About: Bradypnea is a research topic. Over the lifetime, 117 publications have been published within this topic receiving 2190 citations. The topic is also known as: slow respiration & decreased respiratory rate.
TL;DR: A novel method for selective VN stimulation to reduce BP without triggering significant bradycardia and bradypnea is presented and is robust to impedance changes, independent of the electrode's relative position, does not compromise the nerve and can run on implantable, ultra-low power signal processors.
Abstract: Objective. Hypertension is the largest threat to patient health and a burden to health care systems. Despite various options, 30% of patients do not respond sufficiently to medical treatment. Mechanoreceptors in the aortic arch relay blood pressure (BP) levels through vagal nerve (VN) fibers to the brainstem and trigger the baroreflex, lowering the BP. Selective electrical stimulation of these nerve fibers reduced BP in rats. However, there is no technique described to localize and stimulate these fibers inside the VN without inadvertent stimulation of non-baroreceptive fibers causing side effects like bradycardia and bradypnea. Approach. We present a novel method for selective VN stimulation to reduce BP without the aforementioned side effects. Baroreceptor compound activity of rat VN (n = 5) was localized using a multichannel cuff electrode, true tripolar recording and a coherent averaging algorithm triggered by BP or electrocardiogram. Main results. Tripolar stimulation over electrodes near the barofibers reduced the BP without triggering significant bradycardia and bradypnea. The BP drop was adjusted to 60% of the initial value by varying the stimulation pulse width and duration, and lasted up to five times longer than the stimulation. Significance. The presented method is robust to impedance changes, independent of the electrode's relative position, does not compromise the nerve and can run on implantable, ultra-low power signal processors.
TL;DR: The data show that the central cardiovascular and respiratory effects of opioids vary according to injection site and opioid subtype and may differ from findings obtained using cerebroventricular injections.
TL;DR: The pontine region in which μOR agonists produce bradypnea was defined to determine whether antagonism of those μORs reverses brADypnea produced by intravenous remifentanil and Histological examination of fluorescent microsphere injections shows that the sensitive region corresponds to the parabrachial/Kölliker-Fuse complex.
Abstract: Life-threatening side effects such as profound bradypnea or apnea and variable upper airway obstruction limit the use of opioids for analgesia. It is yet unclear which sites containing μ-opioid rec...
TL;DR: Results indicate that mu-opioids at plasma concentrations that cause profound analgesia produce their bradypneic effect via MORs located outside the pre-BötC region through intravenous administration of clinically relevant infusion rates of remifentanil (remi).
Abstract: Systemic administration of μ-opioids at clinical doses for analgesia typically slows respiratory rate. Mu-opioid receptors (MORs) on pre-Botzinger Complex (pre-BotC) respiratory neurons, the putati...