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Critical Review of Evidence for Neonatal Cocaine Intoxication and Withdrawal
Published in Richard J. Konkol, George D. Olsen, Prenatal Cocaine Exposure, 2020
Delia A. Dempsey, Donna M. Ferriero, Sarah N. Jacobson
For years, it has been standard of care in our nursery and in many nurseries to use a single scoring system to monitor all neonates with a history of illicit drug exposure for signs of withdrawal, albeit opiate withdrawal.51Table 7.2 lists the studies that have data on abnormal signs or behaviors noted in cocaine-exposed newborns. Many of the abnormal signs given in Table 7.2 are attributed to cocaine withdrawal because of their similarity to neonatal opiate withdrawal, even though cocaine is a sympathomimetic and opiates are sympatholytics. The assignment of most abnormal signs and behaviors in cocaine-exposed neonates to withdrawal comes from the similarity of these signs to opiate withdrawal. However, there are no reports of significant morbidity or mortality associated with neonatal cocaine withdrawal. Cocaine is a stimulant drug, and intoxication is associated with euphoria, tachycardia, hypertension, tachypnea, hyperactivity, anorexia, hyperthermia, seizures, etc. It is possible that some of the signs listed in Table 7.2 are actually signs of cocaine intoxication.
Adrenergic Antagonists
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Inhibition of adrenoceptors signalling pathways can occur by diverse mechanisms like non-competitive and competitive adrenergic blockers bound to the adrenoceptors in post-synaptic level; by drugs modulating the regulation of catecholamines like catecholamine synthesis blockade by methyltyrosine; vesicular blockade by reserpine which prevents release of noradrenaline; drugs for instances bretylium, guanethidine and 6-hydroxydopamine that act specifically on the sympathetic nerve terminal causing an amassing of neurotransmitter within sympathetic neurones or α2 adrenoceptor agonists acting on α2 adrenoceptor presynaptically and inhibiting postsynaptic activation of adrenoceptors and downstream signalling pathway (Brock et al., 1988). Hence, these medications are clinically important in the therapy of anxiety disorders like GAD, posttraumatic stress disorder (PTSD) and panic disorders (Tyrer, 1992; Kaplan, 1998); in cardiovascular diseases like hypertension; respiratory disorders like asthma, nasal decongestion; ophthalmology for glaucoma; BPH and so on (Brunton et al., 2011). The chapter aims in giving an insight to the readers about various sympatholytic agents affecting the sympathetic system, its action on neurotransmission and explain about specific receptor subtypes bound drugs showing desired pharmacological action thereby rendering it useful clinically.
Motion-Induced Nausea and Vomiting
Published in John Kucharczyk, David J. Stewart, Alan D. Miller, Nausea and Vomiting: Recent Research and Clinical Advances, 2017
Some drugs are known to facilitate motion sickness. A centrally acting cholinesterase inhibitor, physostigmine, produces a motion sickness-like syndrome in subjects not exposed to provocative motion.218 The opiate antagonist, naloxone, enhances motion sickness in humans219 and cats.220 Some sympatholytic drugs also increase susceptibility to motion sickness.193
Incidence and clinical manifestation of iatrogenic opioid withdrawal syndrome in mechanically ventilated patients
Published in Current Medical Research and Opinion, 2021
Suthinee Taesotikul, Pitchaya Dilokpattanamongkol, Viratch Tangsujaritvijit, Chuthamanee Suthisisang
This study demonstrated a higher incidence of IOWS (23.6%) than a previous prospective study conducted by Wang et al. (16.7%)12 based on the same assessment tool and participants with a similar severity score (mean APACHE of 22). The number of patients who received alpha-2 agonists as concomitant medication was higher in Wang et al.’s study than ours (46.3% and 3.6%, respectively). Alpha-2 agonists, including dexmedetomidine and clonidine, have a sympatholytic property which alleviates withdrawal symptoms from sympathetic over-activity15. This presumably resulted in a higher incidence of IOWS in our study. Furthermore, we observed patients at 1, 3, 6 and 24 h after fentanyl discontinuation or dose reduction. This frequent pattern of observations increased the possibility of detecting symptoms that lasted less than 24 h after fentanyl discontinuation or dose reduction such as muscle pain, lacrimation and rhinorrhoea.
Pharmacotherapeutic strategies for treating hypertension in patients with obesity
Published in Expert Opinion on Pharmacotherapy, 2018
Revathy Carnagarin, Vance Matthews, Cynthia Gregory, Markus P. Schlaich
Given the important role of increased sympathetic outflow in the pathogenesis of OHT, it is perhaps surprising that central sympatholytic blockade with imidazoline I1-receptor agonists is not used more frequently in the management of OHT. Some misconceptions may exist relating to the adverse effects of older central sympatholytic agents such as clonidine or α-methyldopa, which were commonly associated with tiredness, sedation, and rebound hypertension when ceased (clonidine). The newer imidazoline I1-receptor agonists such as moxonidine and rilmenidine have been demonstrated to be well tolerated and effective in lowering BP. In contrast to clonidine which binds to central α2 receptors, the newer agents bind to the Imidazoline I1-receptor thereby largely avoiding the clonidine like side effects [66,67]. However, a dry mouth sensation can occur in up to 10% of patients on moxonidine due to its inhibitory effect on salivary flow [68]. From a metabolic perspective, moxonidine has been demonstrated to enhance insulin sensitivity, as shown with an insulin clamp technique in obese spontaneously hypertensive rats [69]. In addition to BP lowering, moxonidine treatment improves insulin sensitivity in patients with obesity hypertension [70]. The BP-lowering effect of moxonidine was comparable to amlodipine, but with additional effects such as the improvement of insulin resistance, reduction of plasma leptin levels and attenuation of sympathetic overdrive [71].
Effects of Traditional Chinese Medicine, Dilong Injection, on Random Skin Flap Survival in Rats
Published in Journal of Investigative Surgery, 2018
Lina Xu, Dingsheng Lin, Bin Cao, Dongnan Ping
Random pattern skin flaps, such as Z-Plasty, Limberg flap, and rotational flaps, are frequently used in plastic and reconstructive surgery to repair local tissue loss and for the reconstruction of several tissue defects for their flexibility and convenience. However, the aspect ratio with great restriction normally cannot be more than 1.5–2:1. The trouble for plastic surgeons is the necrosis of random skin flap, which is one of the most vital problems encountered in flap surgery. Partial or total flap loss may result in a new tissue defect at the flap donor area, increasing the total defect area requiring reconstruction [1]. Such complications may increase the cost of treatment, the length of hospital stay, and, most importantly, may damage the patient's confidence and trust in his/her doctor [1]. Previous studies [2–4] have revealed many factors, such as insufficient arterial flow, ischemia-reperfusion injury, expression of apoptosis-related factors, and inflammation, playing role in the process of flap necrosis. In an attempt to increase viability, numerous surgical and pharmacological methods have been described to increase flap viability. Pharmacological agents, such as sympatholytics, vasodilators, calcium channel blockers, hemorheologics, prostaglandin inhibitors, anticoagulants, glucocorticoids, and free radical scavengers, have been applied topically and administered enterally or parenterally. However, the use of some drugs with proven experimental efficacy has been restricted by side effects, high cost, and/or poor availability [1].