259 arterial pressure fell to about 43 mmHg and renal nerve activity was decreased. A bolus injection of naloxone (3 mg/kg) raised the blood pressure to control levels and increased renal nerve activity by 142 + 30%, to values that were comparable to those measured during non-hypotensive hemorrhage. In contrast, when the blood pressure was raised to the control level by phenylephrine, renal nerve activity increased but not beyond the control level. Thus, in conscious rabbits, hemorrhage elicits a biphasic change in renal nerve activity, which raises initially and then falls when hypotension sets in, the latter phase being mediated mainly by opiate receptors. The pressor effect of naloxone is due to an augmentation of sympathetic nerve activity, while the pressor effect of phenylephrine is due to vasoconstriction. (The Autonomic Nervous System 24: 441-445, 1987)
Noradrenaline content in the urethra and bladder of the dog Shinobu Doukita, Tadashi Nishimoto and Takashi Morita
Department of Urology, Akita University School of Medicine, Japan. In order to assess the distribution of sympathetic nerves in the lower urinary tract, the noradrenaline content was measured in tissue specimens from the bladder dome, bladder base, proximal urethra and distal urethra of male and female dogs, by means of high-pressure liquid chromatography electrochemical detection. In both sexes, the noradrenaline concentration was highest in the proximal urethra and lowest in the bladder dome. In the proximal urethra the noradrenaline concentration was significantly higher in the male than in the female, whereas the opposite was the case in the bladder base and the distal urethra. These results suggest that the sympathetic innervation in the lower urinary tract is at its densest in the proximal urethra, and that there are sex differences in the density of the sympathetic innervation of bladder and urethra. (The Autonomic Nervous System 24: 446-450, 1987)
Sympathetic nerve dysfunction and increased heart-rate response to epinephrine in diabetic patients Masahiko Terada, Hitoshi Yasuda, Atsunori Kashiwagi, Yoshihiko Nishio, Ikuo Hatanaka, Makio Yamashita, Yasuhumi Miyamoto, Ryuichi Kikkawa and Yukio Shigeta
Third Department of Medicine, Shiga University of Medical Science, Otsu, Japan. In an attempt to evaluate sympathetic nerve function in diabetic patients, 6 patients with orthostatic hypotension, 10 patients without orthostatic hypotension and 4 healthy subjects, received an epinephrine infusion test (0.5, 1.5, 3.0 ~g/h). At each rate of infusion, heart rate, mean blood pressure and serum epinephrine concentration were determined. The heart rate response was higher in patients with orthostatic hypotension than in patients without, and it was significantly higher in all the diabetic patients than in the controls. This increase in heart rate response may be attributable to the supersensitivity of cardiac beta-adrenoceptors due to diabetic neuropathy. Mean blood pressure and serum epinephrine concentration were not different in the three groups. The magnitude of the heart rate response to epinephrine correlated well with the resting beat-to-beat coefficient of variation, at 0.5 and 1.5 ~ g / h infusion rates, an observation suggesting that in diabetic patients the sympathetic dysfunction may proceed parallel to a
260 parasympathetic dysfunction. These results suggest that infusion of epinephrine, especially at a rate of t 5 #g/h, is a useful method for evaluating the sympathetic function of diabetic patients. (The Autonomic Nervous System 24:451-456, 1987)
Transient hypothalamie dysfunction associated with acute idiopathic pandysautonomia Kozo Matsubayashi, Kiyohito Okumiya, Kuniaki Otsuka, Akiko Kawamoto. Kazuyuki Shimada and Toshio Ozawa Department of Medicine & Geriatrics, Kochi Medical School, Japan.
A 27-year-old woman with acute idiopathic pandysautonomia was studied. Her initial symptoms were orthostatic hypotension with syncope, paroxysmal coughing spells and body weight loss following common cold-like symptoms lasting about 5 days. Autonomic function tests revealed dysfunction of post-ganglionic sympathetic nerves and parasympathetic nerves. Furthermore, the patient presented hyperprolacfinemia and disappearance of the circadian rhythm of heart rate. The observations suggested a transient hypothalamic dysfunction. The site of lesion in acute idiopathic pandysautonomia is generally assumed to be in the peripheral autonomic nervous system. Our results, however, show. the possibility of an involvement of the central nervous system too. (The Autonomic Nervous System 24: 457-461. 1987)
Shy-Drager syndrome with elliptocytosis. An autopsy case report Shigeo Riku ]. Ko Sahashi 2, Akira Takahashi 3 and Kuniyuki Kawa 3 1 Department of Neurology, Fufita-Gakuen Health Unioersity, 2 Fourth Department of Internal Medicine, Aichi Medical University and 3 Department of Neurology, Nagoya Unioersity School of Medicine, Japan.
The male patient was first admitted to the Aichi Medical University Hospital in 1979, when aged 53. with an 18 months history of progressive autonomic dysfunctions, such as impotence, urinary disorders and postural dizziness, as well as speech disorders and unsteadiness in walking. On examination the patient showed upper gaze palsy, gaze nystagmus, cerebellar speech, dysmetry, ataxic gait. bilateral pyramidal signs and autonomic signs including severe orthostatic hypotension. Routine laboratory tests, including serum lipids, were normal. In peripheral blood smears elliptocytes accounted for 70% of all red blood cells. After discharge, the symptoms worsened, and in 1983 the patients became bedridden. He was then admitted to another hospital and died at the age of 59. The patient had eight siblings. One of them was affected by neurological abnormalities comprising pyramidal signs and ehoreic movements. Two others had elliptocytosis. Neuropathologieal examination revealed severe de,g~neration in the stLbstantia nigra, in the olivo-ponto-cerebellar system and in the intermedio-lateral column of the spinal cord. (The Autonomic Nervous System 24: 462-467. 1987)