[Treatment of the Shy-Drager syndrome].
Explore the source record for details and available documents.
Autonomic Nervous System Diseases↗
Biomedical subjects
E Fritschka
Publications and source records attributed to E Fritschka.
[Ambulatory noradrenaline infusion in refractory Shy-Drager syndrome].
Explore the source record for details and available documents.
Ambulatory Care↗
Sympathetic tone and pressor response to noradrenaline during mineralocorticoid-induced blood pressure rise in man.
To gain insight into the role of the sympathetic nervous system in the development of mineralocorticoid hypertension, we determined noradrenaline and adrenaline in plasma and urine before, during and after administration of the synthetic steroid, fludrocortisone, for a period of 6 weeks in normotensive volunteer subjects. In addition, pressor reactivity to exogenous noradrenaline, platelet alpha 2- and lymphocyte beta 2-receptors, and platelet intracellular free calcium were determined. Fludrocortisone induced a fall in free and sulpho-conjugated plasma noradrenaline and after 6 weeks, a rise in free and sulpho-conjugated noradrenaline excretion. The number of alpha 2- and beta 2-adrenergic binding sites decreased. A marked increase in platelet free intracellular calcium was found after the first week of fludrocortisone administration followed by a decrease in the following weeks. Reactivity to exogenous noradrenaline was found to be enhanced and this could be a factor contributing to the development of hypertension. Whereas the decrease in plasma noradrenaline observed would suggest a diminution in sympathetic tone, the finding of a rise in urinary noradrenaline excretion after 6 weeks of steroid administration in the presence of suppressed plasma levels points to an increased renal sympathetic drive. The decreased number of platelet alpha 2- and lymphocyte beta 2-receptors observed would also be consistent with the assumption of an increased sympathetic tone.
Adult↗
Effect of metoprolol on 24-hour urinary excretion of adrenal steroids and kallikrein in patients with essential hypertension.
Treatment of fifteen patients with essential hypertension over four weeks using the beta 1-adrenoceptor blocking agent, metoprolol, resulted in a decrease in 24 h urinary excretion of kallikrein and aldosterone along with a decrease in plasma renin activity. There was no significant change in 24 h excretion rates of the free adrenal steroids deoxycorticosterone, 18-OH-deoxycorticosterone, corticosterone, cortisol or 18-OH-corticosterone during treatment, which were not significantly different from excretion rates of normal males, thus excluding inhibitory effects of adrenal steroids on urinary kallikrein activity. A positive correlation was found between plasma renin activity and urinary excretion of kallikrein during the control period and after 2 weeks on metoprolol, supporting the assumption of a preserved link between the renin-angiotensin-aldosterone system and the renal excretion of kallikrein in these patients. The decrease in kallikrein excretion during beta 1-adrenoceptor blockade in patients with essential hypertension may be explained by a reduction in sympathetic tone and by reduced activity of the renin-aldosterone system.
18-Hydroxycorticosterone↗
Crossover comparison of nitrendipine with propranolol in patients with essential hypertension.
The antihypertensive effect of nitrendipine (2 X 10 to 2 X 20 mg/day) was compared with that of propranolol (2 X 80 to 2 X 160 mg/day) in a randomized crossover study. Twenty-five patients were treated over two 4-week periods following a placebo period of 2 weeks. Three patients dropped out of the study because of side-effects (two on nitrendipine and one on propranolol). Arterial pressures decreased in a comparable manner from 171/107 mm Hg (measured in a sitting position) to 147/91 mm Hg after 4 weeks on nitrendipine and to 145/93 mm Hg after 4 weeks on propranolol. The frequency of side-effects possibly related to treatment was comparable for both drugs, but decreased with the duration of therapy with nitrendipine only. The antihypertensive effect of nitrendipine, but not of propranolol, correlated positively with age and plasma noradrenaline.
Adult↗
Effect of nifedipine and verapamil on alpha-receptor-activation in patients with essential hypertension.
The question of whether the hypotensive effect of calcium entry blockers involves an interaction with alpha-adrenergic receptors was examined. The effect of nifedipine subl. (20 mg, n = 9) and of verapamil p.o. (160 mg, n = 9) on the pressor effect of the unselective alpha-adrenergic agonist noradrenaline, as well as on 3H-yohimbine binding to platelet alpha 2-adrenoceptors was studied in patients with essential hypertension. In addition, the effect of nifedipine on reactivity to the selective alpha 1-adrenergic agonist phenylephrine was investigated (n = 9). Nifedipine caused a significant reduction of reactivity to noradrenaline (P less than 0.01), along with a significant decrease in binding sites (P less than 0.01). Affinity to the alpha 2-receptors was unchanged. Verapamil, although equally effective in lowering blood pressure, had no effect on the pressor response or binding sites. The pressor effect of the alpha 1-agonist phenylephrine was reduced (P less than 0.01) by nifedipine. Nifedipine may therefore affect both alpha 1- and alpha 2-adrenoceptors in patients with essential hypertension. Since verapamil did not affect the pressor response to noradrenaline or yohimbine-binding, the interaction with alpha 2-adrenoceptors does not appear to be a general prerequisite for the hypotensive action of calcium entry blockers.
Adult↗
The determination of brain water content: microgravimetry versus drying-weighing method.
The microgravimetric technique and the drying-weighing method for the determination of brain water content are analyzed and compared. A new method has been devised for the automatic production of the gradient column. For gravimetry, tissue samples weighing more than 30 mg have proven adequate for measurement. Specific gravity (SG) should be determined as early as 1 minute after tissue is inserted into the gradient column. Calculations of cerebral blood volume (CBV) from changes in SG of both brain tissue and intravascular perfusate have shown that the SG of brain tissue is considerably influenced by changes in CBV. This is because the SG of blood is higher than that of brain tissue, and may lead to a decrease of SG of about 0.002 in anemic cortex and of 0.001 in anemic white matter, which will simulate a false increase in tissue volume as water of 4% and 2%, respectively. This methodological error may be relevant when the early stages of ischemic brain edema development are studied. Water content of brain tissue can also be determined with acceptable accuracy by vacuum freeze-drying samples of brain tissue weighing about 100 mg. In contrast to cortex, white matter shows a wide range of individual and regional differences in water content. Thus, conclusions on the presence of brain edema drawn from tissue water determinations should always be subjected to cautious analysis and criticism.
Animals↗
Neurogenic shock syndrome after experimental subarachnoid hemorrhage in cats.
Explore the source record for details and available documents.
Adrenal Glands↗
Total and regional cerebral blood flow during perfusion from the lateral ventricle to the cisterna magna in the conscious dog: effect of hemorrhagic hypotension and retransfusion on cerebral blood flow.
This study was performed to determine if autoregulation of regional cerebral blood flow (rCBF) occurs in conscious dogs with ventriculocisternal perfusion (VCP) during moderate hypotension. Six dogs were perfused for 360 minutes using mock cerebrospinal fluid (CSF). A 120-minute control period was followed by 180 minutes of moderate hemorrhagic hypotension (mean arterial pressure (SAP) 60-80 mm Hg). The lost blood (approximately 40% of the calculated blood volume) was retransfused after 300 minutes of perfusion, and an additional 60 minutes of observation concluded the study. The rCBF was measured at 120, 240, and 360 minutes of perfusion using labeled microspheres of 15 mu diameter. Cardiac output (CO) was 2.8 +/- 0.41 liters/min at 120 minutes, decreased to 1.4 +/- 0.10 liters/min after hemorrhage, and rose after retransfusion to 2.2 +/- 0.13 liters/min. The percentage of cardiac output (%CO) received by the brain was 1.8 +/- 0.37% at 120 minutes, 3.8 +/- 0.44% at 240 minutes, and 2.2 +/- 0.22% after retransfusion (P < 0.05). There was no significant change in rCBF during hypotension. The regional cerebral blood flow was, however, significantly elevated in the thalamus, mesencephalon, pons, and medulla after retransfusion indicated a local alteration of set point in the plateau of the autoregulatory curve. Cerebral venous pH (measured in internal maxillary venous blood) decreased significantly during hemorrhage to 7.25, while cerebral arteriovenous difference of oxygen and A-VpH increased significantly during hemorrhage. Thus, autoregulation of total cerebral blood flow (CBF) during acute moderate hypotension remains intact during VCP at a rate of 0.2 ml/min using a perfusate of a constant pH and, hence, CSF-pH appears not to be of major significance for the autoregulation of CBF in moderate hypotension.
Animals↗
Increased free fatty acid turnover in CSF during hypotension in dogs.
Cerebrospinal fluid turnover rates of FFA were investigated using ventriculocisternal perfusion techniques. Seven conscious dogs were perfused over a 6-h period from the lateral ventricle to the cisterna magna with mock cerebrospinal fluid (CSF) containing [14C]palmitate and 100 mumol/l of FFA. One hundred and twenty minutes of perfusion were allowed to establish equilibrium of the FFA concentration in the ventricular space. Moderate hemorrhage hypotension was then induced (MABP greater than 60 mmHg) for 3 h, followed by rapid retransfusion and a final hour of perfusion. Cerebral blood flow did not change significantly (45 +/- 6 before, 53 +/- 6 after hemorrhage, and 47 +/- 5 ml.min-1. 100 g-1 after retransfusion). Cerebral arteriovenous difference of O2, glucose, and pH increased significantly during hemorrhage. Hypotension was accompanied by an increased turnover of FFA from 60 to 120 nmol/min (P less than 0.01) in the CSF. FFA turnover was directly correlated with the fatty acid concentration of the CSF (r = 0.77). It is speculated that the increased fatty acid turnover during hypotension may indicate increased phospholipid turnover and/or increased oxidation by tissues lining the ventricular space.
Animals↗
Effect of moderate hemorrhagic hypotension on cerebral metabolism during ventriculocisternal perfusion in the conscious dog.
Early changes in cerebral metabolism during hemorrhagic hypotension in conscious dogs have been studied with a chronic ventriculocisternal perfusion system. The mean arterial blood pressure was held above the lower limit of the cerebral autoregulatory curve. There was a rise of free fatty acids (FFA) in cerebrospinal fluid at 30 minutes after the onset of hemorrhage. The cerebral arteriovenous difference of oxygen (AVDO2), AVD-glucose, and AVD-pH increased significantly after 60 minutes of hemorrhage, while AVD-TCO2 (tissue culture oxygen) rose only slightly. These changes may reflect some of the metabolic alterations that occur in moderate hypotension.
Animals↗
Removal of 14-C-palmitate during ventriculocisternal perfusion in conscious dogs in insulin-induced hypoglycemia.
A detailed description of a method is presented allowing continous ventriculocisternal perfusion of metabolites in the conscious dog. Using this preparation, the loss of the infused albuminbound 14-C-aplmitate, was studied in 14 conscious dogs during ventriculocisternal perfusion with artificial cerebrospinal fluid (CSF). Forty-five percent of the infused 14-C-palmitate was recovered from the cisternal effluent under equilibrium conditions after 60 min of perfusion. The effect of the injection of 2.0 U insulin/kg was also investigated in seven dogs. Plasma glucose concentration decreased to 40--50 mg% and the amount of 14-C-palmitate recovered was significantly higher one hour after insulin compared to the controls receiving saline injections. No significant changes in cerebral arteriovenous differences of glucose or oxygen or in venous 14-C-palmitate concentration were observed during the same time. It is concluded that the combined use of ventriculocisternal perfusion and the analysis of cerebral arteriovenous differences are useful in studying brain metabolism in the consciuos dog.
Animals↗
Cerebral edema following experimental subarachnoid hemorrhage.
The development of cerebral edema after experimental subarachnoid hemorrhage (SAH) was studied in cats by determining regional brain tissue water content with the microgravimetric technique as well as the drying-weighing method. SAH was induced by withdrawing needles previously pierced into one or both infraclinoid internal carotid arteries through a unilateral transorbital approach. Serial determinations of regional cerebral blood flow (rCBF) by labelled microspheres, and monitorings of vital signs such as intracranial pressure (ICP), blood pressure and EEG were carried out up to 24 h after SAH. Animals could be classified into three grades according to the severity of SAH. In grade I, the increase of ICP was transient and minor. In grade II, ICP increased up to 200 mm Hg with a marked reduction of rCBF below 20% of control in cerebral hemispheres. Following subsequent reduction of ICP, rCBF increased over control, indicating reactive hyperemia. Thereafter, a great reduction of rCBF was again observed. In grade III, rCBF was sustained at essentially zero flow with the presence of continuously increased ICP above 100 mm Hg. Cerebral edema was observed particularly in the parasagittal water-shed areas of all grade II animals. It is concluded that cerebral edema complicating SAH is caused by the combination of an initially induced global cerebral ischemia and the subsequent recovery of cerebral circulation. Post SAH hypertension is another factor to exacerbate the development of cerebral edema.
Animals↗
Effects of indomethacin on rCBF during and after focal cerebral ischemia in the cat.
The effect of indomethacin on rCBF was studied in cats anesthetized with Nembutal either under resting conditions or with temporary middle cerebral artery (MCA) occlusion. RCBF was measured by the microsphere method. In control animals (n = 3), indomethacin (4 mg/kg, i.v.) significantly reduced rCBF by about 25% in both cortex (from 44 +/- 6 to 32 +/- 3 ml/100 g/min, p less than 0.001) and white matter (from 36 +/- 4 to 26 +/- 2 ml/100 g/min, p less than 0.001). After MCA occlusion rCBF was markedly decreased in the sylvian region ipsilateral to occlusion (ischemic core) (from 38 +/- 4 to 14 +/- 2 ml/100 g/min in cortex, 4 animals). Although pretreatment with indomethacin (4 mg/kg) (4 animals) 30 min prior to occlusion did not alter rCBF during ischemia, a marked enhancement of reactive hyperemia was observed in the ischemic core immediately upon reperfusion following 2 h occlusion (54 +/- 11 untreated vs 95 +/- 13 treated, p less than 0.05). In the delayed postischemic period, namely 2 h after recirculation, rCBF still remained to be higher in the animals treated with indomethacin (40 +/- 6 untreated vs 96 +/- 9 treated, p less than 0.001). Such an effect of indomethacin for ameliorating postischemic blood flow in both the immediate and delayed period was less prominent in the adjacent area (penumbra) ipsilateral to occlusion. In the contralateral hemisphere, indomethacin caused slight reduction in rCBF during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗