Gotowe bibliografie tematyczne / Cardiovascular physiology

Gotowa bibliografia na temat „Cardiovascular physiology”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 28 lipca 2024

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Artykuły w czasopismach na temat "Cardiovascular physiology"

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Robicsek, Francis. "Cardiovascular physiology". Journal of Vascular Surgery 9, nr 2 (luty 1989): 402. http://dx.doi.org/10.1016/0741-5214(89)90080-3.

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Zierler, R. Eugene. "Cardiovascular physiology". Journal of Vascular Surgery 18, nr 2 (sierpień 1993): 330–31. http://dx.doi.org/10.1016/0741-5214(93)90649-7.

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Lee, Grant de J. "Cardiovascular physiology". International Journal of Cardiology 7, nr 4 (kwiecień 1985): 451. http://dx.doi.org/10.1016/0167-5273(85)90104-4.

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Morgan, H. E. "Cardiovascular Physiology". Annual Review of Physiology 51, nr 1 (marzec 1989): 177–87. http://dx.doi.org/10.1146/annurev.ph.51.030189.001141.

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Desmond, M. "Cardiovascular Physiology". Postgraduate Medical Journal 72, nr 847 (1.05.1996): 319. http://dx.doi.org/10.1136/pgmj.72.847.319.

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Gould, Carla, i Jon Hopper. "Applied cardiovascular physiology". Anaesthesia & Intensive Care Medicine 23, nr 4 (kwiecień 2022): 244–47. http://dx.doi.org/10.1016/j.mpaic.2022.02.005.

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Brodie, D. A. "Modern cardiovascular physiology". British Journal of Sports Medicine 22, nr 4 (1.12.1988): 167. http://dx.doi.org/10.1136/bjsm.22.4.167.

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Teitel, David F. "Developmental cardiovascular physiology". Current Opinion in Cardiology 6, nr 1 (luty 1991): 81–87. http://dx.doi.org/10.1097/00001573-199102000-00013.

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Hines, Michael H. "Neonatal cardiovascular physiology". Seminars in Pediatric Surgery 22, nr 4 (listopad 2013): 174–78. http://dx.doi.org/10.1053/j.sempedsurg.2013.10.004.

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Hainsworth, Roger. "Applied cardiovascular physiology". Anaesthesia & Intensive Care Medicine 5, nr 6 (czerwiec 2004): 184–86. http://dx.doi.org/10.1383/anes.5.6.184.34668.

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Rozprawy doktorskie na temat "Cardiovascular physiology"

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McMurdo, Lorraine. "Endothelin in cardiovascular physiology and pathophysiology". Thesis, Queen Mary, University of London, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321680.

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Spratt, James Christopher Samuel. "Endothelin : cardiovascular pharmacology, physiology & pathophysiology". Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/23202.

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DeGrande, Sean Thomas. "Phosphatase regulation in cardiovascular physiology and disease". University of Iowa, 2012. http://ir.uiowa.edu/etd/3443.

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Reversible protein phosphorylation is an essential component of metazoan signaling and cardiovascular physiology. Protein kinase activity is required for regulation of cardiac ion channel and membrane receptor function, metabolism, and transcription, and aberrant kinase function is widely observed across disparate cardiac pathologies. In fact, multiple generations of cardiac therapies (eg. beta-adrenergic receptor blockers) have targeted cardiac kinase regulatory cascades. In contrast, essentially nothing is known regarding the mechanisms that regulate cardiac phosphatase activity at baseline or in cardiovascular disease. Protein phosphatase 2A (PP2A) is a key phosphatase with multiple roles in cardiac physiology. Here we demonstrate the surprisingly complex regulatory platforms that control PP2A holoenzyme activity in heart. We present the first full characterization of the expression and regulation of the PP2A family of polypeptides in heart. We identify the expression of seventeen different PP2A genes in human heart and define their differential expression and distribution across species and in different cardiac chambers. We show unique subcellular distributions of PP2A regulatory subunits in myocytes, strongly implicating the regulatory subunit in conferring PP2A target specificity in vivo. We report striking differential regulation of PP2A scaffolding, regulatory, and catalytic subunit expression in multiple models of cardiovascular disease as well as in human heart failure samples. Importantly, we demonstrate that PP2A regulation in disease extends far beyond expression and subcellular location, by identifying and describing differential post-translational modifications of the PP2A holoenzyme in human heart failure. Furthermore, we go to characterize a mechanism for this method of post-translational modification that may represent a pathway capable of being therapeutically manipulated in human heart failure. Lastly we provide evidence that dysregulation of phosphatase activity contributes to the cellular pathology associated with a previously described inheritable human arrhythmia syndrome, highlighting the importance of the PP2A in cardiovascular physiology and disease. Together, our findings provide new insight into the functional complexity of PP2A expression, activity, and regulation in heart and in human cardiovascular disease and identify potentially new and specific gene and subcellular targets for the treatment of human arrhythmia and heart failure.
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O'Neill, Mark. "Cardiovascular regulation under physiological stress". Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294358.

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Nyarko-Adomfeh, Charles. "Cardiovascular function in normal man". Thesis, University of Nottingham, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317595.

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Webb, D. J. "The endothelin system in human cardiovascular physiology and pathophysiology". Thesis, University of Edinburgh, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.663587.

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Section 1 is concerned with exploring pharmacological responses to the ET family of peptides, the sarafotoxin analogue peptides, and ET antagonists, in human blood vessels in vivo. This was amongst the first work with ET-1 in humans, and certainly the first to use the sarafotoxins, ET receptor antagonists and ET converting enzyme (ECE) inhibitors. After characterisation of the pharmacological tools, it was possible to show clearly that endogenous ET-1 plays a physiological role in the control of peripheral resistance and blood pressure in healthy humans, suggesting important clinical applications for these agents. It was also shown that the ETA receptor is the major vasocontrictor receptor and that the major role in health of the ETB receptor is endothelium-dependent vasodilatation, enhancement of which may contribute to the beneficial clinical attributes of ETA receptor antagonism. In addition, local ET-1 infusion in the forearm circulation was shown to be a system whereby the clinical efficacy of systematically administered ET receptor antagonists could be modelled pharmacodynamically. Section 2-4 cover work confirming the substantial clinical utility of ET receptor antagonists and ECE inhibitors as vasodilators, particularly in essential hypertension, heart failure and renal failure. Other work, following congenital heart surgery, suggests that a cautious approach may be needed in some cases of pulmonary hypertension. Studies with neutral endopeptidase (NEP) inhibitors show unequivocally, but unexpectedly, that these agents are peripheral vasoconstrictors, and the evidence presented is consistent with this effect occurring because endogenously generated vascular ET-1 is an important substrate for NEP. Section 5 contains some miscellaneous but related studies, together with a series of review articles written from 1991-98 synthesising the literature at each stage and drawing conclusions about potential areas of major clinical interest in cardiovascular disease.
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Muntean, Brian. "Roles of Primary Cilia in Cardiovascular and Renal Physiology". University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1396014586.

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McIntosh, Matthew. "Long-term cardiovascular adaptations to neonatal hypoxia". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110447.

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INTRODUCTION: Previous work from the Rohlicek laboratory has shown that neonatal hypoxia is associated with an increase in systolic blood pressure in two month old male rats. We have asked here whether this increase persists into later maturity, and if it is also present in females. We have further examined separately whether sex hormones or alterations in autonomic control are implicated in this increase. METHODS: Experiments were conducted on adult Sprague Dawley rats of both sexes. An experimental group was raised in hypoxia (FiO2 = 0.12) for the first ten days of life and subsequently raised in normoxia. A second group was reared entirely in normoxia. A subset of males and females were gonadectomized one month prior to recording. At two, three, and six months the rats were instrumented with an intravascular telemetric blood pressure transmitter monitoring abdominal aortic pressure. One week later arterial pressure was recorded for 24 hours in the ambulatory, unrestrained rats. RESULTS: Systolic pressure was significantly higher in neonatally hypoxic male rats at every age during their active (night-time) period and as well at 3 and 6 months during the resting (daytime) period compared to controls. The effect size of neonatal hypoxia increased with age, although this increase did not achieve significance. Neonatally hypoxic females did not show any differences in systemic pressure compared to controls. Castration did not prevent the development of elevated blood pressure in two month neonatally hypoxic males, nor did ovariectomy unveil any differences between neonatally hypoxic and control females at three months of age. In two month male rats hypoxic neonatally, baroreflex sensitivity was significantly decreased during their active (night-time) period. CONCLUSIONS: Our results indicate that the increase in blood pressure experienced by neonatally hypoxic adult male rats persists into later maturity. This effect appears to be sex specific to male animals. The finding of decreased baroreflex sensitivity following neonatal hypoxia at two months indicates that altered autonomic tone with a relative increase in sympathetic activity plays a role in the increase in arterial pressure.
INTRODUCTION: Des travaux antérieurs entrepris au laboratoire Rohlicek ont montré que l'hypoxie néonatale est associée à une élévation de la pression artérielle systolique chez les rats mâles âgés de deux mois. Dans le cadre de la présente étude, on demande si cette élévation persiste plus tard dans la maturité et si elle est également présente chez les femelles. On essaye en outre de déterminer si les hormones sexuelles ou des altérations dans le contrôle autonome jouent un rôle dans cette élévation. MÉTHODE: Des études ont été menées sur des rats adultes Sprague-Dawley des deux sexes. Un groupe expérimental a été élevé en hypoxie (FiO2 = 0,12) durant les dix premiers jours de vie et subséquemment en normaxie. Un second groupe a été élevé entièrement en normaxie. Un sous-ensemble de mâles et de femelles ont été gonadectomisés un mois avant la prise de mesures. À deux, trois et six mois, des rats étaient branchés à un transducteur de pression artérielle intravasculaire avec télémétrie pour surveillance de la pression de l'aorte abdominale. Une semaine plus tard, la pression artérielle a été mesurée durant 24 heures chez des rats ambulatoires et non contenus. RÉSULTATS: La pression systolique a été considérablement plus élevée chez des rats mâles en hypoxie à tout âge durant leur période active (nocturne) et également à 3 et 6 mois durant la période de repos (diurne) par comparaison aux rats du groupe témoin. L'ampleur de l'effet de l'hypoxie néonatale s'est accrue avec l'âge, bien que cette augmentation n'ait pas été statistiquement significative. Les femelles en hypoxie néonatale n'ont montré aucune différence dans la pression artérielle générale par comparaison aux femelles du groupe témoin. Tout comme la castration n'a pu empêcher l'apparition d'une pression artérielle élevée chez les mâles en hypoxie néonatale âgés de deux mois, l'ovariectomie de même n'a pu montrer une quelconque différence entre les femelles en hypoxie néonatale par opposition aux femelles du groupe témoin à l'âge de trois mois. Chez les rats mâles âgés de deux mois en hypoxie néonatale, la sensibilité du baroréflexe a été considérablement atrophiée durant leur période active (nocturne). CONCLUSION: Nos résultats indiquent que l'élévation de la pression artérielle chez les rats mâles adultes en hypoxie néonatale persiste plus tard dans la maturité. Cet effet semble être spécifique selon le sexe chez les animaux mâles. La découverte de la sensibilité du baroréflexe atrophiée à la suite de l'hypoxie néonatale à deux mois indique que le tonus autonome altéré, conjugué à une augmentation relative de l'activité sympathique, jouent un rôle dans l'élévation de la pression artérielle.
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Bearham, D. A. "The cardiovascular consequences of burn injury". Thesis, University of Southampton, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374058.

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Sidery, Michael B. "The cardiovascular effects of food ingestion in man". Thesis, University of Nottingham, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335380.

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Książki na temat "Cardiovascular physiology"

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1922-, Levy Matthew N., red. Cardiovascular physiology. Wyd. 5. St. Louis: Mosby, 1986.

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Priebe, Hans-Joachim, i Karl Skarvan. Cardiovascular physiology. Wyd. 2. London: BMJ Books, 2000.

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Berne, Robert M. Cardiovascular physiology. Wyd. 5. St. Louis: Mosby, 1986.

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Jane, Heller Lois, red. Cardiovascular physiology. Wyd. 2. New York: McGraw-Hill, 1986.

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Berne, Robert M. Cardiovascular physiology. Wyd. 7. St. Louis: Mosby, 1997.

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H, Mines Allan, red. Cardiovascular physiology. New York: Raven Press, 1988.

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Levy, Matthew N. Cardiovascular physiology. Wyd. 9. Philadelphia, Pa: Mosby, 2007.

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1922-, Levy Matthew N., red. Cardiovascular physiology. Wyd. 6. St. Louis: Mosby-Year Book, 1992.

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Jane, Heller Lois, red. Cardiovascular physiology. Wyd. 3. New York: McGraw-Hill, 1991.

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Jane, Heller Lois, red. Cardiovascular physiology. Wyd. 4. New York: McGraw-Hill, Health Professions Division, 1997.

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Części książek na temat "Cardiovascular physiology"

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Farrah, Jason P., R. Shayn Martin i Michael C. Chang. "Cardiovascular Physiology". W Geriatric Trauma and Critical Care, 11–19. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8501-8_2.

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Thiriet, Marc. "Cardiovascular Physiology". W Biomathematical and Biomechanical Modeling of the Circulatory and Ventilatory Systems, 157–352. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9469-0_3.

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Thies, Roger. "Cardiovascular Physiology". W Oklahoma Notes, 75–122. New York, NY: Springer New York, 1995. http://dx.doi.org/10.1007/978-1-4612-4198-0_3.

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Khanna, Sandeep. "Cardiovascular Physiology". W Basic Sciences in Anesthesia, 299–327. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-62067-1_17.

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Mirjalili, S. Ali, Lucy Hinton i Kevin Ellyett. "Cardiovascular Physiology". W Physiology for General Surgical Sciences Examination (GSSE), 55–88. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-2580-9_3.

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Muir, William W. "Cardiovascular Physiology". W Veterinary Anesthesia and Analgesia, 415–72. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119421375.ch22.

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McHale, Philip A., Robert W. Blair i Kenneth J. Dormer. "Cardiovascular Physiology". W Oklahoma Notes, 60–97. New York, NY: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-0292-6_3.

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McHale, Philip A., Kenneth J. Dormer i Robert W. Blair. "Cardiovascular Physiology". W Oklahoma Notes, 72–111. New York, NY: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-0342-8_3.

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Thies, Roger. "Cardiovascular Physiology". W Oklahoma Notes, 73–117. New York, NY: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4684-0522-4_3.

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Vives, Marc. "Cardiovascular Physiology". W Cardiac Anesthesia and Postoperative Care in the 21st Century, 21–45. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-79721-8_2.

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Streszczenia konferencji na temat "Cardiovascular physiology"

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Abbott, Jonathan A. "Cardiovascular physiology: mechanisms of control". W Complex Adaptive Structures, redaktor William B. Spillman, Jr. SPIE, 2001. http://dx.doi.org/10.1117/12.446759.

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Green, Danny, i Raden Argarini. "Exercise as Cardiovascular Medicine: Early Detection and Optimal Prevention". W Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007332400400047.

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Magfirah, Irma, Soebagijo Adi Soelistijo, Hermina Novida i Deasy Ardiany. "Effect of Growth Hormone Deficiency on the Cardiovascular System". W Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007338903420348.

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Bonesi, M., I. Meglinski i S. Matcher. "Doppler optical coherence tomography in cardiovascular physiology". W 1st Canterbury Workshop and School in Optical Coherence Tomography and Adaptive Optics. SPIE, 2008. http://dx.doi.org/10.1117/12.822553.

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Deepankaew, Ronnachit, i Phornphop Naiyanetr. "The simulation of cardiovascular system for physiology study". W 2014 7th Biomedical Engineering International Conference (BMEiCON). IEEE, 2014. http://dx.doi.org/10.1109/bmeicon.2014.7017430.

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Friedrich, I., L. Paschos, T. J. Donovan i A. Paraforos. "Digital Learning: Cardiac Physiology and Pathophysiology". W 51st Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1742908.

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Watrous, R. L. "A Computational Model of Cardiovascular Physiology and Heart Sound Generation". W 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5332548.

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Jelenc, M. "Advanced cardiovascular physiology studied by applying the equivalent electronic circuit". W BIOMEDICINE 2003, redaktorzy T. Podnar, F. Runovc i M. Kordaš. Southampton, UK: WIT Press, 2003. http://dx.doi.org/10.2495/bio030111.

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Avolio, Alberto P., Ke Xu i Mark Butlin. "Application of cardiovascular models in comparative physiology and blood pressure variability". W 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6609476.

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Gok, Caglar, Alan D. Robertson i William Fuller. "BS27 Harnessing the power of palmitoylation to tune NCX1 Physiology". W British Cardiovascular Society Virtual Annual Conference, ‘Cardiology and the Environment’, 7–10 June 2021. BMJ Publishing Group Ltd and British Cardiovascular Society, 2021. http://dx.doi.org/10.1136/heartjnl-2021-bcs.225.

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Raporty organizacyjne na temat "Cardiovascular physiology"

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Brosh, Arieh, David Robertshaw, Yoav Aharoni, Zvi Holzer, Mario Gutman i Amichai Arieli. Estimation of Energy Expenditure of Free Living and Growing Domesticated Ruminants by Heart Rate Measurement. United States Department of Agriculture, kwiecień 2002. http://dx.doi.org/10.32747/2002.7580685.bard.

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Research objectives were: 1) To study the effect of diet energy density, level of exercise, thermal conditions and reproductive state on cardiovascular function as it relates to oxygen (O2) mobilization. 2) To validate the use of heart rate (HR) to predict energy expenditure (EE) of ruminants, by measuring and calculating the energy balance components at different productive and reproductive states. 3) To validate the use of HR to identify changes in the metabolizable energy (ME) and ME intake (MEI) of grazing ruminants. Background: The development of an effective method for the measurement of EE is essential for understanding the management of both grazing and confined feedlot animals. The use of HR as a method of estimating EE in free-ranging large ruminants has been limited by the availability of suitable field monitoring equipment and by the absence of empirical understanding of the relationship between cardiac function and metabolic rate. Recent developments in microelectronics provide a good opportunity to use small HR devices to monitor free-range animals. The estimation of O2 uptake (VO2) of animals from their HR has to be based upon a consistent relationship between HR and VO2. The question as to whether, or to what extent, feeding level, environmental conditions and reproductive state affect such a relationship is still unanswered. Studies on the basic physiology of O2 mobilization (in USA) and field and feedlot-based investigations (in Israel) covered a , variety of conditions in order to investigate the possibilities of using HR to estimate EE. In USA the physiological studies conducted using animals with implanted flow probes, show that: I) although stroke volume decreases during intense exercise, VO2 per one heart beat per kgBW0.75 (O2 Pulse, O2P) actually increases and measurement of EE by HR and constant O2P may underestimate VO2unless the slope of the regression relating to heart rate and VO2 is also determined, 2) alterations in VO2 associated with the level of feeding and the effects of feeding itself have no effect on O2P, 3) both pregnancy and lactation may increase blood volume, especially lactation; but they have no effect on O2P, 4) ambient temperature in the range of 15 to 25°C in the resting animal has no effect on O2P, and 5) severe heat stress, induced by exercise, elevates body temperature to a sufficient extent that 14% of cardiac output may be required to dissipate the heat generated by exercise rather than for O2 transport. However, this is an unusual situation and its affect on EE estimation in a freely grazing animal, especially when heart rate is monitored over several days, is minor. In Israel three experiments were carried out in the hot summer to define changes in O2P attributable to changes in the time of day or In the heat load. The animals used were lambs and young calves in the growing phase and highly yielding dairy cows. In the growing animals the time of day, or the heat load, affected HR and VO2, but had no effect on O2P. On the other hand, the O2P measured in lactating cows was affected by the heat load; this is similar to the finding in the USA study of sheep. Energy balance trials were conducted to compare MEI recovery by the retained energy (RE) and by EE as measured by HR and O2P. The trial hypothesis was that if HR reliably estimated EE, the MEI proportion to (EE+RE) would not be significantly different from 1.0. Beef cows along a year of their reproductive cycle and growing lambs were used. The MEI recoveries of both trials were not significantly different from 1.0, 1.062+0.026 and 0.957+0.024 respectively. The cows' reproductive state did not affect the O2P, which is similar to the finding in the USA study. Pasture ME content and animal variables such as HR, VO2, O2P and EE of cows on grazing and in confinement were measured throughout three years under twenty-nine combinations of herbage quality and cows' reproductive state. In twelve grazing states, individual faecal output (FO) was measured and MEI was calculated. Regression analyses of the EE and RE dependent on MEI were highly significant (P<0.001). The predicted values of EE at zero intake (78 kcal/kgBW0.75), were similar to those estimated by NRC (1984). The EE at maintenance condition of the grazing cows (EE=MEI, 125 kcal/kgBW0.75) which are in the range of 96.1 to 125.5 as presented by NRC (1996 pp 6-7) for beef cows. Average daily HR and EE were significantly increased by lactation, P<0.001 and P<0.02 respectively. Grazing ME significantly increased HR and EE, P<0.001 and P<0.00l respectively. In contradiction to the finding in confined ewes and cows, the O2P of the grazing cows was significantly affected by the combined treatments (P<0.00l ); this effect was significantly related to the diet ME (P<0.00l ) and consequently to the MEI (P<0.03). Grazing significantly increased O2P compared to confinement. So, when EE of grazing animals during a certain season of the year is estimated using the HR method, the O2P must be re measured whenever grazing ME changes. A high correlation (R2>0.96) of group average EE and of HR dependency on MEI was also found in confined cows, which were fed six different diets and in growing lambs on three diets. In conclusion, the studies conducted in USA and in Israel investigated in depth the physiological mechanisms of cardiovascular and O2 mobilization, and went on to investigate a wide variety of ruminant species, ages, reproductive states, diets ME, time of intake and time of day, and compared these variables under grazing and confinement conditions. From these combined studies we can conclude that EE can be determined from HR measurements during several days, multiplied by O2P measured over a short period of time (10-15 min). The study showed that RE could be determined during the growing phase without slaughtering. In the near future the development microelectronic devices will enable wide use of the HR method to determine EE and energy balance. It will open new scopes of physiological and agricultural research with minimizes strain on animals. The method also has a high potential as a tool for herd management.
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