PubMed Health⌕ Search

Biomedical subjects

J Löfgren

Publications and source records attributed to J Löfgren.

At least 19 recordsLinked to original sources
PubMed1993

Vascular dimensions of the cerebral arteries follow the principle of minimum work.

BACKGROUND AND PURPOSE: The principle of minimum work is a parametric optimization model for the growth and adaptation of arterial trees. It establishes a balance between energy dissipation due to frictional resistance of laminar flow (shear stress) and the minimum volume of the vascular system, implying that the radius of the vessel is adjusted to the cube root of the volumetric flow. The purpose of this study is to verify whether the internal carotid artery system obeys the principle of minimum work. METHODS: Measurements of the radius of parent and branch segments of the internal carotid, anterior, and middle cerebral arteries were performed on analog angiographs chosen at random from a set classified as normal. The branch angles were measured from lateral projections in bifurcations of the anterior cerebral artery. The relation of the calibers of parent and branch vessels was analyzed. RESULTS: The area ratio of the bifurcations (N = 174) was 1.2 +/- 0.4 (mean +/- SD). The equation (r0)n = (r1)n + (r2)n was solved for n, resulting in n = 2.9 +/- 0.7 (mean +/- SD, N = 157). Optimum proportions between the radii of parent (r0) and branch (r1 and r2) vessels in the internal carotid artery system were verified in normal carotid angiographs up to four branch generations, according to the theoretical equation r0(3) = r1(3) + r2(3) (r = 0.989, N = 174). No clear correlation was found between the measured branch angles, the relative branch cross-sectional area, and the theoretical optimum angles. CONCLUSIONS: This study demonstrates that the process of branching of the internal carotid artery system obeys the principle of minimum work, as the diameter exponent approximates 3. The principle of minimum work establishes strict functional relations between volumetric flow, flow velocity, and vessel radius. This model was extended to parametric optimization of branch angles, which has proved irrelevant in terms of functional optimization. Our results corroborate this finding. Shear stress-induced endothelial mediation seems to be the regulating mechanism for the maintenance of this optimum vessel design. The magnitude of wall shear stress is the same at every point in a vascular network obeying the principle of minimum work, because the flow rate influences the shear stress proportionally to the third power of the vessel radius. This observation has implications for understanding the remodeling of the cerebral vascular network in the presence of arteriovenous malformations and for the pathogenesis of saccular aneurysms.

Blood Flow Velocity↗
PubMed1993

Optimality principles and flow orderliness at the branching points of cerebral arteries.

BACKGROUND AND PURPOSE: The cerebral arteries present an optimum blood flow/vessel radius relation. However, branch angles may vary widely in the cerebral arteries because the parametric optimization of branch angles is irrelevant in terms of energy cost. The position of the flow divider in extracranial arteries has been suggested to be optimum in flow orderliness. No data exist on the flow divider of cerebral arteries. Thus, we hypothesized that in the cerebral arteries the apex of the bifurcations, which is known to be the site of maximum hemodynamic stress in a vascular network, may normally lie in a non-optimum position relative to the dividing flow streamline in the parent vessel, leading to disturbed laminar flow and increased vessel wall shear stress at the apical region despite the optimum blood flow/vessel radius relation. The objective of this study was to test our hypothesis. METHODS: We measured the branch angles and diameters of parent and branch segments of the anterior cerebral artery system from lateral projections to minimize the measurement error on angiographs chosen at random from normal sets. The position of the apex of the bifurcations in relation to the ostium of the parent artery (gamma) and the ratio of the branch diameters (d2/d1) were compared. Optimum curves for these parameters were calculated by a mathematical model. In addition, the separation of flow streamlines according to gamma was calculated for each bifurcation and related to the division of flow required by each branch according to the optimum blood flow/vessel radius relation. RESULTS: The data points on gamma and d2/d1 and the separation of flow according to gamma and the division of flow required by the branches were found to scatter around the optimum curves. However, a trend toward the theoretical optimum is discernible. The data points are suggested to be a random sample from a normal distribution around the optimum (.40 < P < .50). CONCLUSIONS: The bifurcations of the cerebral arteries appear to be optimized to avoid increased hemodynamic stresses both globally and locally in the same manner as extracranial arteries.

Aneurysm↗
PubMed1990

Cerebral blood flow in experimental intracranial mass lesions. Part I: The compression phase.

We have shown that a rebound of intracranial pressure (ICP) occurring after decompression of an intracranial mass lesion is a threshold phenomenon dependent upon the cerebral perfusion pressure (CPP) during compression and the duration of the compression. In the present study regional cerebral blood flow (rCBF) was measured during balloon compression of a degree critical for the development of a postdecompression rebound. The effects were compared with those of hydrostatically raised pressure which under similar conditions rarely produces a rebound of ICP. Disproportionately marked reductions in flow occurred in the hemisphere ipsilateral to the balloon, especially in white matter and in cortex adjacent to the balloon with flow values of, respectively, 1.1 +/- 0.9 and 6.4 +/- 3.4 ml 100 g-1 min-1. The differences in flow between balloon and hydrostatic compression were found to be due to an increased cerebrovascular resistance (CVR) caused by a direct compressive effect by the balloon overriding the generalized vasodilation which occurs in response to the raised ICP. Thus the increase in CVR attributable to compression by the balloon added to the reduction in CPP caused by the diffuse increase in ICP. As a consequence flow in large regions of the brain was reduced below the thresholds for structural infarction and for ischaemic damage to the blood-brain barrier.

Animals↗
PubMed1990

Cerebral blood flow in experimental intracranial mass lesions. Part II: The postdecompression phase.

Cerebral haemodynamics were evaluated after a period of cerebral compression produced by subarachnoid fluid infusion or inflation of an epidural balloon. Release of the compression resulted in a marked cerebral hyperperfusion which was generalized in the case of hydrostatically raised pressure but restricted to supratentorial structures after balloon compression. A rebound of intracranial pressure (ICP) occurred only after balloon compression, indicating that loss of vasomotor tone per se was not the primary reason for the rebound of ICP. In the balloon compression experiments the hyperaemia passed into a stage of hypoperfusion attributable in part to a reduction in cerebral perfusion pressure due to the rebound of ICP and in part to an increase in flow resistance probably related to external compression of the vascular bed by the accumulation of brain oedema. The observed flow changes, i.e. delayed hypoperfusion preceded by hyperaemia, were similar to those after temporary ischaemia, indicating that the rebound response is a non-specific postischaemic phenomenon.

Animals↗
PubMed1990

Embolization of cerebral arteriovenous malformations with bucrylate. Experience in a first series of 29 patients.

The experience with embolization of intracerebral arteriovenous malformations (AVMs) with bucrylate (isobutyl-2-cyanoacrylate) in 29 patients is reported. In 9 cases (31%) less than 1/3 of the AVM nidus was occluded, in 12 (41%) 1/3 to 2/3, in 4 (14%) more than 2/3, and total occlusion was only seen in 3 cases (10%). One patient was never embolized, owing to procedure complications. At follow-up angiography in 20 patients, partial revascularization was found in 11 AVMs and further occlusion in 2. Complications occurred in 11 cases (38%). Five patients (17%) suffered from hemorrhage: 2 died, one deteriorated severely and 2 recovered. Unintentional embolization or edema resulted in neurologic deficits in 6 patients (21%), permanent in 3 and reversible in 3. Symptomatic improvement was initially found in 13 patients (45%) but was stable only in 9. In 9 patients (38%) embolization was followed by elective surgery or irradiation. The best results were obtained in small and medium-sized AVMs (less than 6 cm) while there was a high risk of complications and an uncertain palliative effect in large AVMs.

Adolescent↗
PubMed1986

Traumatic intracranial hematomas: pathophysiological aspects on their course and treatment.

Hematomas in head injuries as a general rule reach their definite size within minutes after the trauma, the bleeding being effectively checked by an interaction of an increased intracranial pressure and the natural hemostatic processes. In epidural hemorrhage the development of arteriovenous shunting in the epidural space may result in continuing bleeding. In special circumstances vascular injury may produce delayed hemorrhage related to increased transmural pressure in the vascular bed and the development of a hyperfibrinolysis syndrome. The clinical effect of a hematoma is quantitatively related to its volume, but modified to a considerable degree in the particular case by the size of the extraaxial space and the arterial blood pressure. Some implications for treatment are commented upon.

Brain Injuries↗
PubMed1986

Effects of continuously expanding intracranial lesions on vital physiological parameters. An experimental animal study.

The work described in this report confirms and extends the results described in a preliminary communication (Löfgren, J. and Zwetnow, N.N., Acta Neurol. Scand. (1970, 625) which examined the effects in cats of an expanding mass, in the form of an intracranial supratentorial balloon, on vital physiological parameters. In the present study, particular emphasis was placed on the possible significance of the rate of expansion of the mass in the range usually encountered in the clinical situation of intracranial haemorrhages. Results from the experiments on 37 cats and 8 dogs showed that changes in vital parameters appeared when the balloon had reached a volume of about 5% of the intracranial volume (the "reaction volume") while respiratory arrest occurred at an intracranial volume of about 10% (the "apnoea volume"). Both threshold volumes were independent of the rate of expansion within the range used. Alterations in EEG, heart rate, respiratory rate and systemic arterial pressure usually occurred simultaneously with the development of a transtentorial pressure gradient. When respiratory arrest occurred, the cerebral perfusion pressure was markedly reduced, usually to a value of about 30 mm Hg, suggesting that brain tissue ischaemia is an important component in the lethal mechanism underlying intracranial expanding lesions. It is proposed that the volume load tolerance of the organism towards an expanding intracranial lesion, as expressed by the reaction volume and the apnoea volume, may represent a biologically useful parameter potentially suitable for quantitative evaluation of adverse agents and therapeutic procedures.

Animals↗
PubMed1986

Evaluation of intracranial pressure rebound after evacuation of intracranial expanding lesions. An experimental study in dogs.

Sequential magnetic resonance imaging was used to follow brain displacement, signs of herniation and increase in local brain tissue water content during expansion and after evacuation of an extradural balloon in anesthetized, artificially ventilated dogs. A fatal intracranial pressure (ICP) rebound occurred if the cerebral perfusion pressure (CPP) was critically reduced to 20 mm Hg for more than half an hour. Despite reduction of brain displacement after balloon evacuation brain water content continued to increase. Compression of CSF outflow pathways and signs of herniation remained. CPP continuously fell to zero. ICP rebound is a grave situation significantly influenced by a large increase in brain tissue water.

Animals↗
PubMed1985

Regional cerebral blood flow and CSF pressures during the Cushing response induced by an infratentorial expanding mass.

An experimental study was carried out in eight dogs to investigate whether the Cushing response (CR) during intracranial hypertension is due to pressure per se, tissue distortion, or ischemia in the brain stem. To minimize the effects of rostrocaudal displacement, intracranial pressure was raised by an expanding mass lesion located in the posterior fossa. Regional cerebral blood flow (rCBF) was measured with radioactive microspheres and compartmental cerebrospinal fluid (CSF) pressures were recorded during the CR which was induced by the continuous inflation at a constant rate of an infratentorial epidural rubber balloon in two groups of four dogs. In one group (A) rCBF was measured at the onset of the CR and in the other group (B) at the peak of the systemic blood pressure rise. In the animals of group A blood flow in the mesencephalon, pons and upper medulla oblongata was reduced from control values by 32%, 57% and 85% respectively. In group B blood flow in the same areas did not differ significantly from pre-inflation values. In contrast, the recorded balloon volume, which was assumed to be an index of mechanical distortion of the brain stem, varied considerably at the beginning of the blood pressure rise (from 2.5 to 4.7% of the calculated intracranial space). Similarly, CSF pressure in the posterior fossa at the onset of the CR also varied considerably (from 52 to 117 mmHg). Thus, the large quantitative variations meant that both absolute pressure and tissue distortion were poor predictors of the onset of the CR. The findings suggest that ischemia, rather than brain stem distortion per se or pressure by itself, is responsible for the initiation of the CR. The rise in blood pressure elicited during the CR seems capable of restoring blood flow in the brain stem back to control values.

Animals↗
PubMed1985

Influence of blood pressure on tolerance to an intracranial expanding mass.

In 3 groups of 4 dogs with normotensive, induced-hypotensive and induced-hypertensive blood pressure respectively, continuous expansion of an extradural supratentorial balloon led to respiratory arrest at inflation volumes which increased with increasing blood pressure. This positive correlation between the volume tolerance to an expanding lesion and blood pressure was also found in similar experiments on 4 hypotensive and 4 hypertensive cats. Monitoring cerebrospinal fluid pressures in the cerebral lateral ventricles, in the posterior fossa and in the spinal subarachnoid space showed that absolute pressures in the various compartments as well as the intercompartmental pressure gradients at the moment of respiratory arrest were increased in proportion to the level of the systemic arterial pressure in each case. These observations do not support current concepts that brain-stem distortion alone or that stimulation of baroreceptors in the posterior fossa are responsible for eliciting the Cushing response. The fact that the supratentorial perfusion pressure was the only parameter which did not differ significantly under the different experimental conditions suggests that the mechanism responsible for the respiratory arrest is local brain tissue ischemia, probably near the tentorial incisure. The magnitude of gain in volume tolerance, when mean arterial pressure was varied from 60 mmHg to 190 mmHg, was 87% suggesting that the blood pressure may have a critical role in an intracranial lesion. These findings have clinical implications.

Animals↗
PubMed1985

Incidence and prevalence of primary biliary cirrhosis in a defined population in Sweden.

The incidence and prevalence of antimitochondrial antibody-positive primary biliary cirrhosis (PBC) has been studied within a defined area in Sweden served by one hospital. During the period 1976-1983 the yearly incidence of PBC was 1.4/10(5) inhabitants, and on 31 December 1983 the prevalence was 12.8/10(5) inhabitants. The prevalence is the highest reported so far. At the time of diagnosis half of the patients were clinically asymptomatic. Two of the patients also had celiac disease with osteomalacia responding to a gluten-free diet. Gallstone disease occurred in 30% of the patients. Four patients died--two of liver-related complications, one of colonic carcinoma, and one of staphylococcal septicemia and endocarditis. One further patient, who is still alive, developed hypernephroma. Our results indicate that PBC is a fairly benign disease in most patients, with a slow progress during which they lead a fairly normal life.

Adult↗
PubMed1983

Arterio-venous epidural shunting in epidural bleeding radiological and physiological characteristics. An experimental study in dogs.

In order to test the possibility suggested in previous studies that the long bleeding time and the large bleeding volume observed in experimental epidural bleeding can be explained by the development of an arterio-venous shunt, water soluble X-ray contrast was injected into the epidural space in dogs during an epidural bleeding in progress. It was found that the contrast medium left the epidural space through diploic veins in the cranial bone to the neck veins. By draining off epidural blood the arterio-venous shunt counteracts the intracranial pressure tamponade developing in intradural bleeds and thus prolongs bleeding. Perfusion experiments showed the absorption capacity for saline to be about 20 times as large in the epidural space as in the CSF space. While there was no apparent absorption limit for blood in the epidural space the absorption capacity for blood of the subarachnoid space became progressively saturated, leading to a continuously increasing CSF outflow resistance and CSF steady-state pressure. A theory for the formation of epidural haematoma is proposed which in essence implies that the epidural shunt is a major determinant of the clinical outcome of an epidural bleeding.

Animals↗
PubMed1983

Comparative analysis of experimental epidural and subarachnoid bleedings in dogs.

The difference in the course and the lethal mechanism between intracranial, subarachnoid and epidural bleedings was studied in a dog model under varying conditions. Subarachnoid bleedings were usually shortlasting, self-restricting, and generally survivable. The epidural bleedings differed quantitatively and qualitatively from the subarachnoid bleedings in being larger and having a longer duration. The difference seems related mainly to the development of an arterio-venous shunt in the epidural space during the bleeding. It is suggested that the epidural arterio-venous shunt may be of importance for the course and the lethal mechanism in epidural bleeding.

Animals↗
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↗