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Control of breathing
Published in Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson, Ward, Milledge and West's High Altitude Medicine and Physiology, 2021
Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson
Extensive evidence indicates that hypoxia-inducible factors mediate adaptive responses to hypoxemia and are sensed by the carotid body (see Figure 9.3: reviewed in: Semenza and Prabhakar 2018). Kline et al. (2002) studied the importance of the hypoxia-inducible factor-1α (HIF-1α) in the changes in HVR with acclimatization. In this study, heterozygous transgenic mice, with one chromosome for HIF-1α knocked out (homozygous knock-out mice die in utero), were compared with wild-type mice. Whereas there was no difference in response to acute hypoxia, the effect of chronic hypoxia (three days at 0.4 atm) was different. The wild-type mice showed the expected increase in HVR, while the knock-out mice showed reduced HVR. They showed this result both in terms of , especially respiratory rate, and in carotid sinus nerve activity, indicating it was an effect in the carotid body as opposed to a purely central effect.
Resetting of the Arterial Baroreflex: Peripheral and Central Mechanisms
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
Mark W. Chapleau, George Hajduczok, Francois M. Abboud
Central Adaptation of Sympathetic and Parasympathetic Responses to Baroreceptor Stimulation. Studies have demonstrated central resetting or adaptation of both sympathetic and parasympathetic (vagal) responses to baroreceptor stimulation. Electrical stimulation of baroreceptor afferent neurons triggers reflex inhibition of sympathetic nerve activity, but the sympathetic activity may increase or “escape” from inhibition despite the constant sustained baroreceptor input to the CNS (Richter et al., 1970). Electrical stimulation of the carotid sinus nerve also triggers reflex activation of cardiac vagal efferent neurons and a decrease in heart rate (McCloskey and Potter, 1981). The spontaneous activity in single vagal neurons is inhibited for 100–150 ms after the initial excitation induced by a single electrical stimulus to the carotid sinus nerve. The inhibition cannot be attributed to the refractory period of the vagal neuron that lasts for only 10 ms after a spontaneous action potential. When a pair of stimuli are applied to the sinus nerve, the second stimulus has to be given at least 80–100 ms after the first to trigger a second response in the vagal neuron (McCloskey and Potter, 1981).
Cardiovascular receptors, reflexes and central control
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
The carotid sinus is a thin-walled dilatation at the origin of the internal carotid artery. Afferent fibres from the carotid sinus baroreceptors form the carotid sinus nerve. This joins the glossopharyngeal nerve (ninth cranial nerve) to reach the petrous ganglion, where the parent neurons are located. Like all afferent neurons, the petrous neurons are bipolar. Their central axons continue up the glossopharyngeal nerve to the brainstem and terminate in the nucleus tractus solitarius.
The carotid body and associated tumors: updated review with clinical/surgical significance
Published in British Journal of Neurosurgery, 2019
Nasir Butt, Woong Kee Baek, Stefan Lachkar, Joe Iwanaga, Asma Mian, Christa Blaak, Sameer Shah, Christoph Griessenauer, R. Shane Tubbs, Marios Loukas
However, this discovery has often been credited to his mentor Albrecht von Haller, who was known for his interest in the role of the nervous system on the physiology of the heart and blood vessels.2–4 For decades after its description, the function of the carotid body remained a mystery. According to Zappata and Larraín,5 its role as a sensory receptor for chemical changes in the blood was largely based on histological studies by de Castro in 1926.5 By establishing a histological description of the carotid body, de Castro was able to propose its role as a sensory organ, “tasting blood,” before his work was disrupted by the Spanish Civil War.6 At about the same time, the Heymans, a father and son team, were researching the physiological significance of these structures using cross-circulation experiments on dogs.6 These authors ran an experiment in which they severed the connection of the carotid sinus nerve. They then injected potassium cyanide into the carotid arteries and found that severe hyperventilation followed when the connection was intact. However, when the nerve connection to the carotid body was cut, there was no corresponding increase in respiration.6 For their role in discovering the function of the carotid body, the Heymans received the Nobel Prize in 1938.
Strong stimulation triggers full fusion exocytosis and very slow endocytosis of the small dense core granules in carotid glomus cells
Published in Journal of Neurogenetics, 2018
Amy Tse, Andy K. Lee, Noriko Takahashi, Alex Gong, Haruo Kasai, Frederick W. Tse
Our results show that with a large [Ca2+]i rise, exocytosis of glomus SDCGs can shift from the kiss-and-run mode to full fusion, resulting in a more complete release of transmitters. During a severe hypoxic challenge, the cytosolic [Ca2+] of glomus cells (averaged from the entire cell) increased to ∼1 to 1.6 μM (Buckler & Vaughan-Jones, 1994). Since the hypoxia-evoked [Ca2+]i rise is mediated via activation of VGCCs, it is conceivable that the Ca2+ entry via VGCCs generates a spatial Ca2+ gradient, such that the secretory granules near the vicinity of VGCCs are exposed to a local Ca2+ concentration which is higher than the cytosolic average. In chromaffin cells, the local Ca2+ near the VGCCs was estimated to be 10–100 μM (Garcia, Garcia-de-Diego, Gandia, Borges, & Garcia-Sancho, 2006). It is not clear whether secretory granules in glomus cells are tightly coupled to VGCCs. Nevertheless, it is conceivable that some glomus granules near the VGCCs may be exposed to [Ca2+] in the range of 10 μM and thus undergo full fusion for a more complete release of transmitters. This would result in a more robust stimulation of the carotid sinus nerve and the triggering of the respiratory and cardiovascular reflexes.
Does surgical technique influence the postoperative hemodynamic disturbances and neurological outcomes in carotid endarterectomy?
Published in Acta Chirurgica Belgica, 2019
Serkan Burç Deşer, Mustafa Kemal Demirag, Fersat Kolbakir
Carotid endarterectomy (CEA) is a safe and an effective surgical technique which has been used for the treatment of severe extracranial carotid artery stenosis to reduce the risk of stroke for symptomatic and asymptomatic patients under the age of 75 with ≥ 70% stenosis in line with NASCET criteria and with a 3% perioperative risk [1–7]. Surgical options comprise conventional (C-CEA) and eversion carotid endarterectomy (E-CEA) techniques. C-CEA performed through a longitudinal arteriotomy of the internal carotid artery (ICA) followed by primary closure, autologous vein or prosthetic patch angioplasty. Longitudinal arteriotomy minimizes disruption of the carotid sinus nerve fibers during C-CEA [6]. E-CEA which is obliquely transection of the internal carotid artery (ICA) at the carotid bifurcation was initially reported by DeBakey et al [8], later described by Etheredge [9] and improved E-CEA by Raithel [10]. Major stroke, mortality rate, postoperative cranial nerve injury, cerebral ischemia, postoperative blood pressure alterations and early thrombosis or restenosis are main complications of CEA [5,11]. Transaction of the carotid sinus nerve fibers during E-CEA may leads to loss of baroreceptor responses which lead to increase in peripheral vascular resistance, blood pressure and heart rate [12–14]. Consequently, increase in the sympathetic activity may lead to uncontrolled hypertension, heart failure, myocardial infarction and stroke [14]. E-CEA has found to be associated with the loss of the baroreceptor reflex and postoperative hypertension in previously published studies [15]. This study aimed to compare the postoperative hemodynamic changes, postoperative stroke rate and complications between E-CEA and C-CEA.