Levick's Introduction to Cardiovascular Physiology 6th Ed () [PDF] Www. computerescue.info - Ebook download as PDF File .pdf), Text File .txt) or read book. An Introduction to Cardiovascular Physiology 5E Rodney J Levick. A good understanding of cardiovascular physiology is fundamental to An Introduction to Cardiovascular Physiology 5E by Rodney J Levick Free PDF d0wnl0ad, audio books. Book Details Author: Neil Herring,David J. Paterson Pages: Publisher: CRC Press Brand: English ISBN: Publication Date: Release Date: Description A sound knowledge of cardiovascular physiology is fundamental to understanding cardiovascular disease, exercise.
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download An Introduction to Cardiovascular Physiology - 1st Edition. Print Book Authors: J R Levick. eBook ISBN: DRM-free (EPub, PDF, Mobi). × DRM-Free. An introduction to cardiovascular physiology / J. Rodney Levick DSc DPhil MA MRCP BM BCh(Oxon) Emeritus Professor of Physiology St George's Hospital. Introduction to Cardiovascular. Physiology. Sam Dudley, MD, PhD. Office: VA room 2A Tel: Email: [email protected]
This edition is more Department of Cellular and Integrative Physiology than just an introductory textbook. It is comprehensive in its scope and at the same time elegant in its simplicity.
Over the years, we have used its many the focus is on reviews from leading experts in the field, we editions extensively and with great fondness as both students have included classical original research papers throughout. We were therefore honoured to be asked to take References are now ordered with the most contemporary this textbook forward into its sixth edition.
Given Professor reviews and studies cited first.
There is a vast gulf to One of the first things we did when embarking on this be bridged between reading a traditional textbook and read- task, was to consult a broad group of peers and students about ing original research papers, as required when undertaking what they thought of the previous edition. Nevertheless, we students consistently find the most difficult aspect of their have introduced several key changes.
The content has been education. The aim of chapters 19 and 20 is to introduce stu- widely updated given recent advancements, particularly dents to the experimental approach and design, and simply in chapters 4, 5, 9, 12, 13, 15, 16, 17 and 18, and the clinical describe the increasingly complex techniques that are used cases.
Although this is a textbook of cardiovascular physiol- in cardiovascular research as well as their advantages and ogy rather than pathology, it is hard to ignore the significant limitations.
We are very 28 years. In other words, self-expression is vital. To this end, To encourage active learning and clinical relevance, medi- learning objectives are given at the start of each chapter, and cal schools increasingly base teaching on clinical cases, five clinical cases, with questions and answers, are included at although this has serious drawbacks, as well as advantages, the end of the book.
The sections containing the answers are cited after the end of the book, with questions and answers linked to the each learning objective. VO cardiac stress in humans is found in cases of aortic and mitral valve regurgitation, as well as ventricular septal defects, chronic heart failure, and following myocardial infarction We have shown that male rats subjected to 8 wk of VO have significantly higher mortality rates than intact females Further, male rats with VO develop greater ventricular dilatation and a more rapid decline in cardiac function and progression to heart failure than females Our laboratory also found that female rats are able to more successfully adapt to VO-induced myocardial stress by developing compensatory concentric hypertrophy These marked sex differences are ovarian hormone dependent, as ovariectomy abrogates this apparent sex-specific cardioprotection Additionally, we found that estrogen replacement partially restores cardioprotection in ovariectomized rats Our current study sought to determine the estrogen receptor ER dependence of the sex-specific cardioprotection.
ICI , was developed as a pure ER antagonist and has been show to block both endogenous and exogenous estrogen signaling 5 , This potent anti-estrogen binds ERs at a high affinity and downregulates ER levels by reducing intracellular half-life 10 , We therefore hypothesized that ICI , would attenuate female cardioprotection against adverse ventricular remodeling and dysfunction produced by chronic VO. Rats were housed under standard environmental conditions and maintained on commercial rat chow Harlan Teklad and tap water ad libitum.
Rat model of chronic VO stress. Infrarenal aortocaval fistula ACF was surgically created to induce chronic VO, as previously described by our laboratory 14 , Briefly, a ventral laparotomy was performed to expose the abdominal aorta and vena cava. A short-bevel gauge needle was inserted into the abdominal aorta and advanced through the medial wall of the vena cava, creating a shunt below the renal arteries. The needle was withdrawn and the aortic puncture sealed with cyanoacrylate.
Shunting of aortic blood into the vena cava was visually evident and indicated successful creation of VO. Postoperative analgesia was provided by buprenorphine hydrochloride. Experimental timeline. The effects of ER antagonism on cardiac remodeling and dysfunction induced by VO were studied in four age-matched groups: sham-operated controls Sham and fistula-induced volume overload ACF , both with and without ER antagonism by ICI , To ensure complete ER blockade and prevent any transient effects of the drug, treatment with ICI was initiated 1 wk before surgery and was delivered by intraperitoneal injection in the acute 5-day study, or by osmotic minipump in the chronic 6-wk study Alzet models and , at a dose of 0.
These time points were chosen to represent the early and compensated phases of ventricular remodeling At the experimental end points, each rat was weighed and anesthetized. The heart, lungs, and uterus were removed and weighed.
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Capillaries act as a semipermeable membrane allowing the diffusion of gases and transfer of nutrients and waste products. The single layer of flattened endothelial cells of the capillaries facilitate the exchange of substances between capillaries and tissues. Gases, such as O2 and CO2, metabolic waste products, lactate, glucose and other nutrients are transferred across the walls of the capillaries through small slits in the endothelial cells known as pores or fenestrations.
To prevent capillaries from losing vital substances such as plasma proteins, the slits in the endothelial cells are smaller than these proteins. Fluid movement between capillaries and tissues How do gas exchange and nutrient transfer happen between capillaries and tissues?
According to the Starling principle named after physiologist Ernest Starling who described it in , fluid movement through the capillary walls is governed by hydrostatic pressure and oncotic pressure. Like any fluid pushed through a confined space, blood in a capillary exerts pressure on the wall of the vessel because of the pressure exerted upstream by the blood coming from the arteriole.
The blood pressure BP generates hydrostatic pressure, which expels fluid from the pores of the capillary into the interstitial compartment. The size of the pores in the capillary dictates whether particular nutrients are delivered to particular tissues.
Hydrostatic pressure is highest at the arterial end, and lowest at the venous end, of the capillary. The other influencing force is oncotic pressure, which is underpinned by the principle of osmosis; this is the passive movement of water through a semipermeable membrane from a region of low solute concentration to one of high solute concentration, with the aim of achieving equilibrium.
An Introduction to Cardiovascular Physiology
In blood, plasma proteins — which cannot easily pass through the capillary walls — exert an osmotic pressure that tends to pull fluid from the surrounding tissue which has a higher water concentration into the capillary which has a lower water concentration. This is referred to as oncotic pressure. Fig 2 illustrates the interplay between hydrostatic and oncotic pressure.
At the arterial end of the capillary, hydrostatic pressure exceeds oncotic pressure, so fluid moves out of the capillary into the interstitial compartment. At the venous end of the capillary, the two forces are reversed, so fluid moves back from the tissue into the capillary.
In recent years, the Starling principle has been contested. More work is required to fully understand the complex processes taking place in the capillaries Levick and Michel, Another important factor is the architecture of capillaries, which varies according to their site in the body and affects their permeability Table 3. There are site-specific variations in fluid transfers between capillaries; for example, in the glomerulus where capillaries supply and drain the individual kidney units , the capillaries are porous and therefore highly permeable.
Conversely, at the blood-brain barrier in the brain, the very tight architecture of capillaries reduces their permeability. Physiological regulation of BP BP, which is crucial to maintain the perfusion of organs, is influenced by: The total volume of blood in the body; Cardiac output — the amount of blood pumped out by the heart in one minute; Peripheral vascular resistance PVR , resistance to the flow of blood in the arterial system, which is influenced by factors including vessel length, lumen diameter, and blood viscosity.
BP can be affected by a change in cardiac output or PVR. An important measure is the mean arterial pressure MAP , which is the pressure that propels blood towards tissues with each cardiac cycle and generates perfusion pressure to the organs. There are various short- and long-term physiological mechanisms that regulate BP, summarised in Fig 3 and outlined below.
Baroreceptor response The vasomotor centre in the medulla oblongata of the brain, which hosts most of the sympathetic neurons of the nervous system, has a key role in regulating vascular tone. It transmits signals along sympathetic nerve fibres to vascular smooth muscle, mostly at the level of the arterioles. This results in vasoconstriction or vasodilation, with corresponding effects on BP and blood flow to the tissues.
Alterations in BP are detected by mechanical pressure sensors baroreceptors found in the arterial wall of the carotid sinus the site between the internal and the external carotid arteries and the aortic arch. If BP suddenly rises, the walls of these vessels expand, which increases the frequency of nerve impulses sent to the vasomotor centre.
The vasomotor centre is inhibited, causing reflex vasodilation reduced vascular tone due to less sympathetic nerve activity and a decrease in BP.
Conversely, if BP falls, the decreased stretch on the arterial walls causes a decrease in baroreceptor firing and culminates in reflex vasoconstriction and an increase in BP. This is the short-term baroreceptor response regulating BP. Chemoreceptor response A similar phenomenon occurs through a chemically induced reflex via chemoreceptors, which are found in specialised cells in the arteries of the neck common carotid arteries and in the aortic arch.
These peripheral chemoreceptors predominantly detect changes in oxygen, carbon dioxide levels and pH only carotid bodies.Analysis of the collagen matrix. Statistical analyses were performed using Graphpad software Prism 5.
To ensure complete ER blockade and prevent any transient effects of the drug, treatment with ICI was initiated 1 wk before surgery and was delivered by intraperitoneal injection in the acute 5-day study, or by osmotic minipump in the chronic 6-wk study Alzet models and , at a dose of 0. The control of vascular smooth muscle and the wider control of blood vessels in response to intrinsic and extrinsic regulation are dealt with in the following three chapters.
Blood flow into the capillaries is determined by the diameter of the arterioles and can be increased through vasodilation.