[Cerebral vasoparalysis, arterial hypertension and brain edema (author's transl)]. / Cerebrale Vasoparalyse, arterielle Hypertension und Hirnödem

The present studies were performed in order to determine whether "filtration edema" will develop as a consequence of cerebral vasoparalysis, vasoparalysis in combination with arterial hypertension or arterial hypertension alone. A series of dogs, anaesthetised with i.v. Chloralose-Urethane were exposed 1) to cerebral vasoparalysis, produced by hypercapnia (PaCO2 about 150 mm Hg) and hypoxaemia (PaO2 40-60 mm Hg); 2) to arterial hypertension and 3) to a combination of cerebral vasoparalysis and arterial hypertension. Following cerebral vasoparalysis and arterial hypertension, a significant decrease of total cerebrovascular resistance and moderate increase of venous resistance was observed. Regional cerebral blood flow (133Xe), intracranial pressure, as well as the pressure in postcapillary venous outflow (sinus sagittalis wedge pressure and confluence sinuum pressure) were increased. Neither normotonic vasoparalysis nor vasoparalysis in combination with slight arterial hypertension (MABP more than 90 min above 180 mm Hg) resulted in cerebral edema. In contrast, cerebral vasoparalysis in combination with severe arterial hypertension (MABP more than 90 min above 220 mm Hg) resulted in a statistically significant increase in the water content in the white matter without evidence of protein extravasation. Multiple small foci of Evans blue extravasates, however, were found in the cortex following arterial hypertension in combination with vasodilation, indicating a damage of the blood brain barrier. In these blue stained cortical areas the water content was significantly in creased. The following conclusions were drawn from the results. Vasoparalysis during normotension does not produce brain edema despite the slightly elevated hydrostatic pressure gradient between intravasal and extracellular space. Only considerable increase of this hydrostatic pressure gradient caused by a combination of vasoparalysis with severe arterial hypertension is able to produce brain edema in the white matter. In addition, acute hypertension may cause minor multifocal damage of the blood brain barrier in the cerebral cortex. It is concluded that so-called brain swelling, which has been described by several authors in states of cerebral vasoparalysis, is not predominantly caused by brain edema but by vascular congestion. The clinical aspects of the result are discussed.

Circadian rhythm of catecholamines, cortisol and prolactin is altered in patients with apallic syndrome in comparison with normal volunteers.

Circadian rhythms of catecholamines, cortisol and prolactin were investigated in 4 healthy subjects and in 6 patients suffering from an apallic syndrome. The clinical picture of this syndrome is characterized by disturbed consciousness (coma vigile), suspension of the sleeping and waking rhythm, lack of emotional reactions and appearance of primitive motor patterns. With the exception of dopamine a pronounced circadian rhythm was found in the control group for all investigated parameters. Catecholamines and cortisol showed a good correlation in the temporal pattern of plasma concentrations and urinary excreted amounts. In all apallic patients the circadian rhythm of prolactin was abolished. Only in one patient a rhythm of catecholamines and in 2 patients a rhythm of cortisol was still detectable. The data may indicate that the episodic nature of hormone secretion was essentially unaffected by the apallic syndrome. These results are regarded as an indication that endogenous, centrally controlled processes participate in circadian rhythms.

Altered circadian rhythm of catecholamines in patients with apallic syndrome.

Circadian rhythms of catecholamines were investigated in 4 healthy subjects and in 6 patients suffering from an apallic syndrome. The clinical picture of this syndrome is characterized by disturbed consciousness (coma vigile), by suspension of the sleeping and waking rhythm, by lack of emotional reactions and by appearance of primitive motor patterns. 5 of the 6 apallic patients showed an abolished rhythmicity compared with the control group. These results were interpreted as an indication that endogenous, centrally controlled processes are the cause of circadian rhythms.