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Cardiac Hypertrophy, Heart Failure and Cardiomyopathy
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
The pathophysiology that perpetuates the progression of HF is extremely complex with compensatory mechanisms on every level of organization from subcellular all the way through to organ-to-organ interactions. Only when this network of adaptations becomes overwhelmed does HF ensue. Most important among these adaptations are the: Frank-Starling mechanism, in which an increased preload helps to sustain cardiac performance.Alterations in myocyte regeneration and death.Myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented.Activation of neurohumoral systems, especially the release of norepinephrine by adrenergic cardiac nerves, which augments myocardial contractility and includes activation of the RAAS, sympathetic nervous system (SNS) and other neurohumoral adjustments that act to maintain arterial pressure and perfusion of vital organs.
Regulation of Arterial Blood Pressure
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The cell bodies of the efferent vagal parasympathetic cardiac nerves are located in the nucleus ambiguus in the ventrolateral medulla and the dorsal vagal nucleus. They receive baroreceptor input from the nucleus tractus solitarius and discharge synchronously with each cardiac cycle. The medullary inspiratory neurons directly inhibit the parasympathetic activity to cause tachycardia during inspiration, as seen in sinus arrhythmia.
Anatomy and Function of the Intrathoracic Neurons Regulating the Mammalian Heart
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
Sympathetic Neurons. The somata of the efferent postganglionic sympathetic neurons that innervate the canine heart are located primarily throughout the middle cervical ganglia. They are also located in the cranial portions of the stellate ganglia, in the mediastinal ganglia associated with cardiopulmonary nerves as well as adjacent to or on the heart (Armour and Janes, 1988; Armour and Hopkins, 1981; Butler et al., 1988a; Hopkins and Armour, 1984) (cf. Fig. 1); a few are located in the cranial cervical ganglia. In non-human primates they are relatively evenly distributed between the stellate, middle cervical, and superior cervical ganglia (Armour and Hopkins, 1984). Efferent postganglionic sympathetic neurons in any ganglionic locus project axons to widespread regions of the heart. In addition, the somata of some of these neurons project axons into two or more cardiopulmonary nerves (Tomney et al., 1985). This anatomical organization may facilitate interactions between adjacent neurons in a ganglion that innervate different cardiac regions. The efferent sympathetic axons in a cardiopulmonary nerve (Armour and Randall, 1975) or cardiac nerve on the heart (Brandys et al., 1986) innervate relatively specific cardiac regions (Randall et al., 1972), considerable variability occurring in such patterns of innervation for any particular nerve in different dogs (Janes et al., 1986), cats (Phillips et al., 1986) or nonhuman primates (Randall et al., 1971).
Transient receptor potential vanilloid 1-expressing cardiac afferent nerves may contribute to cardiac hypertrophy in accompany with an increased expression of brain-derived neurotrophic factor within nucleus tractus solitarius in a pressure overload model
Published in Clinical and Experimental Hypertension, 2022
Risa Shibata, Keisuke Shinohara, Shota Ikeda, Takeshi Iyonaga, Taku Matsuura, Soichiro Kashihara, Koji Ito, Takuya Kishi, Yoshitaka Hirooka, Hiroyuki Tsutsui
In this study, we hypothesized that TRPV1-expressing cardiac afferent nerves could contribute to cardiac hypertrophy in association with an increased BDNF expression within the NTS, which has been reported to induce sympathoexcitation (14). We investigated whether the pressure overload-induced cardiac hypertrophy was attenuated in TRPV1 knockout (KO) mice and also determined whether the pressure overload cardiac hypertrophy induced BDNF expression in NTS in wild-type, and this induction was attenuated in TRPV1 KO mice. Additionally, we selectively ablated the TRPV1-expressing cardiac nerve endings by chemical intervention and investigated the effects of cardiac sympathetic afferents on pressure overload cardiac hypertrophy in mice.
Utility of the cold pressor test to predict future cardiovascular events
Published in Expert Review of Cardiovascular Therapy, 2019
Sjaak Pouwels, Michel E. Van Genderen, Herman G. Kreeftenberg, Rui Ribeiro, Chetan Parmar, Besir Topal, Alper Celik, Surendra Ugale
The first indication for involvement of the sympathetic ANS was found and shown in experiments by Shapiro et al. [91] Their study described also an increase in cardiac output and they postulated that this finding was the result of hypothalamic discharge along the inferior cardiac nerve [91]. Numbers of studies from the same time period investigated local vascular responses to CPT. After long immersions of the hand, capillary beds initially constrict and then periodically dilate during short periods of time [92]. This wave-like vascular response is known as the Lewis wave, indicating a temporarily weakening of the sympathetic tone [5,92]. This physiological phenomenon is also known as cold-induced vasodilatation.
Transient anisocoria after a traumatic cervical spinal cord injury: A case report
Published in The Journal of Spinal Cord Medicine, 2020
Paul Overdorf, Gary J. Farkas, Natasha Romanoski
Preganglionic sympathetic fibers destined for the head and neck arise from neurons in the intermediolateral cell column of the lateral horn of the upper five thoracic spinal segments (Fig. 1). These fibers ascend through the thoracic and cervical sympathetic trunk to reach the inferior, middle, and/or superior cervical ganglion.11 Some preganglionic fibers synapse at the ganglia and their postganglionic fibers travel through gray rami communicates to access the cervical spinal nerves, while other preganglionic fibers course anteromedially to form the cardiac nerves.11,12