Selecting an MSO. How to assess options and compatibility.

Despite significant changes within the physician practice management and management services industry, physicians across the country are continuing to choose to affiliate with management services organizations (MSO). Now, more than ever, it is crucial that physicians first assess their own unique situation, conduct thorough due diligence of the potential partner and educate themselves on the important terms of any potential deal. As a part of the assessment, physicians must evaluate whether a potential partner's goals are aligned with their own, needed services will be provided at a fair price and the personnel have appropriate expertise and experience. This assessment will enable physicians to effectively determine their options and ensure an informed and strategic decision.

Studies upon the mechanism by which acetylcholine releases surplus acetylcholine in a sympathetic ganglion.

1. Acetylcholine (ACh) releases surplus ACh from the superior cervical ganglion of the cat and the experiments described in this paper tested whether this results from exchange of endogenous ACh with exogenous ACh; the experiments also attempted to characterize pharmacologically the mechanism of this action of ACh. 2. The surplus ACh in the ganglion was radioactively labelled by perfusion of the ganglion with [3H]-choline-Krebs solution containing diisopropylphosphofluoridate, and the release of surplus [3H]-ACh by [14C]-ACh injected close arterially to the ganglion measured. The amount of [3H]-ACh released by [14C]-ACh was 33 +/- 5 times greater than was the amount of [14C]-ACh accumulated by ganglia. The amount of exogenous ACh accumulated by ganglia that had first formed surplus ACh was not different from exogenous ACh accumulation by ganglia that had not formed surplus ACh. Thus, it is concluded that surplus ACh release by ACh is not the result of ACh exchange. 3. In other experiments, surplus [3H]-ACh was accumulated in ganglia exposed to physostigmine. Nicotine, pilocarpine or ACh released surplus ACh; the effect of both nicotine and ACh was blocked by hexamethonium; atropine blocked the effect of ACh but not that of nicotine. It is concluded that both nicotinic and muscarinic receptors can be involved in the release of surplus ACh by cholinomimetic agonists.

Acetylcholine synthesis from recaptured choline by a sympathetic ganglion.

1. The recapture and re-use of choline formed by the hydrolysis of released acetylcholine (ACh) was studied in the superior cervical ganglion of the cat using radioactive tracer techniques. The ganglion's ACh store was labelled by perfusion, during preganglionic nerve stimulation, with Krebs solution containing [(3)H]choline.2. Preganglionic stimulation (5 Hz for 20 min) of ganglia containing [(3)H]ACh released similar amounts of radioactivity when perfusion was with neostigmine-choline-Krebs or with hemicholinium-Krebs. This indicated that neostigmine does not increase transmitter release.3. The amount of radioactivity collected from stimulated ganglia during perfusion with choline-Krebs was 39% of the amount of radioactivity collected during perfusion with medium containing neostigmine or hemi-cholinium. This difference in release was almost (85%) accounted for at the end of the experiment by extra radioactive ACh in the ganglia perfused with choline-Krebs. It is concluded that during preganglionic nerve stimulation approximately 50-60% of endogenously produced choline is recaptured for ACh synthesis; thus, during activity preganglionic nerve terminals appear selectively to accumulate choline.4. However, chronically decentralized ganglia accumulated as much choline as did acutely decentralized ganglia, and this was interpreted as indicating that at rest preganglionic nerve terminals do not selectively accumulate choline.5. Increased exogenous choline concentration increased the amount of radioactivity collected during nerve stimulation in the absence, but not the presence, of an anticholinesterase agent. The spontaneous efflux of radioactivity was little affected by changes in external choline levels. It is concluded that exogenous choline and choline made available from released transmitter compete for uptake into nerve terminals.

The synthesis, turnover and release of surplus acetylcholine in a sympathetic ganglion.

1. Surplus acetylcholine (ACh) is the extra ACh that accumulates in cholinergic nerve endings when they are exposed to an anticholinesterase agent. The synthesis and turnover of this ACh was examined in the cat's superior cervical ganglion.2. Surplus ACh did not accumulate in chronically decentralized ganglia perfused with eserine-choline-Locke solution, and this shows that it is stored in presynaptic nerve terminals.3. Surplus ACh accumulated more rapidly in ganglia perfused with eserine than in ganglia perfused with neostigmine or with ambenonium; accumulation was delayed by 45-60 min when a quaternary anticholinesterase was used. However, the release of ACh upon preganglionic nerve stimulation was the same during perfusion with eserine, neostigmine or ambenonium. It is concluded that intracellular acetylcholinesterase normally destroys surplus ACh, whereas extracellular enzyme destroys released ACh.4. When ganglia were perfused with [(3)H]choline and eserine, the surplus ACh that accumulated was labelled but its specific radioactivity was only 38% of that of the choline added to the perfusion fluid.5. Surplus ACh was not released by nerve stimulation and was not mobilized for release during, or after, prolonged nerve stimulation. It is concluded that ACh released by nerve impulses is replaced by synthesis at the site of ACh storage and not by movement of ACh from the surplus pool.6. The accumulation of surplus ACh no more than doubled the total ACh content of ganglia, but turnover of ACh continued when the total amount was constant. Surplus ACh may contribute to spontaneous ACh output from eserinized preparations.7. When ganglia were perfused with a medium containing high K(+) (56 mM), surplus ACh was released.

The release of acetylcholine by acetylcholine in the cat's superior cervical ganglion.

1. The experiments described in this paper tested the effect of acetylcholine (ACh), carbachol or preganglionic nerve stimulation on the release of ACh from the cat's perfused superior cervical ganglion; radioactive tracer methods were used.2. When the ganglion's transmitter store of ACh had been labelled, radioactive ACh was released by nerve stimulation (5 Hz for 2 min), but there was no release by ACh (0.15-15 mug) or by carbachol (1-10 mug) when these drugs were injected close to the ganglion. Perfusion with low or moderate concentrations of ACh (0.15-5 mug/ml) also failed to release ACh, but high concentrations (15-50 mug/ml) released a small amount of labelled material. There was no correlation between ganglion stimulation by ACh and release of radioactivity.3. Ganglion-blocking concentrations of ACh did not reduce the release of ACh during continuous nerve stimulation.4. When resting (unstimulated) ganglia were perfused with (3)H-choline and eserine, the extra ACh synthesized and stored by such ganglia (surplus ACh) was labelled. Preganglionic nerve stimulation (5 Hz for 2 min) did not release surplus ACh, but perfusion with ACh (0.5-15 mug/ml), or injection of carbachol (0.5-2.5 mug) did.5. Surplus ACh released by ACh or by carbachol did not contribute to the ganglion stimulating effect of either drug.6. It is concluded that the presynaptic effects of ACh are not of physiological importance.