Ultrasound-guided central venous catheter placement through the axillary vein in cardiac critical care patients: safety and feasibility of a novel technique in a prospective observational study.

BACKGROUND: Central venous catheterization is essential for careful administration of fluids and drugs in cardiac critical care patients. The axillary vein might represent an alternative to subclavian and jugular vein accesses, with the advantage of being extra-thoracic, more distal from the pleural space and with more likehood of comfort for the patient. Conventional ultrasound-guided cannulation of the axillary vein is technically demanding and does not guarantee precise visualization of the needle tip. METHODS: We describe a new in-plane technique with a dedicated bracket support for the needle, giving full tip control and continuous visualization of the tip and vessel, making the maneuver easier and safer. In a prospective observational study we also report the feasibility and safety of the novel procedure in a series of 35 cardiac critical care patients, also receiving non-invasive ventilatory support and/or being fully anti-coagulated. RESULTS: With the novel technique, we obtained 97% success with procedural times comparable to other insertion sites and without complications. CONCLUSIONS: Placement of a central line catheter in the axillary vein using a novel ultrasound-guided bracket-assisted technique may be a feasible, safe and rapid alternative to the conventional jugular and subclavian approaches.

Malignant Cough Syncope from Idiopathic Vagal Inflammation.

We describe the case of a patient with malignant vasodepressive cough syncope. We demonstrated a vaso-vagal mechanism related to left vagal neuritis, by means of laryngoscopy and laryngeal electromyography. The condition resolved with steroid therapy. LEARNING POINTS: Left vagal neuritis should be considered in the differential diagnosis of recent onset repetitive loss of consciousness, in particular if cough related.Steroids were used to successfully treat recent onset cough-related syncope.Relatively simple trials of drug therapy can sometimes avoid intensive investigations; in our case, the use of a systemic steroid would probably have avoided many radiological and endoscopic examinations.

Effect of prolonged incubation with copper on endothelium-dependent relaxation in rat isolated aorta.

1 We investigated the effects of prolonged exposure to copper (Cu(2+)) on vascular functioning of isolated rat aorta. 2 Aortic rings were exposed to CuSO(4) (3-24 h) in Dulbecco's modified Eagle medium with or without 10% foetal bovine serum (FBS) and then challenged with vasoconstrictors or vasodilators in the absence of Cu(2+). 3 Exposure to 2 micro M Cu(2+) in the absence of FBS did not modify the response to phenylephrine (PE) or acetylcholine (ACh) in aortic rings incubated for 24 h. Identical exposure in the presence of FBS increased the contractile response to 1 micro M PE by 30% (P<0.05) and impaired the relaxant response to 3 micro M ACh or 1 micro M A23187 (ACh, from 65.7+/-7.1 to 6.2+/-1.1%, n=8; A23187, from 74.6+/-8.2 to 12.0+/-0.8%, n=6; P<0.01 for both). Cu(2+) exposure did not affect the relaxant response to NO-donors. 4 Impairment of vasorelaxation appeared 3 h after incubation with 2 micro M Cu(2+) and required 12 h to attain a steady state. Vasorelaxation to ACh was partially restored by 1 mM tiron (intracellular scavenger of superoxide ions; maximum relaxation 34.2+/-6.4%, n=10, P<0.01 vs Cu(2+) alone), whereas catalase, superoxide dismutase or cycloheximide were ineffective. 5 Twenty-four hour-exposure to 2 micro M Cu(2+) did not affect endothelium integrity or eNOS expression, and increased the Cu content in arterial rings from 6.8+/-1.1 to 18.9+/-2.9 ng mg(-1) wet weight, n=8; P<0.01. 6 Our results show that, in the presence of FBS, prolonged exposure to submicromolar concentrations of Cu(2+) impaired endothelium-dependent vasorelaxation in aortic rings, probably through an intracellular generation of superoxide ions. British Journal of Pharmacology (2002) 136, 1185-1193

Effects of adrenomedullin on the contraction of gastric arteries during reserpine-induced gastric ulcer.

Adrenomedullin (100 ng/kg, s.c.) prevents reserpine-induced damage of gastric mucosa. In the model of in vitro gastric arteries from reserpine-treated rats, adrenomedullin pre-treatment resulted in a decrease of the vasoconstriction in response to 5-hydroxytryptamine. In contrast, adrenomedullin pre-treatment of rat with intact gastric mucosa did not affect the vasoconstriction to 5-hydroxytryptamine. In the presence of the NOS inhibitor N(G)-nitro-L-arginine, the responsiveness to 5-hydroxytryptamine in gastric arteries from rats treated with reserpine + adrenomedullin was enhanced to the same level of rats treated with reserpine alone. The anti-ulcer effect of adrenomedullin could therefore be related, at least in part, to an increase of blood flow at the gastric mucosa, by a mechanism involving nitric oxide.

Secretory and vascular effects of adrenomedullin in gastric ulcer: role of CGRP- and adrenomedullin-receptors.

Adrenomedullin prevents damage of gastric mucosa in either reserpine-treated or pylorus-ligated rats. Pre-treatment with CGRP(8-37) resulted in a decrease of the gastro-protective effect of adrenomedullin in both models and reversed the inhibitory effect of adrenomedullin on gastric acid output in the pylorus-ligated rats. These adrenomedullin actions were less effectively modified by pre-treatment with adrenomedullin(22-52). These data suggest that the anti-ulcer effect of adrenomedullin is mainly related to its anti-secretory action, presumably mediated through CGRP-receptors.

Effects of phenformin on the proliferation of human tumor cell lines.

Phenformin is a biguanide that has been largely used in the past for its anti-diabetic activity. A large body of evidence suggests additional effects of phenformin including antitumoral activity in different animal models in vivo. Thus, the present study has been conducted in order to elucidate possible mechanisms involved in the antitumoral effects of phenformin. In various tumoral cell lines (SH-SY5Y neuroblastoma and LNCaP prostate adenocarcinoma cells), increasing concentrations of phenformin (50-500 microM) induced a concentration-dependent inhibition of cell proliferation. This effect was not dependent on the ability of the drug to reduce glucose levels and was accompanied by induction of apoptotic cell death as measured by cytofluorometric analysis. In addition, a short-time incubation of SH-SY5Y cells with phenformin induced enhanced and transient expression of the cell cycle inhibitor p21 suggesting that phenformin causes inhibition of cell cycle progression prior to induction of apoptosis. These results demonstrate an activity at the cellular level of phenformin that supports its antitumoral effect observed in vivo.

Role of magnesium, coenzyme Q10, riboflavin, and vitamin B12 in migraine prophylaxis.

Migraine is a neurovascular syndrome characterized by recurrent headache associated with other symptoms, eventually preceded by aura. This chapter reviews the involvement of some mineral, coenzyme, and vitamin defects in the pathogenesis of migraine headaches and focuses on their potential therapeutic use in the preventive treatment for migraine. The therapeutic potential of magnesium, coenzyme Q(10), riboflavin, and vitamin B(12) can be cautiously inferred from some published open clinical trials; it should, however, be considered that double-blind randomized larger studies are needed to correctly estimate the impact of the placebo effect in these promising therapies.