Biomedical subjects

J Löfgren

Publications and source records attributed to J Löfgren.

32 records · Page 2Linked to original sources

PubMed1979

Extravasation and arteriovenous shunting after epidural bleeding -- a radiological study.

Eighteen patients with epidural bleeding had preoperative angiography with visualization of the meningeal arteries. Thirteen of these had extravasation of contrast medium from meningeal arteries and eleven also had shunting of contrast medium from meningeal arteries to meningeal or diploic veins. For easier demonstration of these findings, selective external carotid angiography and the use of larger amounts of contrast medium are recommended. Our results support the theory that the arteriovenous shunting has important implications on the pathophysiology of epidural bleeding. Failure to demonstrate extravasation and arteriovenous shunting may be explained in three ways: (1) inadequate angiographic technique; (2) arterial bleeding has stopped; (3) epidural bleeding is not arterial.

Cerebral Angiography↗

PubMed1979

Hysteresis in the relationship between cerebrospinal fluid absorption minus formation and cerebrospinal fluid pressure in the dog.

In this study the difference between cerebrospinal fluid (CSF) absorption and formation (A -- F) was measured as a function of CSF pressure in the living and dead dog. We determined this relationship between A -- F and CSF pressure during both increasing and decreasing CSF pressures. A hysteresis effect was identified in 78% of living animals, but was not seen in the dead animals. This suggests that the mechanism of CSF absorption in the living dog is nonpassive and pressure-sensitive.

Absorption↗

PubMed1978

Communicating exophthalmos: a sign of bilateral orbital roof defects.

The term communicating exophthalmos is suggested for a condition where manual retropulsion of one eye results in proptosis of the other eye. This sign was observed in a patient with bilateral pulsating exophthalmos. The pulsating exophthalmos was ascribed to orbital roof defects in combination with post-traumatic hydrocephalus. It was controlled by a shunting procedure.

Adult↗

PubMed1978

Cerebral blood flow and metabolism in the acute phase of experimental subarachnoid bleed.

Our experiment seems to confirm the hypothesis, implying an active CBF autoregulation as one of the interacting four survival mechanisms during an intracranial hemorrhage. While our present study has indicated that the autoregulation operates during the initial bleed, it is fully conceivable that the autoregulatory capacity may be exhausted after recurrent hemorrhages. Earlier experiments (Häggendal et al. [1970]) showed that autoregulation is easily abolished for prolonged periods after periods of intracranial hypertension. Further experiments are necessary to evaluate the capacity of the cerebral autoregulation to withstand repeated intracranial bleeds.

Animals↗

PubMed1975

Characteristics and limits of tolerance in repeated subarachnoid hemorrhage in dogs.

The effects of repeated subarachnoid hemorrhages have been investigated experimentally in dogs. The main objectives were to determine the tolerance to repeated hemorrhage and to study the changes occurring during the repeated bleeds, in intracranial pressure, EEG, ECG, systemic arterial pressure and respiration. The natural course of an intracranial hemorrhage was simulated by shunting blood from a femoral artery through a drop recorder into five different sites in the craniospinal system: the chiasmatic cistern, a lateral ventricle, the cisterna magna, the lumbar subarachnoid space and into the cerebral tissue of the left frontal lobe. The hemorrhage was allowed to continue until it stopped spontaneously. Each bleed resulted in a transient rise in intracranial pressure to the level of the arterial pressure, followed by a return to a steady state value. The time taken for the attainment of the steady state was increasingly prolonged. The final steady state pressure increased with each bleed. Ultimately, a stage was reached where the hemorrhage resulted in a sustained high pressure at the level of the arterial blood pressure, producing failure of vital functions and an irreversibly isoelectric electroencephalogram. The average number of bleeds necessary to produce this state in the case of hemorrhage into brain parenchyma was 3 (range 2-4), into the lateral ventricle, 4 range 3-5), and into the cisterna chiasmatica, 5 (range 2-7). After 5 hemorrhages into the cisterna magna and the spinal subarachnoid space, a local resistance at the bleeding site was built up which prevented further bleeding.

Animals↗

PubMed1975

Lethal mechanism in repeated subarachnoid hemorrhage in dogs.

The mechanism limiting the tolerance to repeated subarachnoid hemorrhages was analysed experimentally. Blood introduced by an extracorporeal femorointrathecal shunt or by injection, into five different sites of the cranio-spinal system in living and dead dogs, produced a progressive increase in the steady state CSF pressure after each subsequent bleed. The pressure increase was quantitatively related to the amount of blood entering the system. A comparison of the respective effects of injections of whole blood and of erythrocytes indicated that the red blood cells were the component which induced an increase in the outflow resistance by clogging the pathways of the cerebrospinal fluid. The increase in outflow resistance with each bleed resulted in a stepwise rise in pressure to a level incompatible with survival. The lethal volume of bleed was specific for each site of hemorrhage: namely for brain parenchyma 8.1 ml, lateral ventricle 16.2 ml, cisterna chiasmatica 17.7 ml, cisterna magna 30 ml, and spinal subarachnoid space 55 ml. The assumption that death might be a random event was discarded, the failure of vital functions being considered to be the result of the high intracranial pressure. Mock bleeds using intrathecal infusions of saline suggested that spatial decompensation rather than cumulative ischemic effects caused death.

Animals↗

PubMed1974