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Pulmonary autonomic neuropathy in diabetic patients
110 Orthostatic hypertension is a rare syndrome usually associated with nephroptosis and/or supine hypertension. Orthostatic hypertension may develop as a consequence of cardiovascular autonomic dysfunction, considering that the majority of cases of orthostatic hypotension, the opposite condition, are of neurogenic origin. We investigated 330 patients with neurologic degenerative diseases to find out the cases of neurogenic orthostatic hypertension. Subjects and Methods: A test of 70° passive head-up tilt was performed on 142 patients with Parkinson's disease, 64 with multiple system atrophy, 64 with motor neurone disease, 21 with hereditary ataxias, 20 with Alzheimer's disease, 4 with corticobasal degeneration and 15 with other degenerative diseases. The diagnosis of orthostatic hypertension was made when a rise in systolic blood pressure exceeded 20 mmHg. Results: Among 330 subjects, we found 6 cases (1.8%) of orthostatic hypertension (3 with motor neurone disease, 2 with Parkinson's disease, and 1 with corticobasal degeneration). The autonomic function tests (Valsalva's manoeuvre, cold pressor test, plasma catecholamine measurement etc.) revealed that they had an increased cardiovascular sympathetic tone. Conclusion: Orthostatic hypertension may result from the increased sympathetic tone. This is the first report of neurogenic orthostatic hypertension associated with neurologic degenerative diseases.
142 Pulmonary Autonomic Neuropathy in Diabetic Patients C. Tantucci% L. Scionti 2, M.L. Dottorini% P. Bottini 2, E. Puxeddu 2, G. Casucci 2, V. Grassi3 and C.A. Sorbini I
1Institute of Semeiotica Medica, University of Ancona, Ancona, ltaly, 2Institute of Patologia Medica, University of Perugia, Perugia, Italy, and 3Institute of Patologia Medica, University of Brescia, Brescia, Italy Recently, we speculated that autonomic lung neuropathy could impair the control of breathing on the basis of a lower mouth occlusion pressure (P0.1) response, following methacholine-induced bronchoconstriction, in diabetics with autonomic disorders. In view of this, we investigated the ventilatory response to progressive hyperoxic hypercapnia in diabetics with autonomic neuropathy. Methods: 19 diabetic patients, 9 with (N) and 10 without (D) autonomic neuropathy, were studied with a control group (C) of 10 subjects. All patients and subjects had pulmonary function test, including M W , and measurements of maximal in- and expiratory pressures (Plmax and PEmax). Following basal evaluation of I;'E, Vt, R-R and P0.1, both diabetics and C underwent a CO2 rebreathing test; for each test changes of I?E, R-
R, Vt and Po.l were plotted against increasing PetCOl and fitted according to least-square regression method. Results: No significant differences were found in the baseline lung function tests and Plm~xand PEmax. Resting P0.b I?E, R-R and Vt were also similar for D, N and C. During CO2 rebreathing N (as a whole group) did not show any significant differences in terms of P0.1/P~tCO2, ~'E/PetCO2, Vt/PetCO2 and R-R/PetCO2 slopes with C: on the contrary, as C did, N showed significantly higher P0.1/PetCO2, IYg/PetCO2slopes in respect to D (P<0.05). If N were split, however, in patients with only cholinergic dysautonomy (No; n = 4) and with both cholinergic and adrenergic dysautonomy (Nca; n = 5), Nca displayed even significantly higher P0.1/PetCO2, ~'E/PetCO2, Vt/PetCO2 and R-R/PetCO2 slopes (P<0.01) in respect to either D and Nc which in turn behaved similarly (Nc~ vs. D and vs. No: 0.77+0.10 vs. 0.23---0.10 and vs. 0.20±0.04 cm H20/mmHg; 4.95+2.84 vs. 2.02+__0.79 and vs. 2.34:t:0.37 l/min/mmHg; 144-t-64 vs. 88_+33 and vs. 9 0 + 2 2 ml/mmHg; 0.91_+0.57 vs. 0.21±0.16 and vs. 0.17±0.14 b/min/mmHg, respectively). Conclusions: Our data suggest that abnormality by the central component of respiratory control is present both in D and No. The presumable decrease of sympathetic nerve traffic (removal of afferent pulmonary inhibitory sympathetic activity or more likely a dysfunction in the control of cerebral blood flow) seems able to completely reverse the effects of this abnormality in N~.
143 An Integrated Study of Pupiilary and Cardiovascular Response to Cold Presser Test C. Tassorelli% (3. Micieli% V. Osipova 2 and G. Nappi
~Autonomic Unit, III Department of Neurology. 'C Mondino' Foundation, University of Pavia, Italy, and 2Russian Center of Autonomic Pathology, Moscow, Russia The Cold Pressor Test (CPT) (immersion of the nondominant hand in ice-cold water) induces an increase in blood pressure (BP) and heart rate (HR) and, as we have recently demonstrated, changes in cerebral blood flow velocity. In the present study, pupillary response to a 5-min CPT and a possible relationship with cardiovascular reactions were investigated in 11 healthy young sub)ects. The pupil responded after 30 s with a bilateral and symmetrical mydriasis (+25% vs. basal diameter) which lasted through the second minute. Then, from the third to the fifth minute, an evident miosis (-20/25% vs. basal diameter) was observable. BP rose slightly, while HR showed a biphasic increase. Pretreatment with thymoxamine (an al-bloeaker) reduced the mydriatic response significantly, while homatropine (a
142 Pulmonary Autonomic Neuropathy in Diabetic Patients C. Tantucci% L. Scionti 2, M.L. Dottorini% P. Bottini 2, E. Puxeddu 2, G. Casucci 2, V. Grassi3 and C.A. Sorbini I
1Institute of Semeiotica Medica, University of Ancona, Ancona, ltaly, 2Institute of Patologia Medica, University of Perugia, Perugia, Italy, and 3Institute of Patologia Medica, University of Brescia, Brescia, Italy Recently, we speculated that autonomic lung neuropathy could impair the control of breathing on the basis of a lower mouth occlusion pressure (P0.1) response, following methacholine-induced bronchoconstriction, in diabetics with autonomic disorders. In view of this, we investigated the ventilatory response to progressive hyperoxic hypercapnia in diabetics with autonomic neuropathy. Methods: 19 diabetic patients, 9 with (N) and 10 without (D) autonomic neuropathy, were studied with a control group (C) of 10 subjects. All patients and subjects had pulmonary function test, including M W , and measurements of maximal in- and expiratory pressures (Plmax and PEmax). Following basal evaluation of I;'E, Vt, R-R and P0.1, both diabetics and C underwent a CO2 rebreathing test; for each test changes of I?E, R-
R, Vt and Po.l were plotted against increasing PetCOl and fitted according to least-square regression method. Results: No significant differences were found in the baseline lung function tests and Plm~xand PEmax. Resting P0.b I?E, R-R and Vt were also similar for D, N and C. During CO2 rebreathing N (as a whole group) did not show any significant differences in terms of P0.1/P~tCO2, ~'E/PetCO2, Vt/PetCO2 and R-R/PetCO2 slopes with C: on the contrary, as C did, N showed significantly higher P0.1/PetCO2, IYg/PetCO2slopes in respect to D (P<0.05). If N were split, however, in patients with only cholinergic dysautonomy (No; n = 4) and with both cholinergic and adrenergic dysautonomy (Nca; n = 5), Nca displayed even significantly higher P0.1/PetCO2, ~'E/PetCO2, Vt/PetCO2 and R-R/PetCO2 slopes (P<0.01) in respect to either D and Nc which in turn behaved similarly (Nc~ vs. D and vs. No: 0.77+0.10 vs. 0.23---0.10 and vs. 0.20±0.04 cm H20/mmHg; 4.95+2.84 vs. 2.02+__0.79 and vs. 2.34:t:0.37 l/min/mmHg; 144-t-64 vs. 88_+33 and vs. 9 0 + 2 2 ml/mmHg; 0.91_+0.57 vs. 0.21±0.16 and vs. 0.17±0.14 b/min/mmHg, respectively). Conclusions: Our data suggest that abnormality by the central component of respiratory control is present both in D and No. The presumable decrease of sympathetic nerve traffic (removal of afferent pulmonary inhibitory sympathetic activity or more likely a dysfunction in the control of cerebral blood flow) seems able to completely reverse the effects of this abnormality in N~.
143 An Integrated Study of Pupiilary and Cardiovascular Response to Cold Presser Test C. Tassorelli% (3. Micieli% V. Osipova 2 and G. Nappi
~Autonomic Unit, III Department of Neurology. 'C Mondino' Foundation, University of Pavia, Italy, and 2Russian Center of Autonomic Pathology, Moscow, Russia The Cold Pressor Test (CPT) (immersion of the nondominant hand in ice-cold water) induces an increase in blood pressure (BP) and heart rate (HR) and, as we have recently demonstrated, changes in cerebral blood flow velocity. In the present study, pupillary response to a 5-min CPT and a possible relationship with cardiovascular reactions were investigated in 11 healthy young sub)ects. The pupil responded after 30 s with a bilateral and symmetrical mydriasis (+25% vs. basal diameter) which lasted through the second minute. Then, from the third to the fifth minute, an evident miosis (-20/25% vs. basal diameter) was observable. BP rose slightly, while HR showed a biphasic increase. Pretreatment with thymoxamine (an al-bloeaker) reduced the mydriatic response significantly, while homatropine (a