Biomedical subjects
Publications and source records attributed to L Auer.
In 30 patients with severe brain injury a double-blind study was performed. The effectiveness of the aldosterone-antagonist Aldactone pro injectione was examined in therapy of traumatic brain edema. The results indicate elimination of sodium and water from brain cells and white matter. Concomitantly faster improvement of state of consciousness was observed.
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From a series of 74 patients with severe head injuries and massive brain lesions, we measured the changes in haptoglobulin in 33 cases. On average, the globulin was, after a short drop in the first two days, increased about three times towards the seventh day, and was still above normal after ten days. Seen together with the total alpha-2-globulin increase after head injury this rise seems mainly to be caused by the haptoglobulin changes. Haptoglobulin was found to be a good indicator of the extent of brain tissue damage. It cannot on its own be used for prediction of survival chances.
This study in cats investigates the action of sodium nitroprusside on the pial vessels by systemic and local administration, with an intravital microscopic window technique and a photometric technique for graphic documentation of vessel diameter changes. Intravenous infusion caused vasodilatation parallel with decreasing blood pressure. Pial arterioles dilated more than venules, smaller vessels more than larger ones. Local administration caused maximal dilatation within 5--10 seconds. With blood pressure returning to normal after i.v. therapy, pial vessels remained wider than they were before hypotension at the same pressure level. From these data it is concluded that the substance acts longer on the brain vessels than on vessels elsewhere in the body, and that cerebrovascular autoregulation to blood pressure changes is disturbed during this period.
This is an investigation into thromboplastin time, partial thromboplastin time, plasma thrombin time, fibrinogen, and platelets in 30 patients with severe brain injury over 7--14 days. Platelets showed a very marked initial decrease and a slow return to normal around the seventh day. Fibrinogen was initially lowered in most of the cases, and raised from the second day onward. Changes in the other laboratory values were less definite. Latent signs of consumption coagulopathy were not accompanied by bleeding disorders, or by disseminated intravascular coagulation at autopsy. The severity of laboratory value changes clearly correlated with the extent of brain damage, and was significantly higher when the patient did not survive the first week after injury.
We have investigated serum urea, uric acid, and creatinin crealinine levels in 39 patients with craniocerebral trauma. The most impressive observation was a change in serum urea, which was found significantly increased up to 237 mg% on the seventh day (mean value) after severe injury, and turned out to be of great prognostic value. Patients with a serum urea above 100 mg% did not survive the acute stage. Uric acid and creatinine were only significantly increased in patients with lethal outcomes, the first being elevated by about 300% in the first week, the second remaining normal for four days increasing thereafter. It is concluded from these first data that a hypercatabolic state due to shock, central dysregulation, or both, is responsible for the dissociated behaviour of urea, uric acid and creatinine during the first four days, after which renal failure as a secondary change is shown by the rise in serum creatinine.
Pial microcirculation was observed in cats during acutely induced blood pressure increase using the window technique. Measurements of arteriolar diameter changes in situations of preserved and altered cerebrovascular autoregulation were made, when diffuse vasoconstriction and sausage-like dilation, respectively, occurred. Comparison of percentage changes of narrow segments between sausage-like dilated arterioles and diffusely constricted (= autoregulating) vessels gave evidence that a failure of autoregulation in this situation is not associated with vasospasm but with dilation. Individual narrow segments did not constrict more--but on an average even rather less--than diffusely constricted vessels. Evans blue extravasation occurred only with dilation, never with vascular constriction. From these data it is concluded that extravasation due to acute blood pressure increase is not of ischemic nature, but a consequence of high filtration pressure due to arteriolar and venous congestion.
An intravital-microscopic study on cat pial vessels for the localization of Evans blue extravasation during acute hypertension was performed. The onset of extravasation was seen 10 sec to 2 min after the beginning of hypertension. The localization of initial extravasation turned out to be little venules, not arterioles. Venular congestion by an overload of venous outflow seemed to be the origin of extravasation.
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Sodium nitroprusside (Nipride) was used in 35 patients between 16 and 72 years for induced hypotension. The fast and dose-dependent effect on the smooth muscles of the vessels made it superior to other methods of lowering blood pressure. Sodium nitroprusside was used to achieve hypotension in 11 patients (group I) with an aneurysm of a cerebral vessel and in 16 patients (group II) with highly vascularized cerebral tumors. In 8 patients (group III) from the neurosurgical intensive care unit a hypertensive crisis was interrupted. 10 patients (group IV) without induced hypotension were used as controls to compare the action of our standardized method of anesthesia on the observed parameters of blood pressure lowering. The average dose of sodium nitroprusside was 2.74 mcg/kg/min. in group I, 1.77 mcg/kg/min in group II and 1.27 mcg/kg/min in group III. The initial blood pressure was lowered between 30--40% in the mean in all 3 groups. Careful monitoring of the intra-arterial blood pressure, the central venous pressure, the cerebral fluid pressure, the arterial blood gases and the function of the kidneys during and after induced hypotension with sodium nitroprusside made it possible to take advantage of the blood pressure lowering effect also in patients with increased intracranial pressure.
Sodium Nitroprusside (Nipride) was administered by infusion pump intravenously in 27 neurosurgical patients for intraoperative, postoperative and posttraumatic blood pressure lowering. This was accomplished with intension to reduce the risk of hemorrhage during operation on highly vascularized tumors or aneurysms and to combat hypertensive crisis after surgery and brain injury. The effect was documented by direct arterial blood pressure registration and the drug proved to be fast acting, potent and readily reversible. Dosage varied between 1 and 10 microgram/kg/min with systolic pressure decreasing about 6 to 60% of the initial value. There was ill correlation between infusion rate and blood pressure drop which demanded particular caution at the beginning and the end of infusion. A decrease in pulse pressure and a moderate tachycardia were generally observed, however no complications were seen due to a Sodium Nitroprusside administration over less than 12 hours duration in our series.
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A fluorescence-angiographic investigation is presented of pital vessel reactions to acute drug-induced hypertension in cats. Observations and documentation were carried out by an intravital-microscopic technique. Acute hypertension, where pressure values of 220 to 260 mm Hg were reached within 10 to 20 sec, was followed by marked vasodilatation: Arterioles under 50 mu in diameter and capillaries were dilated to between 200 to 300% of the resting diameter, whilst arterioles of 50 to 100 mu showed an increase of 50 to 60%. Reddening of veins and acceleration of the blood flow occurred. Vasodilatation persisted after the blood pressure values had returned to normal. In connexion with investigations of the blood pressure immediately after a head injury, the role of acute hypertension in the development of hydrostatic brain oedema is discussed.
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