabolism in experimental CHF. CHF was modeled in white outbred rats by administering doxorubicin. The study drugs were administered intragastrically—new drug Hypertril (1-(β-phenylethyl)-4-amino-1,2,4-triazolium bromide)-3.5 mg/kg, Metoprolol—15 mg/kg, Nebivolol −10 mg/kg, Carvedilol 50 mg/kg, and Bisoprolol, 10 mg/kg. In the myocardium, the main indices of energy metabolism were determined—ATP, ADP, AMP, malate, lactate, pyruvate, succinate dehydrogenase (SDH) activity, and NAD-dependent malate dehydrogenase (NAD-MDH) activity. Traditional second-generation beta-blockers (Metoprolol and Bisoprolol) did not affect the studied indices of energy metabolism, and third-generation beta-blockers with additional properties—Carvedilol and, especially, Nebivalol and Hypertril—improved myocardial energy metabolism. The obtained results will help to expand our understanding of the effect of beta-blockers of various generations used to treat cardiovascular diseases on energy metabolism, and are also an experimental justification for the practical choice of these drugs in the complex therapy of CHF. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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13 pages, 3030 KiB  
Article
Loss of c-Kit in Endothelial Cells Protects against Hindlimb Ischemia
by Gustavo Falero-Diaz, Catarina de A. Barboza, Roberto I. Vazquez-Padron, Omaida C. Velazquez and Roberta M. Lassance-Soares
Biomedicines 2024, 12(6), 1358; https://doi.org/10.3390/biomedicines12061358 - 19 Jun 2024
Viewed by 1045
Abstract
Background: Critical limb ischemia (CLI) is the end stage of peripheral artery disease (PAD), and around 30% of CLI patients are ineligible for current treatments. The angiogenic benefits of c-Kit have been reported in the ischemia scenario; however, the present study demonstrates the [...] Read more.
Background: Critical limb ischemia (CLI) is the end stage of peripheral artery disease (PAD), and around 30% of CLI patients are ineligible for current treatments. The angiogenic benefits of c-Kit have been reported in the ischemia scenario; however, the present study demonstrates the effects of specific endothelial c-Kit signaling in arteriogenesis during hindlimb ischemia. Methods: We created conditional knockout mouse models that decrease c-Kit (c-Kit VE-Cadherin CreERT2—c-Kit) or its ligand (SCF VE-Cadherin CreERT2—SCF) specifically in endothelial cells (ECs) after tamoxifen treatment. These mice and a control group (wild-type VE-Cadherin CreERT2—WT) were subjected to hindlimb ischemia or aortic crush to evaluate perfusion/arteriogenesis and endothelial barrier permeability, respectively. Results: Our data confirmed the lower gene expression of c-Kit and SCF in the ECs of c-Kit and SCF mice, respectively. In addition, we confirmed the lower percentage of ECs positive for c-Kit in c-Kit mice. Further, we found that c-Kit and SCF mice had better limb perfusion and arteriogenesis compared to WT mice. We also demonstrated that c-Kit and SCF mice had a preserved endothelial barrier after aortic crush compared to WT. Conclusions: Our data demonstrate the deleterious effects of endothelial SCF/c-Kit signaling on arteriogenesis and endothelial barrier integrity. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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14 pages, 3423 KiB  
Article
Pigs as Models to Test Cardiovascular Devices
by Yanina L. Rusakova, Denis S. Grankin, Kseniya S. Podolskaya and Irina Yu. Zhuravleva
Biomedicines 2024, 12(6), 1245; https://doi.org/10.3390/biomedicines12061245 - 3 Jun 2024
Cited by 1 | Viewed by 1253
Abstract
Pigs as laboratory animals are used in preclinical studies aimed at developing medical devices for cardiac surgery. The anatomy of the cardiovascular system of these animals has been well studied and acknowledged as suitable for use and the testing of new cardiovascular devices [...] Read more.
Pigs as laboratory animals are used in preclinical studies aimed at developing medical devices for cardiac surgery. The anatomy of the cardiovascular system of these animals has been well studied and acknowledged as suitable for use and the testing of new cardiovascular devices developed for humans. However, there are no morphometric characteristics of the aortic root and thoraco-abdominal part of porcine aorta. This can lead to difficulties in experimental surgery and even result in the death of experimental animals due to the mismatch in the size of the implantable devices. Thus, such information is essential to enhance the efficiency of surgical technologies used for eliminating aortic pathologies in their various sections. The purpose of our research is to study the anatomy of the aorta in mini pigs and to assess whether the size, age, and sex of the animals affect the size of the main structures in their aortas. In addition, we attempted to compare the results obtained by transesophageal echocardiography (TEE) and angiography. We studied 28 laboratory mini pigs, dividing them into three groups by body weight (40–70 kg, 71–90 kg, and 90 kg). We did not find any relationship between the external somatometric characteristics of the animals and the size of their aortas. Animals have individual anatomical variability in their cardiovascular systems, which means that they need to be examined in terms of preoperative planning by any available method—echocardiography, angiography, or multispiral computed tomography (CT). Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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18 pages, 2035 KiB  
Article
Blockade of Inflammatory Markers Attenuates Cardiac Remodeling and Fibrosis in Rats with Supravalvular Aortic Stenosis
by Francine Duchatsch, Danyelle S. Miotto, Lidieli P. Tardelli, Thiago J. Dionísio, Dijon S. Campos, Carlos F. Santos, Katashi Okoshi and Sandra L. Amaral
Biomedicines 2023, 11(12), 3219; https://doi.org/10.3390/biomedicines11123219 - 5 Dec 2023
Viewed by 1299
Abstract
Since cardiac inflammation has been considered an important mechanism involved in heart failure, an anti-inflammatory treatment could control cardiac inflammation and mitigate the worsening of cardiac remodeling. This study evaluated the effects of dexamethasone (DEX) and ramipril treatment on inflammation and cardiac fibrosis [...] Read more.
Since cardiac inflammation has been considered an important mechanism involved in heart failure, an anti-inflammatory treatment could control cardiac inflammation and mitigate the worsening of cardiac remodeling. This study evaluated the effects of dexamethasone (DEX) and ramipril treatment on inflammation and cardiac fibrosis in an experimental model of heart failure induced by supravalvular aortic stenosis. Wistar rats (21d) were submitted to an aortic stenosis (AS) protocol. After 21 weeks, an echocardiogram and a maximal exercise test were performed, and after 24 weeks, rats were treated with DEX, ramipril or saline for 14d. The left ventricle (LV) was removed for histological and inflammatory marker analyses. The AS group showed exercise intolerance (−32% vs. Sham), higher relative wall thickness (+63%), collagen deposition and capillary rarefaction, followed by cardiac disfunction. Both treatments were effective in reducing cardiac inflammation, but only DEX attenuated the increased relative wall thickness (−17%) and only ramipril reduced LV fibrosis. In conclusion, both DEX and ramipril decreased cardiac inflammatory markers, which probably contributed to the reduced cardiac fibrosis and relative wall thickness; however, treated AS rats did not show any improvement in cardiac function. Despite the complex pharmacological treatment of heart failure, treatment with an anti-inflammatory could delay the patient’s poor prognosis. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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Review

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18 pages, 506 KiB  
Review
Advancing Atrial Fibrillation Research: The Role of Animal Models, Emerging Technologies and Translational Challenges
by Monica Ferreira, Vera Geraldes, Ana Clara Felix, Mario Oliveira, Sergio Laranjo and Isabel Rocha
Biomedicines 2025, 13(2), 307; https://doi.org/10.3390/biomedicines13020307 - 27 Jan 2025
Viewed by 446
Abstract
Atrial fibrillation (AF) is the most prevalent sustained cardiac arrhythmia, presenting a significant global healthcare challenge due to its rising incidence, association with increased morbidity and mortality, and economic burden. This arrhythmia is driven by a complex interplay of electrical, structural, and autonomic [...] Read more.
Atrial fibrillation (AF) is the most prevalent sustained cardiac arrhythmia, presenting a significant global healthcare challenge due to its rising incidence, association with increased morbidity and mortality, and economic burden. This arrhythmia is driven by a complex interplay of electrical, structural, and autonomic remodelling, compounded by genetic predisposition, systemic inflammation, and oxidative stress. Despite advances in understanding its pathophysiology, AF management remains suboptimal, with ongoing debates surrounding rhythm control, rate control, and anticoagulation strategies. Animal models have been instrumental in elucidating AF mechanisms, facilitating preclinical research, and advancing therapeutic development. This review critically evaluates the role of animal models in studying AF, emphasizing their utility in exploring electrical, structural, and autonomic remodelling. It highlights the strengths and limitations of various models, from rodents to large animals, in replicating human AF pathophysiology and advancing translational research. Emerging approaches, including optogenetics, advanced imaging, computational modelling, and tissue engineering, are reshaping AF research, bridging the gap between preclinical and clinical applications. We also briefly discuss ethical considerations, the translational challenges of animal studies and future directions, including integrative multi-species approaches, omics technologies and personalized computational models. By addressing these challenges and addressing emerging methodologies, this review underscores the importance of refining experimental models and integrating innovative technologies to improve AF management and outcomes. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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12 pages, 1545 KiB  
Review
The Monocrotaline Rat Model of Right Heart Disease Induced by Pulmonary Artery Hypertension
by Anna Maria Krstic, Timothy L. M. Jones, Amelia S. Power and Marie-Louise Ward
Biomedicines 2024, 12(9), 1944; https://doi.org/10.3390/biomedicines12091944 - 23 Aug 2024
Viewed by 1566
Abstract
Pulmonary artery hypertension (PAH) is characterised by increased pulmonary vascular resistance (PVR) resulting in elevated pressure in the pulmonary artery supplying the pulmonary circulation. Disease of the right ventricle (RV) often manifests as a result of PAH placing excessive pressure on the right [...] Read more.
Pulmonary artery hypertension (PAH) is characterised by increased pulmonary vascular resistance (PVR) resulting in elevated pressure in the pulmonary artery supplying the pulmonary circulation. Disease of the right ventricle (RV) often manifests as a result of PAH placing excessive pressure on the right side of the heart. Although a relatively rare disease in humans, the impact of sustained PAH is severe, with poor outcomes even in treated individuals. As PAH develops, the blood flow is restricted through the pulmonary arteries and the right ventricle hypertrophies due to the increased strain of pumping blood through the pulmonary circulation. With time, RV hypertrophy progresses to right heart failure, impacting the supply of blood to the left ventricle and systemic circulation. Although right heart failure can currently be treated, it cannot be cured. There is therefore a need for more research into the physiological changes that cause the heart to fail under pressure overload. This review aims to evaluate the monocrotaline (MCT) rat model of PAH as a means of studying the cellular mechanisms associated with the development of RV hypertrophy and right heart failure. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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