American journal of physiology. Heart and circulatory physiology最新文献

{"title":"Improved vascular health linked to increased physical activity levels and reduced sedentary behavior in rheumatoid arthritis.","authors":"K Meireles, T Peçanha, A J Pinto, L P Santos, B C Mazzolani, F I Smaira, D Rezende, A C M Ribeiro, A L de Sá Pinto, F R Lima, N D da Silva Junior, C L M Forjaz, B Gualano, H Roschel","doi":"10.1152/ajpheart.00640.2024","DOIUrl":"10.1152/ajpheart.00640.2024","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is characterized by deteriorated vascular health and increased cardiovascular risk. Physical activity (PA) is recommended for cardiovascular management in RA, but evidence on the associations between objectively measured PA and vascular health markers in RA is limited. In this cross-sectional study, 82 postmenopausal women with RA (62 ± 7 yr) undertook ultrasound assessments of vascular function and structure, including brachial and superficial femoral artery (BA and SFA) flow-mediated dilation; baseline and post-hyperemia peak diameters; and carotid intima-media thickness. Participants also performed a 7-day accelerometer-based assessment of PA and sedentary behavior (SB). Fitted regression models controlled for age, body mass index, and disease activity were conducted to examine associations between vascular and PA outcomes. Regression analyses revealed that prolonged SB (bouts >60 min) and total sedentary time were inversely associated with both baseline and peak BA diameters, with each additional hour of SB resulting in decreases of 0.08-0.1 mm in these diameters (<i>P</i> ≤ 0.01). Total sedentary time also showed similar negative associations with peak SFA diameters (β = -0.14 [-0.24 to -0.05], <i>P</i> < 0.01). Conversely, light-intensity PA and stepping time were positively associated with both baseline and peak BA diameters, with each additional hour increasing these diameters by 0.10-0.24 mm (<i>P</i> ≤ 0.02). Finally, standing time was positively associated with SFA peak diameter (β = 0.11 [0.01-0.20], <i>P</i> = 0.02). No associations were found between moderate-to-vigorous PA and vascular outcomes. In conclusion, in patients with RA, SB was negatively, whereas light PA was positively, associated with BA and SFA diameters. These findings suggest that reducing SB and increasing PA, even at light intensities, may improve vascular health in RA.<b>NEW & NOTEWORTHY</b> This was the first study to investigate associations between objectively measured physical activity and markers of vascular health in rheumatoid arthritis (RA). The findings suggest that reducing sedentary behavior and increasing light or total physical activity are associated with improved vascular outcomes in RA. These results support further investigation into interventions aimed at reducing sedentary time and replacing with any type of physical activity as a potential strategy for improving cardiovascular outcomes in individuals with RA.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1590-H1598"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142556960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developmental nicotine exposure alters cardiovascular structure and function in neonatal and juvenile rats.","authors":"Emily G Flanigan, Gerrie P Farman, Melissa R Dennis, Lila Wollman, Marloes Van Den Berg, Henk Granzier, Christopher T Banek, Ralph F Fregosi","doi":"10.1152/ajpheart.00558.2024","DOIUrl":"10.1152/ajpheart.00558.2024","url":null,"abstract":"<p><p>Here we test the hypothesis that continuous nicotine exposure throughout pre- and postnatal development (developmental nicotine exposure, DNE) alters the cardiovascular structure and function in neonatal and juvenile rats. Echocardiography showed that DNE reduced left ventricular mass, left ventricular outflow tract (LVOT) diameter, and posterior wall thickness, but only in females. Both male and female DNE rats had a lower end-systolic volume, higher ejection fraction, and increased fractional shortening, with unchanged stroke volume and cardiac output. Left ventricular single cardiac myocytes from male and female DNE animals exhibited increased calcium-evoked maximal tension with no effect on EC₅₀. Tail-cuff plethysmography in awake rats showed that DNE males had lower systolic blood pressure and higher heart rate than control males. No significant changes in preload, afterload, or the in vitro renal artery response to vasodilators were observed. The results suggest that DNE enhances myocyte tension-generating capacity, possibly compensating for an unknown developmental insult, which may differ in males and females. Although this adaptation maintains normal resting cardiac function, it may lead to reduced cardiac reserve, increased energy demand, and elevated oxidative stress, potentially compromising both short- and long-term cardiovascular health in developing neonates.<b>NEW & NOTEWORTHY</b> Developmental nicotine exposure (DNE) induced cardiovascular changes in neonatal/juvenile rats. Relative to controls, females had reduced left ventricular mass and dimensions, while both sexes had increased ejection fraction and fractional shortening. DNE increased calcium-evoked tension in cardiac myocytes, suggesting an adaptive mechanism as resting cardiac output was preserved. Despite normal resting function, these changes may reduce cardiac reserve, potentially compromising long-term cardiovascular health. These novel findings highlight how DNE disrupts cardiovascular development and function.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1442-H1454"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thy and mighty: the importance of T3 thyroid hormone on dyadic structure and function in cardiac health and disease.","authors":"Charlotte E R Smith","doi":"10.1152/ajpheart.00735.2024","DOIUrl":"10.1152/ajpheart.00735.2024","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1384-H1386"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684938/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142556963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vascular chemerin from PVAT contributes to norepinephrine and serotonin-induced vasoconstriction and vascular stiffness in a sex-dependent manner.","authors":"Emma A Wabel, Teresa Krieger-Burke, Stephanie W Watts","doi":"10.1152/ajpheart.00475.2024","DOIUrl":"10.1152/ajpheart.00475.2024","url":null,"abstract":"<p><p>The adipokine chemerin supports normal blood pressure and contributes to adiposity-associated hypertension, evidenced by falls in mean arterial pressure in Dahl SS rats given an antisense oligonucleotide against chemerin. In humans, circulating chemerin is positively associated with hypertension and aortic stiffness. Mechanisms of chemerin's influence on vascular health and disease remain unknown. We identified chemerin production in the vasculature-the blood vessel and its perivascular adipose tissue (PVAT). Here, using RNAScope, qPCR, isometric contractility, high-frequency ultrasound imaging, and Western blot in the Dahl SS rat, we test the hypothesis that endogenous chemerin amplifies agonist-induced vasoconstriction through the chemerin1 receptor and that chemerin drives aortic stiffness in the thoracic aorta. <i>CMKLR1</i> (chemerin1) expression was higher in the media, and <i>Rarres2</i> (chemerin) expression was higher in the PVAT. Chemerin1 receptor antagonism via selective inhibitor CCX832 reduced maximal contraction to norepinephrine (NE) and serotonin (5-HT), but not angiotensin II, in isolated thoracic aorta (PVAT intact) from male Dahl SS rat. In females, CCX832 did not alter contraction to NE or 5-HT. Male, but not female, genetic chemerin knockout Dahl SS rats had lower aortic arch pulse wave velocity than wild types, indicating chemerin's role in aortic stiffness. Aortic PVAT from females expressed less chemerin protein than males, suggesting PVAT as the primary source of active chemerin. We show that chemerin made by the PVAT amplifies NE and 5-HT-induced contraction and potentially induces aortic stiffening in a sex-dependent manner, highlighting the potential for chemerin to be a key factor in blood pressure control and aortic stiffening.<b>NEW & NOTEWORTHY</b> Chemerin1 receptor inhibition reduced norepinephrine (NE) and 5-HT-induced vasoconstriction in males. Genetic chemerin knockout (KO) resulted in lower pulse wave velocity in males. Differences in chemerin abundance in aorta perivascular adipose tissue (APVAT) may explain sex-dependent role of chemerin.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1577-H1589"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolites and metabolism in vascular calcification: links between adenosine signaling and the methionine cycle.","authors":"Parya Behzadi, Cynthia St Hilaire","doi":"10.1152/ajpheart.00267.2024","DOIUrl":"10.1152/ajpheart.00267.2024","url":null,"abstract":"<p><p>The global population of individuals with cardiovascular disease is expanding, and a key risk factor for major adverse cardiovascular events is vascular calcification. The pathogenesis of cardiovascular calcification is complex and multifaceted, with external cues driving epigenetic, transcriptional, and metabolic changes that promote vascular calcification. This review provides an overview of some of the lesser understood molecular processes involved in vascular calcification and discusses the links between calcification pathogenesis and aspects of adenosine signaling and the methionine pathway; the latter of which salvages the essential amino acid methionine, but also provides the substrate critical for methylation, a modification that regulates the function and activity of DNA and proteins. We explore the complex and dynamic nature of osteogenic reprogramming underlying intimal atherosclerotic calcification and medial arterial calcification (MAC). Atherosclerotic calcification is more widely studied; however, emerging studies now show that MAC is a significant pathology independent from atherosclerosis. Furthermore, we emphasize metabolite and metabolic-modulating factors that influence vascular calcification pathogenesis. Although the contributions of these mechanisms are more well-define in relation to atherosclerotic intimal calcification, understanding these pathways may provide crucial mechanistic insights into MAC and inform future therapeutic approaches. Herein, we highlight the significance of adenosine and methyltransferase pathways as key regulators of vascular calcification pathogenesis.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1361-H1375"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11588312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Perivascular fat is where it is at: fat-derived chemerin regulates aortic function in a sex-dependent manner.","authors":"Lisa A Cassis","doi":"10.1152/ajpheart.00749.2024","DOIUrl":"10.1152/ajpheart.00749.2024","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1522-H1523"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142612482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of T cells in vascular aging, hypertension, and atherosclerosis.","authors":"Theodore M DeConne, David J Buckley, Daniel W Trott, Christopher R Martens","doi":"10.1152/ajpheart.00570.2024","DOIUrl":"10.1152/ajpheart.00570.2024","url":null,"abstract":"<p><p>Vascular dysfunction has emerged as a significant risk factor for the development of cardio- and cerebrovascular diseases (CVDs), which are currently the leading cause of morbidity and mortality worldwide. T lymphocytes (T cells) have been shown to be important modulators of vascular function in primary aging and CVDs, likely by producing inflammatory cytokines and reactive oxygen species that influence vasoprotective molecules. This review summarizes the role of T cells on vascular function in aging, hypertension, and atherosclerosis in animals and humans, and discusses potential T-cell targeted therapeutics to prevent, delay, or reverse vascular dysfunction.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1345-H1360"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142456050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertension-induced heart failure disrupts cardiac sympathetic innervation.","authors":"Arianna Scalco, Ethan N Lee, Morgan A Johnson, Michelle L Sorensen, Thomas N Hilton, Riley K Omonaka, Shae Zeimantz, Sue A Aicher, William R Woodward, Beth A Habecker","doi":"10.1152/ajpheart.00380.2024","DOIUrl":"10.1152/ajpheart.00380.2024","url":null,"abstract":"<p><p>About 26 million people worldwide live with heart failure (HF), and hypertension is the primary cause in 25% of these cases. Autonomic dysfunction and sympathetic hyperactivity accompany cardiovascular diseases, including HF. However, changes in cardiac sympathetic innervation in HF are not well understood. We hypothesized that cardiac sympathetic innervation is disrupted in hypertension-induced HF. Male and female C57BL6/J mice were infused with angiotensin II (ANG II) for 4 wk to generate hypertension leading to HF; controls were infused with saline. ANG II-treated mice displayed HF phenotype, including reduced cardiac function, hypertrophy, and fibrosis. ANG II-treated mice also had significantly reduced sympathetic nerve density in the left ventricle, intraventricular septum, and right ventricle. In the left ventricle, the subepicardium remained normally innervated, whereas the subendocardium was almost devoid of sympathetic nerves. Loss of sympathetic fibers led to loss of norepinephrine content in the left ventricle. Several potential triggers for axon degeneration were tested and ruled out. ANG II-treated mice had increased premature ventricular contractions after isoproterenol and caffeine injection. Although HF can induce a cholinergic phenotype and neuronal hypertrophy in stellate ganglia, ANG II treatment did not induce a cholinergic phenotype or activation of trophic factors in this study. Cardiac neurons in the left stellate ganglion were significantly smaller in ANG II-treated mice, whereas neurons in the right stellate were unchanged. Our findings show that ANG II-induced HF disrupts sympathetic innervation, particularly in the left ventricle. Further investigations are imperative to unveil the mechanisms of denervation in HF and to develop neuromodulatory therapies for patients with autonomic imbalance.<b>NEW & NOTEWORTHY</b> Angiotensin II (ANG II)-induced hypertension leads to a heart failure phenotype and cardiac sympathetic denervation with the endocardial region of the left ventricle being the most affected. Denervation is accompanied by loss of norepinephrine content in the left ventricle and increased premature ventricular contractions (PVCs) after isoproterenol and caffeine injection. ANG II treatment also causes morphological changes in cardiac-projecting left stellate ganglion neurons.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1544-H1558"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684885/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142556959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensin receptor-neprilysin inhibition and improved ventricular-arterial coupling in heart failure with reduced ejection fraction.","authors":"Tina Stegmann, Luisa Parentin, Stephan H Schirmer, Philipp Lavall, Andreas Hagendorff, Ulrich Laufs, Daniel Lavall","doi":"10.1152/ajpheart.00410.2024","DOIUrl":"10.1152/ajpheart.00410.2024","url":null,"abstract":"<p><p>Sacubitril/valsartan improves outcomes in chronic heart failure (HF) with reduced ejection fraction (EF). The underlying mechanisms on left ventricular (LV) myocardial function are incompletely understood. In this study, 117 patients with symptomatic HF and LVEF ≤ 40% were enrolled prospectively. Noninvasive pressure-volume analysis was calculated from transthoracic echocardiography with simultaneous arm-cuff blood pressure measurements. Primary outcome parameters were LV end-systolic elastance (<i>E</i>_es; a measure of LV contractility), effective arterial elastance (<i>E</i>_a; a measure of afterload), and the ventricular-arterial coupling ratio (<i>E</i>_a/<i>E</i>_es). The mean age was 65 ± 13 yr, 30% were female, and 54.7% had ischemic heart disease. During 6 mo of follow-up, eight patients died, three withdrew their consent, and four were lost to follow-up. About 102 patients were included in pressure-volume analyses. After 6 mo of sacubitril/valsartan treatment, <i>E</i>_es increased (0.66 mmHg/mL [IQR 0.45-0.94] vs. 0.78 mmHg/mL [IQR 0.57-1.10], <i>P</i> = 0.001), <i>E</i>_a decreased (1.76 mmHg/mL [IQR 1.48-2.13] vs. 1.62 mmHg/mL [IQR 1.36-1.96], <i>P</i> = 0.014), and the <i>E</i>_a/<i>E</i>_es ratio improved (2.52 [IQR 1.88-4.05] vs. 1.93 [IQR 1.50-2.63], <i>P</i> < 0.001). LV end-diastolic pressure and LV volumes were reduced, and LVEF increased from 33% to 43% (both <i>P</i> < 0.001). Clinical improvement occurred in NYHA functional class, NT-proBNP level, and 6-min walking distance. Change in LVEF correlated with change in <i>E</i>_es (<i>r</i> = 0.33, <i>P</i> = 0.0008), while change in NT-proBNP was associated with change in LV end-diastolic pressure (LVEDP) (<i>r</i> = 0.42, <i>P</i> < 0.0001). In conclusion, sacubitril/valsartan is associated with improved ventricular-arterial coupling by enhancing LV contractility and reducing afterload. Beyond LV reverse remodeling, optimized ventricular-arterial interaction may contribute to the favorable outcome of sacubitril/valsartan treatment in HF with reduced EF.<b>NEW & NOTEWORTHY</b> The study demonstrates that 6-mo treatment with sacubitril/valsartan in patients with heart failure with reduced ejection fraction is associated with increased left ventricular contractility, reduced afterload, and improved ventricular-arterial coupling. Together with reverse remodeling, these changes indicate a leftward shift of the operating left ventricular pressure-volume relationship. These data provide new insights into the understanding of pharmacological mechanisms in the failing heart and may facilitate tailored medical therapy.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1477-H1489"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Procurement and preservation of neonatal porcine cardiac tissue.","authors":"Lauren M Gilbertsen, Tara L Goertzen, Mallery L Larson, Lucelia M Pereira, Aidan S Bradshaw, Raney L Hazan, Georgia F Patyna, Abigail H Thomas, Emma S Scudder, Jennifer A Sexton, Jeff Olivarez, Alyssa M Marre, Lais Malavasi, Daniel P Fitzsimons","doi":"10.1152/ajpheart.00362.2024","DOIUrl":"10.1152/ajpheart.00362.2024","url":null,"abstract":"<p><p>The porcine and human heart are remarkably similar in cardiac physiology and biochemistry. Translational research involving the porcine biomedical model is becoming increasingly applicable for the study of human cardiac function in health and disease. Presently, few protocols exist for collecting experimentally viable cardiac tissue from large animal models, particularly during neonatal maturation. To address this deficiency, we have developed a technique to procure and preserve ventricular tissue from neonatal piglets at <i>day 3</i> (<i>n</i> = 4) and <i>day 30</i> (<i>n</i> = 6) postpartum. Piglets were subjected to a strict sedation, anesthesia, and analgesia regimen. During surgery, cardiopulmonary indices of electrocardiogram, heart rate, systolic and diastolic blood pressure, respiration rate, peripheral O₂ saturation, and end-tidal CO₂ were monitored continuously to ensure normal cardiac function. Before cardiectomy, each heart was perfused with an intravenous administration of heparin (10 mL/kg) and ice-cold Custodiol HTK cardioplegia solution (10 mL/kg). After cardiac explantation, myocardial samples (dimensions: 1 × 1 × 1 cm) were dissected from the left and right ventricles and snap-frozen in liquid nitrogen. Analysis via SDS-PAGE densitometry demonstrated that myofibrillar proteins are stable and undegraded. Western Blots showed full expression of protein. These results suggest that the detailed cardiac tissue procurement technique preserves the experimental viability of the cardiac tissue and prevents the degradation of myofibrillar proteins.<b>NEW & NOTEWORTHY</b> This project's objective was to develop a technique for procuring and preserving cardiac tissue from a porcine model. Porcine is a rapidly emerging animal model to study cardiovascular disease and has recently been popularized due to advancements in CRISPR-cas9 technology. The technique, originally derived from human heart transplant protocols, involves full anesthetic and analgesic regimens and the use of saline heparin and cardioplegia solution to preserve tissue integrity.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1455-H1466"},"PeriodicalIF":4.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}