PubMed Health⌕ Search

Biomedical subjects

U Bagge

Publications and source records attributed to U Bagge.

At least 37 records · Page 2Linked to original sources
PubMed1992

Calcium depletion reduces the destruction of fibrosarcoma cells in the microvasculature of artificially perfused rat hearts.

Earlier studies have shown that most tumour cells (TCs) injected into the circulation die rapidly. The mechanisms behind this rapid elimination of TCs are not known, but some experimental data suggest that mechanical trauma to the cells in the capillary bed plays a role. In the present investigation 725,000 rat fibrosarcoma cells (250,000/ml) were infused into the coronary microcirculation of isolated and artificially perfused (flow rate approx. 6 ml/min), beating and non-beating (Ca2+ excluded from the perfusate) rat hearts. The analyses included calculations of the number of TCs retained in the myocardium 5 min after start of TC infusion and their distribution within the ventricular wall. In addition, ultrastructural studies were performed to identify possible structural changes of trapped TCs and myocardial tissue. Intact and viable TCs in the effluent perfusate were counted. In beating hearts about 20% of the infused TCs were collected microscopically intact after passage through the heart circulation, and of these cells only 32% were viable (in-flow viability 87-91%). In Ca(2+)-depleted hearts the corresponding figures were 29 and 48%, respectively. The difference in viable cell counts was statistically significant (P less than 0.001). The TCs trapped in the left ventricular wall of the myocardium of beating hearts were mainly found in the subepicardial third of the wall, whereas in non-beating hearts the trapped cells were distributed randomly. The ultrastructural appearance of trapped cells differed between the two groups: 82% of cells trapped in beating hearts showed signs of severe damage, with subcellular vacuolization and plasmalemmal disruption, whereas 65% of cells trapped in Ca(2+)-depleted hearts seemed undamaged with intact cell membranes and cytoplasmic organization. The remaining 35% showed variable subcellular disorganization. The results cannot entirely be explained by mechanical TC damage in the microcirculation due to intracapillary deformation. The observations require additional explanatory mechanisms. One possible important TC damaging mechanism, dependent on extracellular Ca2+ levels, could be endothelial cell release of reactive oxygen species.

Animals↗
PubMed1992

Flow resistance and its components in hypertensive men treated with the calcium antagonist isradipine.

The components of blood flow resistance were investigated in 14 men with essential hypertension (diastolic blood pressure higher or equal to 100 mm Hg) before and after treatment with the dihydropyridine calcium antagonist-isradipine. Isradipine reduced intraarterial blood pressure by decreasing the total (placebo 5.1 U.mPa-1.s-1; isradipine 3.9 U.mPa-1.s-1), and renal (placebo 48.9 U.mPa-1.s-1, isradipine 35.4 U.mPa-1.s-1) vascular hindrance, the blood viscosity being unchanged. Arterial compliance was increased by isradipine (placebo 1.03 ml.mmHg-1; isradipine 1,25 ml.mmHg-1). The pressor response to adrenergic alpha stimulation with phenylephrine was decreased during treatment with the calcium antagonist. The compliance of the venous system was not changed by the treatment with isradipine. Haemorheological parameters were stable throughout the study but some changes in the correlations between the different rheological parameters were observed. The present study indicates that the antihypertensive effect of the dihydropyridine calcium antagonist isradipine was the result of functional modulation of the small and large arteries, the venous system and the flow properties of blood being unaffected.

Adult↗
PubMed1991

The morphology, deformability and microvascular arrest of rat fibrosarcoma and adenocarcinoma cells.

The deformation and flow properties of tumour cells may play a role in their arrest in the microvasculature of different organs. In the present investigation the morphology, deformability and microvascular arrest in the liver of rat fibrosarcoma cells (FSCs) and adenocarcinoma cells (ACCs) were compared using electron microscopy, deformability measurements in narrow glass pipettes and isotope-labelling techniques. The ACCs had a larger mean diameter (13.9 microns) than the FSCs (10.9 microns) and showed a slower rate of deformation into 6.5 microns glass pipettes. A significantly larger percentage of ACCSs (52.4%) than of FSCs (19.9%) remained in the livers 5 min after intraportal injection. The results indicate that for the particular tumour cells studied here, there exists a relationship between cell deformability and the tendency for microvascular trapping in the liver, i.e. less deformable cells have a greater tendency for retention in the liver.

Adenocarcinoma↗
PubMed1991

Hemorheological disturbances, metabolic parameters and blood pressure in different types of obesity.

Body fat distribution characterized by a high waist/hip ratio (WHR) has been described as a risk factor in the incidence of cardiovascular diseases and associated mortality. Hemorheological changes have been shown to accompany several risk factors. Gynoid and android obese women were compared in the present study with respect to hemorheological and metabolic variables and blood pressure. The android obese women had a significantly higher hematocrit and red blood cell count and showed higher blood viscosity at both high and low shear rates than women with the gynoid obesity type. Blood pressure was also higher in the android group. No significant differences were shown in concentration of cholesterol or triglycerides in serum nor in the microrheological properties of the red blood cells. The filterability index, which mirrors the number of rigid erythrocytes in the blood, was found to correlate with the plasma insulin concentration (r = 0.78, P less than 0.05) in the android but not in the gynoid obese women. It is concluded that the pathological changes in blood rheology observed in the android obese women may contribute to the high rate of cardiovascular events and associated mortality reported in this type of obesity.

Adipose Tissue↗
PubMed1991

Changes in gastric mucosal microcirculation and purine nucleotide metabolism during hemorrhagic shock in rats.

Intravital fluorescence microscopy and morphometry were used to study the microcirculation in the rat gastric mucosa during and after hemorrhagic shock. Under control conditions the circulation appeared homogeneous and unaffected by superfusion with 0.1 N HCl. During hemorrhagic shock, scattered areas of the mucosa lost circulation. Morphometry showed that the number of perfused mucosal vessels decreased significantly in the abluminal part of the mucosa both in perfused and ischemic areas, the reduction being most pronounced in the ischemic areas, where the number of perfused luminal vessels also decreased significantly. During reperfusion, bleedings occurred from the mucosa. A key finding was that the bleedings always had their origin at the border zone between ischemic and perfused areas. After hemorrhagic shock adenosine triphosphate and energy charge levels dropped significantly in both perfused and ischemic areas but with significantly lower levels in the ischemic areas. The hypoxanthine levels increased in both perfused and ischemic areas. The experiments show that local mucosal ischemia and accelerated nucleotide degradation are of pathogenetic importance in the development of stress ulcers after hemorrhagic shock. The border zone between circulated and ischemic areas seems to be an area of special interest.

Animals↗
PubMed1990

The influence of different flow velocities on tumor cell survival in micropore filters.

Earlier studies have shown a lower degree of lodgement and early survival of tumor cells in muscle than in liver after infusion via the femoral artery and portal vein, respectively. A possible explanation to this difference might be that the tumor cells are mechanically destroyed, and thus die more rapidly in muscle because they enter this capillary network at a much higher flow velocity. In the present study, the effect on early tumor cell (rat fibrosarcoma) survival of a high and a low flow velocity/deformation rate was evaluated in micropore (5 microns) filters, using isotope (Cr51) technique. These experiments were combined with scanning electron microscopic (SEM) analyses. The filter experiments showed no significant differences in the rate of cell death in the filters between tumor cells subjected to high or low deformation rates, and there were no qualitative differences in tumor cell appearance in the SEM study. It is, therefore, concluded that the difference in tumor cell lodgement and survival between muscle and liver is not primarily caused by differences in the rate of cell deformation upon entry of the organ capillary network.

Animals↗
PubMed1989

Effects of experimental graded compression on blood flow in spinal nerve roots. A vital microscopic study on the porcine cauda equina.

Compression injuries of spinal nerve roots are very common. However, the basic pathophysiology of these conditions is not fully understood. In this study a model is presented for experimental graded compression of the nerve roots of the pig cauda equina, including a technique for vital microscopic studies on the microcirculation flow of the intrinsic vessels of the nerve roots during compression. With this model critical pressure levels for compression-induced occlusion of the arterioles, capillaries, and venules of the intrinsic vasculature of the nerve roots were determined. The study showed that the average minimum pressure in the inflated balloon required to stop the flow in the arterioles was 127 mm Hg (SD = 18, n = 11), in the capillaries 40 mm Hg (SD = 6, n = 12), and in the venules 30 mm Hg (SD = 10, n = 12). The average mean arterial pressure (MAP) was 150 mm Hg (SD = 14, n = 12). There was a statistically significant correlation (p greater than 0.001) between the MAP and the pressure required to stop the flow in the arterioles (r = 0.83, n = 14), but no correlation between MAP and capillary (r = 0.09 NS, n = 20) or venular (r = -0.28 NS, n = 34) occlusion pressure. After the nerve roots had been compressed at 50 or 200 mm Hg for 10 min or 2 h, the recirculation started immediately. There was a hyperemia during the first 10 min, with a dilatation of the vessels, particularly the venules. In nerve roots exposed to compression for 2 h at either 50 or 200 mm Hg, an intraneural edema developed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Leukocyte effects on microcirculation in artificially perfused rat lungs.

Evidence indicates that leukocyte microvascular flow obstructions play an important role in no-reflow phenomena after ischemia and that leukocytes may cause significant disturbances of capillary perfusion in low flow states. In the present study, a cell-free colloid perfusion (20-60 ml.kg-1.min-1) of isolated ventilated rat lungs was interrupted by bolus injections of leukocytes in varying numbers. Leukocyte effects on flow resistance, tracer gas exchange, and micromorphology were evaluated. The vast majority of the infused leukocytes remained trapped in the lungs after repeated infusions regardless of the number of leukocytes given, although leukocyte trapping decreased at the higher flow rates. The functional and morphological analyses showed that the polymorphonuclear granulocytes had a greater tendency than the mononuclear cells to become permanently trapped in the pulmonary capillaries. The tracer gas analyses indicated that the trapped leukocytes were scattered in the alveolar capillary networks and did not cause complete exclusion of flow from the affected alveoli. This was probably due to the anatomy of the pulmonary microvasculature, with its abundancy in interconnecting pathways.

Animals↗
PubMed1989

Leukocyte deformability--a comparison between different methods for separation of rat leukocytes from whole blood.

The deformability of rat leukocytes isolated by three different methods (Ficoll-Sodium Metrizoate, Ficoll-Hexabrix and Percoll) was studied with micropipette technique. The internal diameter of the micropipette tip was 4.0 microns and a constant aspiration pressure of -15 cm H2O was suddenly applied. The time course of deformation of the cells was analysed with video technique. The rat leukocytes showed the same viscoelastic deformation pattern as has been described earlier for human leukocytes. There was no significant difference in deformability between the three different lymphocyte (LC) fractions or between the two different polymorphonuclear granulocyte (PMN) fractions that were studied. The initial, rapid phase deformation was similar for LCs and PMNs, whereas the PMNs showed a considerably slower second phase deformation. This difference between LCs and PMNs is probably due to the larger size of the PMNs and the larger adhesive shear stresses acting on these cells. It is concluded that the three methods used for separation of rat leukocytes are equivalent in respect to the deformability of the cells produced.

Animals↗
PubMed1988

Arterial occlusion reduces tumour cell lodgement in the rat liver.

The lodgement of tumour cells (TCs) is a key event in the development of metastases in distant organs. Experimental and clinical studies have shown that ligation of the hepatic artery may reduce the mass of established metastases. In the present study the effect of hepatic artery or portal vein occlusion on the early phase of metastasis development, i.e. TC lodgement, was investigated. Occlusion of the hepatic artery immediately before intraportal TC infusion reduced TC lodgement, while a temporary occlusion of the portal vein directly after the TC infusion led to increased TC lodgement. It is speculated that the decrease in TC lodgement after arterial occlusion is due to local increase in blood flow, which might enhance the passage of the TCs through the liver, and to a decrease in pH causing an increased rate of TC destruction. The increased TC lodgement after portal vein occlusion, on the other hand, should mainly be due to flow reduction, promoting TC trapping in the liver microvasculature.

Animals↗
PubMed1987

Leukocytes and the risk of ischemic diseases.

Predictive indexes for atherosclerotic risk are imperfect, suggesting that there are predictive factors not commonly considered. Such a factor may be the white blood cell (WBC) count. Epidemiologic studies have shown correlations between the WBC count and the risk of myocardial infarction and stroke. The risk of acute myocardial infarction is approximately four times as great in persons with WBC counts high in the normal range (greater than 9000/microL [9 X 10(9)/L]) as in persons with WBC counts low in the normal range (less than 6000/microL [6 X 10(9)/L]); only 50% to 65% of the excess risk of the high-count individuals is explainable by tobacco smoking (which covaries with WBC count). A high WBC count also predicts greater risk of reinfarction and of in-hospital death. Less rigorously studied, the constitutional neutropenia of Yemenite Jews appears to afford protection against atherosclerotic disease. Among WBC types, the strongest epidemiologic association has been with the neutrophil count. Such a predictive value of WBC count is plausible and satisfying, because WBCs make a major contribution to the rheologic properties of blood; alter adhesive properties under stress--including the stress of ischemia, enhancing their rheologic importance; and participate in endothelial injury, both acutely and chronically, by adhering to endothelium and damaging it with toxic oxygen compounds and proteolytic enzymes. Techniques newly developed or under development may allow us to refine the predictive value of the WBC count by combining it with measures of cell activation and/or activatability.

Blood Vessels↗
PubMed1987

Haemodynamic and haemorheological effects of hypervolaemic haemodilution in men with primary hypertension.

The haemorheological disturbances observed in primary hypertension arise mainly from haemoconcentration, which leads to an elevation of blood and plasma viscosity and increased aggregation of red blood cells (RBCs). We evaluated the rheological properties of blood and central haemodynamic indices in 13 men with untreated primary hypertension (WHO stage I and II), during a baseline period and after intravenous infusion of 1000 ml of 0.9% NaCl (within 12-15 min). The rheological properties studied were: whole blood viscosity (WBV), plasma viscosity (PV), haematocrit (HCT) and plasma fibrinogen concentration (PF). The central haemodynamic indices were: mean intra-arterial blood pressure (MAP), central venous pressure (CVP), cardiac index (CI), stroke volume index (SVI), total peripheral resistance index (TPRI) and the vascular hindrance index (VHI). Plasma renin activity (PRA) and plasma noradrenaline concentration (P-NA) were also measured. Volume expansion with saline caused haemodilution as expressed by a fall in HCT (P less than 0.001), WBV (P less than 0.001) and PV (P less than 0.01). At the same time, CVP, MAP and VHI increased (P less than 0.05) while PRA decreased (P less than 0.05) and P-NA remained unchanged. Mean values of the cardiac index (CI) and stroke volume index (SVI) did not change significantly. We did not observe any significant relationship between haemodynamic and haemorheological parameters, during baseline or between their respective changes after the infusion. The results indicate that although hypervolaemic haemodilution produced by saline infusion in hypertensive patients may improve blood flow properties (HCT, WBV, PV), blood pressure (BP) is not reduced; rather the converse is true. The reduction in HCT and hence the improved blood rheology, did not affect calculated vascular resistance. Thus, correction of WBV does not acutely normalize BP in primary hypertension.

Adult↗
PubMed1987

Vital microscopic studies on the capillary distribution of leukocytes in the rat cremaster muscle.

Leukocyte capillary distribution was studied with vital fluorescence microscopy in the rat cremaster muscle. Ten terminal arterioles, each in a different animal, with 2 to 7 capillaries and with a total leukocyte flux ranging from 97 to 571 cells, were analysed. Nonparametric statistics was used for the analyses of the experimental data. In order to characterize the pathways for leukocyte flux in the networks, the leukocyte concentration for each capillary was calculated in relation to the network inflow leukocyte concentration and to the bifurcation inflow leukocyte concentration. The study shows a strong positive correlation between the relative capillary leukocyte concentration and the capillary volume flow and the position of the capillary in the network, respectively. There was no correlation between the relative capillary leukocyte concentration and capillary branching angle. A relative leukocyte concentration above unity, indicating an enrichment of leukocytes, was found in capillaries with a high volume flow and in capillaries located at the downstream end of the arterioles. In addition, the analyses show a very strong correlation between capillary volume flow and the position of the capillary along the arteriole, the capillaries located at the downstream end having the highest volume flows. In conclusion, the present study provides evidence for the existence of volume flow dependent preferential pathways for leukocyte passage across the capillary network in the rat cremaster muscle.

Animals↗
PubMed1986

Acute synovitis induced by preformed immune complexes.

The morphology of acute immune complex (IC) elicited synovitis in rabbit knee joints was studied, as well as IC-induced leukocyte activation in vivo and in vitro. Acute synovitis was induced by intra-articular injection of in vitro preformed, complement activating bovine serum albumin (BSA)-anti-BSA IC. Within 30 min, migration of polymorphonuclear granulocytes (PMNGs) was observed. Scanning electron microscopy showed that adhering, apparently activated leukocytes were attached to the synovial lining, often forming clusters. Phagocytosis of IC was evident, as immunoglobulins were detected within the leukocyte cytoplasm by the direct immunofluorescence technique. At the peak accumulation of PMNGs, focal erosions of the synovial lining were observed. Later, monocytes and macrophages appeared and degenerated PMNGs were found, sometimes within the cytoplasm of large macrophages. Chemiluminescence experiments showed a maximum in vitro activation of leukocytes by complement activating IC formed near optimal precipitation proportions and in slight antigen excess, whereas IC in large antigen excess gave a smaller and later response.

Acute Disease↗
PubMed1986

Leukocyte effects on the vascular resistance and glomerular filtration of the isolated rat kidney at normal and low flow states.

Because of their large volume and high internal viscosity, leukocytes may obstruct capillary blood flow, particularly in low flow states. In the present study rat kidneys were isolated and perfused with a cell-free colloid solution. The urine production was continuously measured and samples were taken for determination of inulin clearance. In this way changes in glomerular filtration rate (GFR) and tubular reabsorption (TR) could be followed before, during, and after a bolus injection of leukocytes separated from whole blood. The experiments showed that leukocyte infusion caused a sustained increase of the renal vascular resistance, which at low flows ranged from 5 to 20%, whereas at normal flow rates only small and transient increases occurred. The passage of a leukocyte bolus caused, in addition, a decrease in GFR and to a small degree also in TR. The study indicates that leukocytes may disturb the perfusion of glomeruli and peritubular vessels in low flow states.

Animals↗
PubMed1985

Involvement of platelet-released 5-HT in tumor cell lodgement.

Adherence of circulating tumor cells in the microvasculature (lodgement) is a key event in metastasis formation, once cells released from a primary neoplasm have reached the bloodstream. Platelets appear to be involved in tumor cell lodgement, since thrombocytopenia significantly reduces the number of lodged tumor cells. Platelets activated by tumor cells are known to release 5-HT, and therefore the present study was focused on the influence of this amine on hepatic lodgement of intraportally injected fibrosarcoma cells in rats. Lodgement was quantified by labeling of tumor cells with [5-125I]iodo-2-deoxy-uridine. 5-HT levels were simultaneously determined using liquid chromatography with electrochemical detection (LCED) from hepatic areas with lodged tumor cells, as seen in vital microscopy. Injection of tumor cells increased hepatic 5-HT levels twofold (614 +/- 64 micrograms/g) compared with the levels found in rapidly killed (284 +/- 22 micrograms/g) or saline-injected animals (231 +/- 75 micrograms/g). In thrombocytopenia lodgement was reduced by 47% and hepatic 5-HT levels by 52% in comparison with tumor cell-injected controls. Peripheral blockade of 5-HT2 receptors with ketanserin (0.6 mg/kg sc) also reduced lodgement by 28% and hepatic 5-HT levels by 36%, strongly indicating involvement of platelet-released 5-HT in the lodgement process. Immunocytochemical studies of hepatic tissue in untreated rats demonstrated presence of 5-HT only in mast cells, while as early as 15 min after tumor cell injection 5-HT immunopositive nerves were also seen. This implies an active uptake of circulating 5-HT by neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The effect of different cooling temperatures and immersion fluids on post-burn oedema and survival of the partially scalded hairy mouse ear.

One ear of NMRI hairy mice was first scalded and then immediately immersed in cold water or saline at 8 degrees C, 15 degrees C, 20 degrees C, 25 degrees C or 30 degrees C for a period of 30 min in order to study oedema formation and the therapeutic effect at 4 days. Oedema was determined by wet-dry weight measurements of punch biopsies from the ear and expressed as an increase in tissue water content. The therapeutic effects at 4 days were determined by observing the survival of the ear; the area of necrosis was expressed in per cent of the total area of the ear. Significant oedema was found in all scalded ears. A partial (15 per cent) dry necrosis of the untreated burned ear had developed within 4 days. Cooling in 8 degrees C water or saline for 30 min post-burn significantly reduced oedema in this model as determined 2h post-burn. However, 4 days post-burn all cooled ears showed a 15 per cent necrosis.

Animals↗