A New Approach to Percutaneous Subclavian Venipuncture to Avoid Lead Fracture or Central Venous Catheter Occlusion

Pacemaker and defibrillator leads and central venous catheters placed by commonly recommended techniques have been found to pass through the subclavius muscle, the costocaracoid ligament, or the costoclavicular ligament before entering veins medial to the first rib. Entrapment by these soft tissues subjects leads and catheters to stresses imposed by movements of the ipsilateral upper extremity. Accordingly, a new approach has been developed that introduces the lead or catheter into the subciavian vein near the lateral border of the first rib. This placement avoids soft tissue entrapment and may extend the longevity of leads and catheters.     

TEENAGE HEAVY DRINKERS: ALCOHOL-RELATED KNOWLEDGE, BELIEFS, EXPERIENCES, MOTIVATION AND THE SOCIAL CONTEXT OF DRINKING

During 1988 and 1989 a survey was conducted of the drinkinghabits and alcohol-related beliefs of a national sample of teenagersin England. Data were obtained from 6,244 respondents virtuallyall aged 14–16. Heavy drinkers were significantly morelikely to report drinking in a mixed sex group than were otherteenagers. They were also more likely than others to have drunkillegally in licensed premises, and were distinctive from otherteenagers in relation to their self-reported reasons for drinkingand their alcohol-related beliefs.     

Isoflurane attenuates dynorphin-induced cytotoxicity and downregulation of Bcl-2 expression in differentiated neuroblastoma SH-SY5Y cells

Background: It has been proposed that the volatile anesthetic isoflurane induces neuroprotection and that the endogenous opioid peptide dynorphin induces neurocytotoxicity in cells. The levels of dynorphin are often significantly elevated in neuropathophysiological conditions, and dynorphin can directly induce toxicity. However, the neuroprotective effects of isoflurane on dynorphin-induced cytotoxicity are still unclear.
Methods: In order to determine the effect of isoflurane on dynorphin-induced cytotoxicity in neuronal cells, we have designed a device wherein cultured human neuroblastoma SH-SY5Y cells can be exposed to isoflurane. Fully differentiated SH-SY5Y cells were obtained by treating the cells with retinoic acid for 6 days. We examined SH-SY5Y cell survival, apoptosis, and antiapoptotic protein expression by cell viability, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling stain, and Western blot analysis, respectively.
Results: After 16 h of dynorphin (10 μM) treatment, the SH-SY5Y cells showed significant cytotoxicity, apoptosis, and downregulation of the antiapoptotic Bcl-2 protein expression. These effects of dynorphin were significantly inhibited by isoflurane exposure for 32 h [pretreatment for 16 h and posttreatment (after dynorphin treatment) for 16 h].
Conclusion: Thus, our results suggest that isoflurane exerts neuroprotective effects in the case of dynorphin-induced pathophysiological disruption.     

Sotalol: From "Just Another Beta Blocker" to "The Prototype of Class III Antidysrhythmic Compound"

Sotalol is a beta-blocking drug devoid of membrane stabilizing properties, as well as intrinsic sympathomimetic actions, or cardioselectivity. In addition, sotalol prolongs atrial and ventricular repolarization (Class III antiarrhythmic activity). It appears to have less myocardial depressant effect than other beta-blocking agents. Given orally, bioavailability of the drug reaches 100%. Sotalol's plasma half-life is 15 hours (range 7–18) and is dependent only on renal function. In clinical practice, it has been found effective in the suppression of nearly all supraventricular and ventricular dysrrhythmias except those related to prolonged ventricular repolarization. Most common adverse effects are dyspnea, bradycardia, and fatigue, which results in drug termination in 16% of the cases. Torsades de pointes usually associated with bradycardia and drug induced QTc prolongation has been reported in 1.9%–3.5% of the patients receiving sotalol. This complication may be reduced by limiting the dose (< 640 mg/day) especially in patients with impaired renal function. In addition hypokalemia must be avoided. To sum up, the combination of Class II and Class III effects may carry additional benefits. However, further studies are required to test such hypotheses.     

Estrogen inhibition of noradrenaline release in the rabbit oviduct1

In the present study, we investigated the influence of estrogen on ³H-noradrenaline (³H-NA) release induced in the oviductal isthmus by electrical stimulation, potassium and calcium. The fractional release of ³H-NA was measured in oviducts isolated from ovariectomized rabbits and from ovariectomized rabbits treated with estradiol cypionate, 70 μg/kg im 72 h before an experiment. Electrical field stimulation of the intramural nerves induced muscle contraction and augmented the release of labelled NA from the muscle. The ³H-NA release was reduced after estrogen treatment when reuptake of NA into the nerve terminals was blocked by desipramine, 10^-6 M. Estrogen also reduced the ³H-NA release evoked by exposure of the oviducts to 121 mM KCI in the presence of calcium (2.5 mM) and in a high potassium, calcium-free medium upon the addition of 2.5 mM calcium. In the presence of desipramine a small fraction of ³H-NA was released in high potassium, calcium-free medium. This release was unaffected by estrogen. These results suggest that estrogen reduces the release of NA from the adrenergic nerves within the oviduct and that this action is exerted primarily on the calcium-dependent release. It therefore might be due to a reduction in the entry of calcium into the nerve terminal.     

The involvement of intramural nerves in cholera toxin induced intestinal secretion

In previous reports we have suggested that nervous reflexes are involved in the pathophysiology of cholera secretion and that these nervous reflexes involve a cholinergic synapse and a neuron with vasoactive intestinal polypeptide (VIP) as neurotransmitter. These proposals were further analyzed in this study. Tetrodotoxin (TTX) and lidocaine applied on the serosal surface inhibited cholera secretion in segments of rat small intestine. Fluid absorption in control rats was not significantly changed. Hexamethonium given i. v. decreased cholera secretion in the cat. No additional inhibition of cholera secretion was observed after giving TTX close i. a. Furthermore, the intestinal secretion evoked by VIP was not influenced by hexamethonium given i. v. or TTX given close i. a. The present observations support the hypothesis of a role for nervous reflexes in cholera secretion. The results suggest that at least a major part of the proposed nervous reflex(es) in cholera have a cholinergic synapse. Furthermore, the VIP-ergic neuron is situated “distal” to the cholinergic neuron in the reflex(es) closer to the effector cells.