Cholinergic-opioid interactions at brainstem respiratory chemosensitive areas in cats.

Central respiratory chemosensitivity has been ascribed to CO2-sensitive neurons located on the ventral brainstem surface. The effects of cholinergic mechanisms on CO2-sensitive neuronal activity recorded extracellularly at the brainstem respiratory chemosensitive area at the caudal ventral medullary surface (cVMS) were investigated in cats (n = 14) anesthetized with chloralose-urethane. The neurons increased their firing rate from 10.4 +/- 1.6 Hz to 33.9 +/- 5.2 Hz when the mock cerebrospinal fluid (mCSF) superfusing buffer solution was changed from pH 7.4 (control) to pH 7.0 (acidic). Atropine (ATR) applied topically to the cVMS depressed the H(+)-ion-induced increase in neuronal frequency from 32.8 +/- 4.8 Hz to 13.4 +/- 2.2 Hz. ATR also depressed the inspired-CO2-induced increase in neuronal activity from 33.2 +/- 8.3 Hz to 18.9 +/- 4.9 Hz, suggesting the possibility of a muscarinic cholinergic involvement in cVMS neuronal responses to changes in PCO2 and mCSF-pH. Acetylcholine (ACh) increased the activity of cVMS CO2-sensitive neurons by 237.5% +/- 34.9%, and naloxone applied topically to the cVMS augmented the ACh responsiveness to 338.6% +/- 52.7%. Physostigmine (PHY) increased neuronal activity by 254.3% +/- 42.9%, and this increase was augmented to 435.4% +/- 61.2% by naloxone. Although responses of the CO2-sensitive neurons to PHY were biphasic, the depressant phase failed to appear whenever the cVMS was pretreated with naloxone. Naloxone also augmented the responsiveness of cVMS neurons to increased H+ ion superfusion. These findings suggest that the endogenous opiates may be involved in the central regulation of respiration by interaction with CO2-sensitive cholinergic structures at the cVMS.(ABSTRACT TRUNCATED AT 250 WORDS)

An outbreak of gastrointestinal illness caused by Staphylococcus aureus in a prison population.

Overcrowded conditions in a closed setting may contribute to the occurrence of disease outbreaks among the population.

Is passive surveillance always insensitive? An evaluation of shigellosis surveillance in Oklahoma.

The authors studied the reporting of shigellosis in Oklahoma to evaluate the sensitivity of the state-based passive surveillance system for shigellosis. They found that passive surveillance for shigellosis can be more sensitive than has been previously observed. Laboratory-based reporting was found to be far superior to reporting by physicians.

The role of hypoxia in organophosphorus nerve agent intoxication.

Effectiveness of the standard therapy for organophosphorus (OP) anticholinesterase poisoning has been questioned because of the relative resistance of the cholinesterase (ChE) enzymes to reactivation by oximes (Harris et al., 1968). Because tissue hypoxia may be a significant lethal component of OP nerve agent intoxication, oxygen therapy should be beneficial. Although there have been no systematic investigations of the value of oxygen therapy in OP poisoning, it may improve the efficiency of ChE reactivation by the standard therapies of cholinolytics and oximes. Because tissue hypoxia may be generated by arterial hypoxemia due to respiratory failure, oxygen therapy should limit concomitant metabolic disturbances associated with anaerobiosis. This review addresses the interspecies variations and experimental model developments that should challenge neuroscientists to adopt an integrated, physiological approach to understanding the precise role of hypoxia in neurotoxicity. The significance of tissue hypoxia to protection and recovery of humans from OP nerve agent intoxication is also discussed.