1625915643-5d53d156c9525bd62bd0d3434ecdc231 (843955), страница 31
Текст из файла (страница 31)
The myocardium is innervated by sympathetic nerves. Arterial and venous vessels throughout most of the body are innervated by sympatheticnerves, whereas the parasympathetic nervous system innervates vessels in the genital organs and lower GItract. Autonomic efferent activity is regulated by the baroreceptor reflex, in response to changes in arterialpressure detected at the carotid sinus and aortic arch baroreceptors. The response to a change in postureis illustrated.
ACh, acetylcholine; E, epinephrine; MAP, mean arterial pressure; NE, norepinephrine.the SA nodal pacemaker rate, myocardial contractility, andvascular smooth muscle tone (Fig. 11.2). Sympathetic nerveendings at the heart and vessels release norepinephrine, whileparasympathetic nerves release acetylcholine at the heart (primarily the SA node) and in a few vascular beds (vessels inmost regions do not have parasympathetic innervation). Inaddition to direct release of catecholamines by sympatheticnerves in the heart and vessels, circulating catecholamines(predominantly epinephrine) released by the adrenal glandcontribute to cardiovascular regulation when the sympatheticnervous system is strongly activated.Heart Rate RegulationThe arterial baroreceptor reflex is a key mechanism involvedin autonomic regulation of cardiovascular function (seeFig. 11.2).
The baroreceptors consist of specialized cells in thevascular wall of the carotid sinuses and aortic arch. Barorecep-The Cardiac Pumptors respond to the stretch associated with elevation of arterialpressure by increasing afferent impulses to the medullary cardiovascular center, where autonomic nervous system activityis regulated. In response to increased afferent input, sympathetic nerve activity is reduced, and parasympathetic outflowis increased. The effects of these autonomic responses on theheart and vessels result in a return of arterial blood pressuretoward its original level; specific aspects of this regulation arediscussed in the following text.Mechanisms that contribute to regulation of heart rate includethe following:■■■The autonomic nervous system and baroreceptors.The Bainbridge reflex response to atrial stretch.Effects of thoracic pressure changes during respirationon venous return.Under normal conditions, heart rate regulation is accomplished primarily by the autonomic nervous system and baroreceptor reflexes.
Sympathetic nerves release norepinephrineat the SA node, which acts at β1 receptors, increasing cAMPproduction and ultimately raising the activity of the pacemaker and elevating heart rate. Parasympathetic activationreduces heart rate through release of the neurotransmitteracetylcholine. Thus, when arterial pressure rises, the baroreceptor reflex results in a fall in the SA node pacemaker rate.The resulting reduction in heart rate contributes to a fall inCO, and a return to normal arterial pressure (see Fig.
11.2).Conversely, reduced arterial pressure will result in less stretchof baroreceptors, reduced afferent impulses to the cardiovascular center, greater sympathetic activity, and reduced parasympathetic activity, raising heart rate and returning arterialblood pressure to the normal level.Another reflex potentially regulating heart rate is the Bainbridge reflex.
When right atrial volume is increased, low-pressure stretch receptors (that is, receptors responding to stretchat the low pressures typical in the atria) initiate a neural reflexthat increases heart rate through sympathetic nerves. Notethat arterial baroreceptors respond to stretch by decreasingheart rate, whereas atrial baroreceptors respond to stretch byincreasing heart rate. In the former case, the response is partof a mechanism to regulate arterial pressure, and in the lattercase, the response is to increased blood volume. When atrialstretch results in increased HR, blood volume will be redistributed.
In addition, a number of other mechanisms for regulating blood volume and pressure will be activated; these willbe considered subsequently (see “Regulation of Arterial BloodPressure” in Chapter 12).Heart rate may also be affected by the respiratory cycle, particularly in infants and children.
In so-called respiratory sinusarrhythmia, heart rate is increased during inspiration anddecreased during expiration. The low-pressure baroreceptorswithin the atria are stretched by increased venous returnduring inspiration, producing the cyclic variation in HR.117The Bainbridge reflex and the arterial baroreceptorreflex produce opposite responses to an intravenousinfusion. The Bainbridge reflex is usually observed when a rapidintravenous infusion is administered to a subject with a slowheart rate. Stretch of atrial receptors produces a reflexiveincrease in heart rate under these circumstances.
On the otherhand, when heart rate is high to begin with, for example, afterhemorrhage, intravenous infusion usually decreases heart rate.In this circumstance, the increased ventricular filling associatedwith the infusion produces an increase in cardiac output andtherefore an increase in arterial pressure. The rise in arterialpressure causes stretch of arterial baroreceptors, resulting indiminished sympathetic nervous system activity and enhancedparasympathetic activity, and a slowing of heart rate.Stroke Volume RegulationStroke volume regulationparameters:■■■isdependentonseveralPreload: The degree of stretch of myocardial fibers priorto contraction. Preload in the intact heart is closelyrelated to end-diastolic volume of the ventricle. Increasedpreload is associated with increased force of contraction,and hence, increased stroke volume.Afterload: The force against which the heart contracts.In the intact heart, afterload is closely related to arterialpressure or left ventricular pressure during systole.Increased afterload opposes ejection by the heart andtherefore will tend to reduce stroke volume.Contractility (inotropism): The intrinsic ability ofcardiac muscle to generate force at a given fiber length.Specifically, contractility is not synonymous with forceof contraction, because force of contraction is dependent on degree of initial stretch of the muscle fibers(preload).The Frank-Starling RelationshipThe Frank-Starling relationship is named for Otto Frank,who described the relationship between pressure generated inthe frog heart and the diastolic volume, and for Earnest Starling, who demonstrated, in an intact, canine heart-lungpreparation, the relationship between stroke volume andend-diastolic volume.
The cardiac function curve illustratesthis relationship (Fig. 11.3A). When preload is increased byraising atrial pressure, stroke volume (and therefore, cardiacoutput) rises, up to the optimum level of preload. This is anintrinsic mechanism for regulation of stroke volume and isnot associated with a change in inotropism. The molecularbasis for this relationship involves stretch of sarcomeres; atoptimal preload, conditions for subsequent crossbridge formation and recycling are best.Sympathetic Regulation of Stroke VolumeStroke volume is also regulated by the sympathetic nervoussystem (Fig. 11.3B). Cardiac muscle is directly innervated by118Cardiovascular PhysiologyCardiacFunction CurveStrokevolume orcardiacoutputDevelopedtensionRight atrial pressureATimeSympathetic stimulationNormal resting stateHeart failureStrokevolume orcardiacoutputBRight atrial pressureFigure 11.3 The Frank-Starling Relationship A, An increase inpreload of the ventricle results in an increase in stroke volume and thuscardiac output.
B, Sympathetic stimulation of the heart shifts this curveupward and to the left; heart failure results in a lower slope of the curve.The slope of the cardiac function curve is one measure of contractilityof the heart. In this graph, it is assumed that afterload (arterial pressure)is held constant.The Frank-Starling relationship is an important mechanism for matching cardiac output and venous return,and left- and right-side cardiac output.
If output from the rightventricle is suddenly increased (for example, due to a change inposture), return to the left ventricle will be rapidly elevated. Theresulting stretch of the left ventricle will cause an increase in itsoutput, matching the rise in output that occurred on the rightside. Thus, the Frank-Starling relationship maintains balancebetween right- and left-side output. It is also an importantmechanism in the adjustment of stroke volume and cardiacoutput during the complex physiological changes associatedwith exercise or volume depletion (for example, inhemorrhage).Figure 11.4 Effect of Heart Rate on Force of Contraction(Treppe or Staircase Effect) When the intervals between cardiacmuscle contractions are long, the tension developed is low.
![](https://s.studizba.com/z.php?f=/templates/si/i/noavatar.png&w=100&h=100&t=1"){kind=avatar}
