PubMed Health⌕ Search

Biomedical subjects

J W O'Brien

Publications and source records attributed to J W O'Brien.

7 recordsLinked to original sources
PubMed1997

Current induction in a fiberglass guidewire compared to conventional wires during simulated papillotomy.

BACKGROUND: Current induced in a guidewire during papillotomy poses a danger of injury to the bile duct. We measured currents induced in three commercially available guidewires and a prototype fiberglass wire during simulated sphincterotomy under standard and nonstandard conditions. METHODS: Blended current at 55 W was applied to a double-lumen papillotome grounded through a 1000 omega resistor. For extreme conditions, power was increased to 70 W using a single-lumen papillotome. Fault conditions were created with a break in the insulation at the distal end of each wire. Guidewire-induced current was measured, and safety calculations performed for adherence to accepted standards for electrosurgical devices. RESULTS: Induced current was within safety limits for all wires tested under standard conditions. With insulation faults, one of the commercially available wires was unsafe. Under extreme conditions, with or without faults, the three commercial wires produced currents ranging from 9% to 225% above acceptable levels, while only the prototype wire remained safe. CONCLUSIONS: Most guidewires contain metal cores that function as capacitors. Because its core is primarily fiberglass, the prototype wire generates less induced current under nonstandard conditions, thus achieving a greater margin of safety during wire-guided sphincterotomy.

Bile Ducts↗
PubMed1991

Effects of internal mammary artery dissection on phrenic nerve perfusion and function.

The effects of left internal mammary artery (LIMA) dissection and distal division on phrenic nerve perfusion and function were examined in an adult swine model. Phrenic nerve perfusion was determined by left atrial injection of radioactively labeled microspheres. Phrenic nerve function was determined by measuring nerve and diaphragm potentials evoked by bilateral phrenic nerve stimulation. In the first group of animals (n = 9), the LIMA was dissected with ligation of all its branches. Left phrenic nerve perfusion and function decreased after LIMA dissection in every animal studied, whereas only minimal changes were observed on the right. Sixty minutes after LIMA dissection, left phrenic nerve mean perfusion decreased 71%. Left phrenic nerve and left diaphragm mean action potential amplitudes decreased 54% and 80%, respectively. In the second group of animals (n = 4), the LIMA dissection was performed without division of the pericardiacophrenic artery, a small proximal branch of the internal mammary artery that supplies the phrenic nerve. Sixty minutes after LIMA dissection, left phrenic nerve perfusion had decreased by 21% from control values, with a corresponding decrease in left phrenic nerve and diaphragm mean action potential amplitudes of 19% and 23%, respectively. These results indicate that LIMA dissection with division of all its branches in this model is associated with a significant impairment in left phrenic nerve perfusion and function and suggests a causal relationship. These results may also explain the apparent increased phrenic nerve cold sensitivity and increased incidence of phrenic nerve dysfunction associated with LIMA grafting.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1988

Activities of octopamine and synephrine stereoisomers on alpha-adrenoceptors.

1. The activities of the (-)- and (+)-forms of m- and p-octopamine and m- and p-synephrine on alpha 1-adrenoceptors from rat aorta and anococcygeus and alpha 2-adrenoceptors from rabbit saphenous vein were compared with those of noradrenaline (NA). 2. The rank order of potency of the (-)-forms on alpha 1-adrenoceptors from rat aorta and alpha 2-adrenoceptors was NA greater than m-octopamine = m-synephrine greater than p-octopamine = p-synephrine. The two m-compounds were 6 fold less active than NA on alpha 1-adrenoceptors from rat aorta and 150 fold less active on alpha 2-adrenoceptors. The two p- compounds were 1,000 fold less active than NA on both alpha 1-adrenoceptors from rat aorta and alpha 2-adrenoceptors. The rank order of potency of the (-)- forms on alpha 1-adrenoceptors from rat anococcygeus was NA = m-synephrine greater than m-octopamine greater than p-octopamine = p-synephrine. m-Octopamine was 4 fold less active than NA and (-)-m-synephrine. The two p- compounds were 30 fold less active than NA. 3. The rank order of potency of the (+)- forms was NA greater than m-octopamine greater than m-synephrine greater than p-octopamine greater than p-synephrine on both alpha 1- and alpha 2-adrenoceptors. The potency of each (+)- form was 1-2 orders of magnitude less than that of the (-) counterpart, the differences being greater for the stereoisomers of synephrine than for those of octopamine on both alpha 1- and alpha 2-adrenoceptors. 4. The yohimbine diastereoisomer antagonists, rauwolscine and corynanthine, were tested against (-)-NA and (-)-m-octopamine-induced contractions in both preparations. Based upon the known selectivities of these isomers for alpha-adrenoceptor subtypes, it is concluded that the rat aorta contains only alpha 1-adrenoceptors while the rabbit saphenous vein possesses predominantly alpha 2-adrenoceptors. 5. Ligand binding data for the octopamine and synephrine stereoisomers at alpha 1- and alpha 2-binding sites from rat cerebral cortex was also obtained. (-)-Forms were more active than (+)-forms. The rank order of affinity of the (-)-forms for both alpha 1- and alpha 2-binding sites was NA greater than m-octopamine = m-synephrine greater than p-synephrine greater than p-octopamine. The relative affinities of the members of the series against alpha 1-binding sites were very similar to their relative functional activities on rat aorta. However, the affinities of both m- and p-compounds relative to that of ( -)-NA were much greater at the x2-binding sites than were the relative activities in rabbit saphenous vein, possibly suggesting low intrinsic efficacy. Functional antagonist responses to NA by the (-)-octopamine and synephrines could not, however, be demonstrated on rat aorta or rabbit saphenous vein. 6. The activities of m-octopamine and m-synephrine were not significantly different from each other on either a,-adrenoceptors from rat aorta or x2-adrenoceptors; however, m-synephrine is more active than m-octopamine on a,-adrenoceptors from rat anococcygeus. Both m-octopamine and msynephrine can be considered to be naturally occurring x,-selective amines. However, if m- and poctopamine are co-released with NA in amounts proportional to their concentration, it is concluded that their activities on m,- and x2-adrenoceptors are too low to be physiologically significant.

2-Hydroxyphenethylamine↗
PubMed1987

Blockade by nifedipine of responses to intravenous bolus injection or infusion of alpha 1- and alpha 2-adrenoceptor agonists in the pithed rat.

Nifedipine was tested against pressor responses in the pithed rat to ten agonists with varying selectivity for alpha 1- and alpha 2-adrenoceptors, injected as a bolus or infused intravenously: i.e. amidephrine, azepexole, cirazoline, indanidine, M7, methoxamine, noradrenaline (NA), oxymetazoline, phenylephrine and xylazine. Nifedipine, administered before the agonists, inhibited responses initiated by all agonists, usually for both the bolus and infusion responses. With a bolus, blockade was significantly greater against the more prolonged, secondary components of the pressor responses. This demonstrates that calcium-entry occurs during the secondary component of the alpha-adrenoceptor-mediated response and can be initiated by either alpha 1- or alpha 2-adrenoceptor subtypes. The time courses of responses to infusion varied. Selective alpha 1-adrenoceptor agonists, with the exception of indanidine, did not produce a stable pressor response during the 20 min infusion time but alpha 2-adrenoceptor agonists did. Nifedipine reduced responses to infusion with no preference for alpha 1- or alpha 2-agonists. Phenylephrine and NA produced pressor responses which reached a peak and then declined during the remainder of the infusion. The levels of NA in arterial and venous plasma were measured by h.p.l.c. during the infusion of NA. Arterial NA levels rose throughout the infusion whereas venous levels remained relatively unaffected. The absolute levels of plasma NA suggest that a large proportion of intravenously administered NA is removed in the pulmonary circulation and the remainder is removed in the systemic circulation with negligible recirculation. The consequences of these results, for assessment of the mechanisms of action of adrenoceptor agonists and calcium entry blockers, are discussed.

Adrenergic Agonists↗
PubMed1985

Influence of blood gases, Ca2+-entry blockade and angiotensin converting enzyme inhibition on pressor responses to alpha-adrenoceptor agonists: evidence in vivo for subtypes of response independent of receptor subtype?

The pressor responses in the pithed rat to alpha-adrenoceptor agonists can be modified by alterations in arterial blood gas levels or by drugs which interfere with excitation-contraction coupling processes in the vascular smooth muscle, e.g. Ca2+-entry blockers or angiotensin converting enzyme (ACE) inhibitors. However, the extent of these influences depends on which agonist is used. The pressor response to intravenous injection of alpha-adrenoceptor agonists consists of two phases: an initial rapid but transient response (phase I) is followed by a response of slower onset but longer duration (phase II). We have examined the effects of manipulation of arterial blood gases, a Ca2+-entry blocker, nifedipine, and an ACE inhibitor, teprotide, on the pressor responses to a series of alpha-adrenoceptor agonists. In each case, the effects showed selectivity for one or other of the two phases and the differences in susceptibility between agonists could be explained by the relative sizes of the two phases in their responses. In general, phase II was more susceptible to alkalosis, nifedipine and teprotide, so that drugs in which this component predominated were more susceptible to these factors. In contrast there was no direct correlation with the receptor subtypes activated by the agonists.

Adrenergic alpha-Agonists↗
PubMed1985

The influence of blood gases on alpha 1- and alpha 2- adrenoceptor-mediated pressor responses in the pithed rat.

The influence of blood gases on alpha 1- and alpha 2-adrenoceptor-mediated pressor responses was studied in the pithed rat by varying the inspired gas mixture or the ventilation stroke volume. Acidosis favoured the peak responses to the alpha 2-adrenoceptor agonist, xylazine, while alkalosis favoured the peak responses to the alpha 1-adrenoceptor agonist, phenylephrine. A combination of hypoxia and hypercapnia greatly depressed the alpha 1 response to phenylephrine whereas the alpha 2 response to xylazine remained relatively unaffected. When Pao2 was varied in either acidotic or alkalotic conditions the response to the phenylephrine increased as Pao2 increased. To prevent hypoxia in air ventilated rats, large stroke volumes were required. This caused alkalosis and hence decreased responsiveness to xylazine. Consequently, air ventilated pithed rats gave poorer responses to xylazine than did those ventilated on 100% O2. The results show that alpha 1- and alpha 2-adrenoceptor-mediated pressor responses can be differentially affected by blood gases. The relative contribution of alpha 1- and alpha 2-adrenoceptors to vascular tone may be either under- or over-estimated depending on the arterial blood gases.

Animals↗