Properties of a projection pathway from the medial preoptic nucleus to the midbrain periaqueductal gray of the rat and its role in the regulation of cardiovascular function

In this study we examined (1) the effect of stimulation of the MPO on the firing activity of neurons in the PAG, (2) the role of glutamic acid in this interaction and, (3) whether reversible blockade of neuronal activity in the PAG by lidocaine can alter the effect of stimulation of the MPO on arterial blood pressure. Single pulse stimulation of the MPO produced a biphasic response in232 cells and inhibited332 cells. Train electrical stimulation excited2154 cells and inhibited1254 cells. The latencies to the onset of the excitatory and the inhibitory effects were not different, but the duration of the excitatory effect was slightly longer than that of the inhibitory effect. Chemical stimulation of the MPO excited1797 cells and inhibited1697 cells. The latency to onset of the excitatory response to stimulation of the MPO was longer but the duration was shorter than that of the inhibitory response. In 83% of the animals (2935), stimulation of the MPO produced a decrease in mean arterial pressure (MAP). The duration of the response was 196.9 ± 20.9 s and the average decrease in the MAP was 18.2 ± 1.4 mmHg. Application of KYN blocked the excitatory response to stimulation of the MPO in816 cells and the inhibitory response of310 cells. Injection of lidocaine into the PAG by itself had no effect on the arterial blood pressure. However, in all animals (n = 10) lidocaine totally or significantly reduced the magnitude of the blood pressure change produced by stimulation of the MPO in a reversible manner. These studies electrophysiologically confirm a pathway between the MPO and the PAG that is, in part, under glutamatergic control. In addition, our results demonstrate that stimulation of the MPO produces a distinctive depressor effect that is mediated through the PAG.     

Action of some ganglion-stimulating substances on the secretion of saliva from the submandibular gland

An attempt has been made to determine whether the ganglionic actions of pilocarpine and of 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride (McN-A-343) contribute to their effect on salivary secretion. Salivary flow was measured from the submandibular glands of spinal cats. Destruction of the superior cervical ganglion and adrenalectomy failed to reduce the stimulant effect of pilocarpine and McN-A-343. Substances known to interfere with the ganglionic actions of pilocarpine (cocaine, methadone and choline 2:6-xylyl ether bromide) likewise failed to modify the response. It is concluded that stimulation of autonomic ganglia and of the adrenal medulla does not contribute to the salivary secretion observed after intravenous injections of pilocarpine and of McN-A-343. Dimethylphenylpiperazinium, a nicotine-like ganglion-stimulating substance, causes salivary flow by stimulating the adrenal medulla as well as parasympathetic ganglion cells; stimulation of the superior cervical ganglion by this substance does not contribute to the salivary response.     

Longitudinal Monitoring of Intracranial Arterial Stenoses with Transcranial Doppler Ultrasonography

The natural history of intracranial arterial stenoses remains relatively unknown. To monitor the progression of these lesions over time, the authors reviewed transcranial Doppler (TCD) laboratory reports at five hospitals for patients with angiographically documented intracranial arterial stenoses along the internal carotid artery distribution, and at least two TCD studies conducted more than 2 months apart. Twenty-two patients (19 men and 3 women; mean age, 64 years) with 29 stenoses were identified. The findings were compared to reproducibility data obtained from 11 age-matched control subjects with repeat TCD studies. During a mean follow-up period of 21 months, peak systolic flow velocities corresponding to the areas of stenosis increased in 9 arteries with lesions, and new collateral flow patterns, indicating further hemodynamic compromise distal to the lesions, developed in 2; one of the latter also had increased corresponding velocities. Thus, 10 (35%) arteries with lesions had TCD evidence of progression. Flow velocities remained the same in 13 (45%) stenotic vessels and dropped in 2 (7%). Findings were considered inconclusive for 4 lesions (14%). These findings suggest that intracranial arterial stenoses are dynamic lesions, and that they can evolve and cause further reductions of the arterial diameters after relatively short periods of time. TCD can noninvasively detect their hemodynamic efects.     

Hodgkin's disease in HIV-infected patients

Eight patients with Hodgkin's disease who were seropositive to human immunodeficiency virus (HIV), 6 of them being heroin addicts and one a homosexual, were studied. Histological examination showed 4 cases of lymphocytic depletion, 2 cases of mixed cellularity, 1 nodular sclerosis, and one not classifiable. There were five cases of stage IV-B and 3 IIIs-B. The response to treatment was poor, with disproportionate cytopenia and severe infectious complications. We suggest that the atypical nature of Hodgkin's disease in patients who are seropositive for HIV might be considered to be a part of the Acquired Immunodeficiency Syndrome (AIDS).     

Renin and angiotensinogen expression during the evolution of diabetes.

The expression of renin and angiotensinogen genes and their proteins were studied during the progression of diabetes using adult BioBreeding spontaneously diabetic rats at 1 day and 2-12 months of diabetes. The number of renin-stained cells per juxtaglomerular apparatus was determined by immunocytochemistry. Initially, at 2 months of diabetes the number of renin-stained cells per juxtaglomerular apparatus increased significantly (p less than 0.0001, 2 months versus resistant groups) and was followed by a decrease in the number and intensity of renin-stained cells after 12 months of diabetes (p = 0.007, 2 months versus 12 months). A significant negative correlation was observed between the number of renin-containing cells and the duration of diabetes (r = 0.99, p = 0.014). Immunoreactive angiotensinogen was restricted to the proximal tubule and appeared increased after 4 and 8 months of diabetes as compared with the 2- and 12-month diabetic groups. Renin messenger RNA (mRNA) levels increased with the onset of diabetes and decreased markedly during chronic diabetes. At 1 day of diabetes, renin mRNA levels were 700% higher than at 12 months of diabetes. Angiotensinogen mRNA levels were unchanged. We conclude that diabetes results in an initial increase in renin gene expression, and as the duration of diabetes lengthens, there is a progressive decrease in renin gene expression and in the number of cells containing renin. These findings suggest that as the duration of diabetes and the age of the animal lengthens, there is a decrease in the number of cells expressing the renin gene.