Bulbus arteriosus of the bivalve mollusc Mercenaria mercenaria: Morphology and pharmacology.

We examined the morphology and pharmacology of the bulbus arteriosus of the marine bivalve mollusc Mercenaria mercenaria. The bulbus arteriosus is an organ of unknown function associated with the posterior aorta and the ventricle. It is composed of connective tissue interspersed with muscle bundles. In contrast to the lumen of the ventricle, which has an extensive trabecular network, the lumen of the bulbus arteriosus has no trabeculae. No valve is present in the posterior aorta connecting the lumina of the ventricle and the bulbus arteriosus. Scattered neuronal profiles are present in the wall and the axonal processes contain vesicles that may contain neurosecretory products. We did not, however, find synapses or evidence of vesicular release into the lumen of the bulbus arteriosus. The bulbus arteriosus contains acetylcholine, 5-hydroxytryptamine (5HT), and the molluscan neuropeptides FMRFamide (phenyl-alanyl-methionyl-arginyl-phenylalaninylamide) and FLRFamide (phenylalanyl-leucinyl-arginyl-phenylalanylamide). The isolated bulbus arteriosus contracts tonically in response to mechanical stress and exposure to 5HT or FMRFamide, while acetylcholine relaxes it. We surmise that the bulbus arteriosus probably functions as a mechanism for regulating the relative amounts of hemolymph pumped into the anterior and posterior aortae by the ventricle and that the bulbus arteriosus may be a neurohemal site.

Three-dimensional brain metabolic imaging in patients with toxic encephalopathy.

Thirty-three workers, ages 24 to 63, developed clinical toxic encephalopathy after exposure to neurotoxins and were studied by SPECT brain scans. Five were exposed to pesticides, 13 were acutely exposed to mixtures of solvents, 8 were chronically exposed to mixtures of hazardous wastes that contained organic solvents, 2 were acutely exposed to phosgene and other toxins, and 5 had exposures to hydrogen sulfide. Twenty-nine had neuropsychological testing and all had a medical history and physical. Of the workers who had a clinical diagnosis of toxic encephalopathy, 31 (93.9%) had abnormal SPECT brain scans with the most frequent areas of abnormality being temporal lobes (67.7%), frontal lobes (61.3%), basal ganglia (45.2%), thalamus (29.0%), parietal lobes (12.9%), motorstrip (9.68%), cerebral hemisphere (6.45%), occipital lobes (3.23%), and caudate nucleus (3.23%). Twenty-three out of 29 (79.3%) neuropsychological evaluations were abnormal. Other modalities when performed included the following percentages of abnormals: NCV, 33.3%; CPT sensory nerve testing, 91.3%; vestibular function testing, 71.4%; olfactory testing, 89.2%; sleep EEG analysis, 85.7%; EEG, 8.33%; CT, 7.14%; and MRI brain scans, 28.6%. The complex of symptoms seen in toxic encephalopathy implies dysfunction involving several CNS regions. This series of patients adds to the previous experience of brain metabolic imaging and demonstrates that certain areas of the brain are typically affected despite differences in toxin structure, that these lesions can be globally defined by SPECT/PET brain scans, that these lesion correlate well with clinical and neuropsychological testing, and that such testing is a useful adjunct to previous methods. EEG and structural brain imaging such as CT and MRI are observed to have poor sensitivity in this type of patient. Additional metabolic imaging studies need to be done to explore dose, time, and specific toxin effects as well as mechanisms of toxicity and olfactory migration.