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The present study was undertaken to determine the central and peripheral actions of trout angiotensin III (ANG III) on heart rate (HR) and mean dorsal aortic blood pressure (P(DA)) in the unanaesthetized rainbow trout. Intracerebroventricular injection of ANG III (5-100 pmol) produced a significant and dose-dependent increase in HR without significant change in P(DA). In contrast, when injected peripherally ANG III (5-50 pmol) evoked a significant and dose-dependent increase in P(DA). The hypertensive responses were accompanied by a bradycardia that reached significance only for the highest dose of ANG III tested. In conclusion, our results have shown that ANG III has potent and contrasting cardiovascular actions depending on whether its site of action is the brain or the peripheral circulation. Endogenous ANG III may have important physiological functions in teleost fishes.

International audience; Although in most vertebrate species urotensin-II (UII) is synthesized in neurons of the central nervous system, little is known regarding the physiological actions of UII in the brain. We have investigated the effects of intracerebroventricular (ICV) administration of synthetic trout UII (1, 5, and 50 pmol) on total motor activity (ACT), ventilatory frequency (VF), ventilatory amplitude (VA), and heart rate (HR) in the unanesthetized trout. ICV injection of UII increased ACT in a dose-dependent manner, and the maximal effect was observed at a dose of 5 pmol. At doses of 1 and 5 pmol, UII did not affect VF, VA, or HR. At the highest dose tested (50 pmol), UII not only increased ACT, but also significantly activated VF, VA, and HR. In contrast, ICV injection of synthetic trout angiotensin-II (5 pmol) did not produce any effect on ACT, VF, or VA, but sharply increased HR. These data provide the first evidence that UII can act centrally to induce motor activity in a nonmammalian vertebrate species.

The visual evoked potentials (VEPs), somatosensory evoked potentials (SEPs) and the electroencephalogram (EEG) have been studied in 16 subjects presenting chronic respiratory insufficiency (CRI) with normal consciousness. The SEPs latencies were increased but the VEPs latencies were not. The EEG was little disturbed and did not seem to provide useful information in CRI without encephalopathy.

Eleven patients with bronchial epidermoid carcinoma and undergoing treatment with cis-D.D.P. (II) were kept under electrophysiological and clinical surveillance. No other neurotoxic medication was added. The total dose of cis-D.D.P. was 300 mg/m2 over a period of three months: namely, three courses of 100 mg/m2 distributed over 5 days. Following the pretreatment check-up, the patients were divided into two groups: those without any electrophysiological abnormality (group A), and those without clinical abnormality but with a delayed latency H of the Hoffmann Reflex (group B). Patients in group A showed a slowing down of the motor nerve conduction velocity of the Median and Peroneal Nerves after a course of 100 mg, without accompanying worsening of the conduction velocity after 300 mg/m2, and prolongation of the distal latency of the sensory Median Nerve after 300 mg/m2; in group B, no significant change of electrophysiological clinical features were noted. In the two groups a non-significant reduction in amplitude of evoked responses were noted. These findings are more consistent with an axonal injury than with functional myelin injury. The authors review the existing literature and discuss the physiopathologic mechanisms of cis-D.D.P. peripheral neuropathies.

The authors report two cases of infant encephalopathies with psychomotor retardation. The cerebrospinal fluid, the electroretinogram, the electromyogram and the motor conduction velocity are normal. The neuromuscular cutaneous conjunctival biopsies are normal. No biochemical abnormalities are found. The electroencephalogram presents continuous high voltage fast rhythms (250-400 microV) with reduced or absent evoked responses. Early infantile neuroaxonal dystrophy and lissencephaly are suggested.

Ten subjects from 2 families with adrenoleukodystrophy (ALD) and adrenomyeloneuropathy (AMN), hereditary X-linked diseases, were systematically explored. We performed endocrinological, biochemical assays and neurophysiological tests; the latter consisted of nerve conductions (CNV), Hoffmann's reflex and multimodal evoked potentials: visual (flash and pattern, VEP), brainstem auditory (BAEP) and somesthetic (SEP) using median nerve stimulation at the wrist. We only considered values above 2 SD. The purpose of our study was to determine the correlation between neurophysiological and endocrinological perturbations and the presence of pathological traits. Our results suggest that the correlation is high in diseased male patients, lower for the ALD carriers (BAEP, SEP and CNV were more frequently abnormal) and very low for the AMN carriers. Only the biochemical assays appeared to have any value for the characterization of female carriers of ALD and AMN.

Brain-stem auditory evoked potentials (BAEPs) were obtained from 25 chronic alcoholic patients. The patients had been drinking heavily for an average of 15 years and a minimum of 5 years. All patients were totally abstinent for a minimum of 3 weeks. The morphology of waves were often altered. All presented prolonged I-III, III-V, inter-peak latencies (IPLs) and a loss of amplitude of wave V. The I-III, III-V and I-VIPLs were increased between 30 and 40 years, and III-V and I-VIPLs between 40 and 50 years. The incidence of abnormal BAEPs in patients with alcoholic epilepsy was not different from that of patients without a history of alcoholic seizures. Patients with clinical manifestations of alcoholic polyneuropathy had the highest incidence of abnormal BAEPs. BAEPs are more reliable in chronic alcoholic patients than EEG. The mechanisms of the increase in neural transmission time within the auditory brain-stem are discussed.

In order to better evaluate the influence of glycemic control on diabetic neuropathy, 73 diabetic patients were considered: 42 males and 31 females who had been treated with insulin during 9 years. Twenty-one subjects were examined during 2-12 months. Motor nerve conduction velocity (MCV) was measured on the external sciatic popliteus (ESP). The H reflex parameters from soleus were: latency time for H response (HL), the ratio between the maximum amplitude of the H reflex response and the M motor response: (formula: see text) was determined by a chromatographic method. The reduction of MCV, the rise in HL and the decrease of E in diabetics are more pronounced according to the duration of the disease and are significantly correlated with the rate of HbA1c (respectively MCV: r = -0.39, P less than 0.001; HL: r = 0.42, P less than 0.001; E: r = -0.37, P less than 0.01). There is a slight correlation between HbA1c level and the duration of diabetes. For the 21 diabetics observed during many months there is a very significant correlation between the slope of the evolution curves of HbA2c, MCV and HL.

The central and peripheral cardiovascular effects of synthetic trout urotensin II (UII) were investigated in the conscious rainbow trout. Intracerebroventricular injection of 50 pmol UII produced a slight (3%) but significant (P < 0.05) increase in heart rate but had no effect on mean arterial blood pressure. Injection of 500 pmol UII icv produced a significant (P < 0.05) rise (8%) in blood pressure with no change in heart rate. In contrast to the weak pressor effect of centrally administered UII, intra-arterial injection of UII produced a dose-dependent increase in arterial blood pressure and decrease in heart rate with significant (P < 0.05) effects on both parameters observed at a dose of 25 pmol. Higher doses of the peptide produced a sustained decrease in cardiac output that accompanied the bradycardia and rise in arterial blood pressure. The UII-induced bradycardia, but not the increase in pressure, was abolished by pretreatment with phentolamine. Trout UII produced a sustained and dose-dependent contraction of isolated vascular rings prepared from trout efferent branchial [-log 50% of the concentration producing maximal contraction (pD2) = 8.30] and celiacomesenteric (pD2 = 8.22) arteries but was without effects on vascular rings from the anterior cardinal vein. The data indicate that the pressor effect of UII in trout is mediated predominantly, if not exclusively, by an increase in systemic vascular resistance. The UII-induced hypertensive response does not seem to involve release of catecholamines, but the bradycardia may arise from adrenergic-mediated activation of cardioinhibitory baroreflexes.

Laboratoire de Physiologie des Régulations, Faculté des Sciences Biologiques, Avenue du Général Ledere, 35031 Rennes Cedex, France (Received 31 May 1977) Reports of the response of the hypothalamo-hypophysial-adrenal axis to stress have involved measurement of the levels of corticosterone and/or adrenocorticotrophin (ACTH) in the plasma of intact and adrenalectomized rats. It is known that the size and kinetics of the adrenal response are dependent on the nature of the stress and the sex of the rat (Kitay, 1961; Lescoat, Jego, Beraud & Maniey, 1970). From work on the effect of stress on plasma ACTH (Lutz, Koch & Miahle, 1969; Cook, Kendall, Greer, & Kramer 1973; Usategui, Oliver, Vaudry, Lombardi, Rosenberg & Mourre, 1976), the nature of the stress and the parameters of the response appear to be related and Barrett (1960) reported that the release of ACTH in response to stress is greater in female than in male rats. This