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Biomedical subjects

F S Larsen

Publications and source records attributed to F S Larsen.

At least 73 records · Page 4Linked to original sources
PubMed1995

Cerebral blood flow autoregulation and transcranial Doppler sonography in patients with cirrhosis.

Impairment of cerebral blood flow (CBF) autoregulation may have serious implications for patients with cirrhosis if arterial hypotension occurs during coma, anesthesia, bleeding, or sepsis. In this study, CBF autoregulation was investigated in patients with cirrhosis with no or mild encephalopathy. Ten patients (median age, 45 years; range, 30 to 61 years) and six healthy volunteers (median age, 30 years; range 21 to 61 years) were included. Catheters were placed in a radial artery and in the internal jugular veins. Baseline CBF was measured using single-photon emission computed tomography (SPECT) with concomitant measurements of cerebral arteriovenous oxygen content differences (AVDO2). CBF autoregulation was evaluated using the AVDO2 method and changes in mean flow velocity in the middle cerebral artery (Vmean) as determined by transcranial Doppler (TCD). Mean arterial pressure (MAP) was increased by 30 mm Hg by intravenous norepinephrine, and subsequently decreased by a combination of lower body negative pressure and ganglion blockade, whereas AVDO2 and Vmean were measured at each 5 mm Hg change in MAP. CBF was 61 (range, 45 to 78) mL 100 g-1 min-1 in patients with cirrhosis and 65 (range < 53 to 88) mL 100 g-1 min-1 in volunteers (not significant [NS]). There were no regional differences in CBF between the two groups. Arterial carbon dioxide tension was 31 (23 to 35) mm Hg in patients with cirrhosis and lower, compared with 36 (range, 34 to 47) mm Hg in the volunteers (P < .01). For evaluation of autoregulation, MAP was raised to 116 (range, 100 to 145) and then decreased to 39 (range, 34 to 50) mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Systemic vascular resistance during high-volume plasmapheresis in patients with fulminant hepatic failure: relationship with oxygen consumption.

BACKGROUND: In patients with fulminant hepatic failure, systemic vascular resistance and blood pressure are often reduced. OBJECTIVE: To determine whether systemic vascular resistance increases during high-volume plasmapheresis, which is assumed to eliminate endogenous vasodilatory substances from the bloodstream. DESIGN: A prospective study. PATIENTS AND METHODS: Ten patients [median age 48 (range 21-53) years] were admitted for liver transplantation. Systemic haemodynamic variables were determined using a catheter in a radial artery and a thermodilution catheter placed in a pulmonary artery. Ten (range 8-15) litres of fresh frozen plasma were exchanged, while body temperature [37.6 (range 36.6-38.4) degrees C], blood partial pressure of carbon dioxide [3.75 (range 3.30-4.50) kPa] and peak inspiratory ventilatory pressure [24 (range 20-26) mmHg] were kept constant. RESULTS: Mean arterial pressure increased from 74 (range 61-110) to 96 (range 68-103) mmHg and cardiac index decreased from 5.2 (range 3.6-7.5) to 4.2 (range 3.4-6.6) l/min/m2. The systemic vascular resistance index increased from 662 (range 430-1270) to 1060 (range 621-1520) dyn s/cm5/m2. In contrast, the pulmonary vascular resistance index [42 (range 20-110) dyn s/cm5/m2) remained constant. As cardiac index decreased, oxygen delivery decreased from 939 (range 680-1496) to 745 (range 601-1189) ml/min/m2 with no effect on oxygen consumption [171 (87-231) ml/min/m2], as the arteriovenous oxygen extraction ratio increased from 17 (range 9-22) to 25 (range 8-31)% (P < 0.02). CONCLUSION: In patients with fulminant hepatic failure, cardiac output, systemic vascular resistance and arterial blood pressure improved during high-volume plasmapheresis.

Acute Disease↗
PubMed1994

ELISA for the core protein of the cartilage large aggregating proteoglycan, aggrecan: comparison with the concentrations of immunogenic keratan sulphate in synovial fluid, serum and urine.

Immunological assays for fragments of the cartilage large aggregating proteoglycan, aggrecan, have been widely used to monitor cartilage turnover. These assays have commonly employed the monoclonal keratan sulphate antibody, 5D4. Keratan sulphate, however, is present in many tissues and 5D4 affinity is critically dependent on antigen structure. We have therefore raised and characterized a monoclonal antibody (1-F21) that reacts with the core protein of aggrecan without interference from the glycosaminoglycan side chains and, using this antibody, we have optimized a sensitive, competitive ELISA. The within-assay and between-assay coefficients of variation were 4.9-8.9% and 11.1-13.0%, respectively. The mean concentrations of core protein in synovial fluid, serum and urine were 76.4 micrograms/ml, 104.0 ng/ml and 81.0 ng/ml, respectively. In synovial fluids the concentrations were closely correlated with the concentrations of keratan sulphate as determined by 5D4 (r = 0.94), whereas in serum and urine there was no obvious correlation between the determinations. These findings show that measurement of both core protein and keratan sulphate results in a more precise description of aggrecan turnover.

Aggrecans↗
PubMed1994

Cerebral blood flow autoregulation is absent in rats with thioacetamide-induced hepatic failure.

Cerebral blood flow normally remains constant within a wide range of mean arterial blood pressure values. In fulminant hepatic failure, however, it is not known whether autoregulation of cerebral blood flow is maintained. In the present study, cerebral blood flow autoregulation was investigated in rats 3 days after induction of fulminant hepatic failure. Wistar rats were given intraperitoneal thioacetamide or saline injections. The mean arterial blood pressure was varied by means of norepinephrine infusion or venesection, respectively. As mean arterial blood pressure declined, repeated cerebral blood flow measurements were performed by the intracarotid 113Xenon injection method. The relation between mean arterial blood pressure and cerebral blood flow was examined by statistical regression analysis, and the lower limit of autoregulation was determined in each rat. Cerebral blood flow baseline values were unaltered in liver failure compared to the control group (73 (36-92) vs. 79 (57-87) ml.100 g-1.min-1, median and range). Baseline mean arterial blood pressure was also similar in the two groups (90 (75-113) vs. 95 (70-112)). Mean arterial blood pressure varied between 40 (35-50) and 110 (90-135) mmHg in the control rats and between 50 (45-68) and 110 (95-126) mmHg in the rats with liver failure. A lower limit of autoregulation was identified in all control rats at a mean arterial blood pressure of 67 (55-78) mmHg. Below this limit, cerebral blood flow declined in parallel with mean arterial blood pressure. None of the rats with liver failure exhibited autoregulation, and cerebral blood flow changed in parallel with mean arterial blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Comparative effects of IGF-I and insulin on the glucose transporter system in rat muscle.

The acute effect of insulin-like growth factor I (IGF-I) and insulin on glucose uptake and the glucose transport system in in vitro incubated rat soleus muscles was examined using 3-O-methylglucose and the ATB-[3H]BMPA exofacial photolabeling technique. IGF-I and insulin both stimulated 3-O-methylglucose uptake and GLUT-4 translocation in a dose-dependent manner with a maximal effect six- to sevenfold above basal. No additive effects of IGF-I and insulin on maximal 3-O-methylglucose uptake were found. On a molar basis, IGF-I was 13 times less potent than insulin. Receptor binding experiments showed that IGF-I exhibited a much lower affinity for the insulin receptor [half-maximal effective dose (ED50) = 28.5 nM] than that of insulin (ED50 = 0.20 nM). In contrast, IGF-I bound to the partially purified IGF-I receptor with an apparent affinity (ED50 = 3.7 nM) that was similar to the concentrations of IGF-I which caused half-maximal activation of 3-O-methylglucose uptake (ED50 = 2.4 nM) and GLUT-4 translocation (ED50 = 2.5 nM). Our findings suggest that IGF-I exerts its insulin-like effects on glucose uptake primarily through its own specific receptor and that the molecular events underlying IGF-I and insulin actions on glucose uptake in skeletal muscle are similar, namely caused by a translocation of the GLUT-4 transporter from an intracellular pool to the cell surface.

3-O-Methylglucose↗
PubMed1994

Transcranial Doppler is valid for determination of the lower limit of cerebral blood flow autoregulation.

BACKGROUND AND PURPOSE: This study validates transcranial Doppler sonography (TCD) for determination of the lower limit of cerebral blood flow (CBF) autoregulation and establishes a relation between global CBF and mean flow velocity (Vmean) in the middle cerebral artery. METHODS: Relative changes in CBF and in Vmean were compared in 12 normal volunteers (2 women and 10 men; median age, 30 years [range, 21 to 61 years]). Catheters was placed in the left radial artery and in the bulb of the right internal jugular vein, respectively. Baseline CBF was measured by single-photon emission computed tomography scanning; concomitantly, blood samples were drawn for calculation of the cerebral arteriovenous oxygen difference. Then changes in mean arterial pressure (MAP) were induced, and relative changes in global CBF were calculated according to Fick's principle assuming a constant cerebral oxygen metabolism. MAP was increased 30 mm Hg by norepinephrine infusion and was decreased by lower body negative pressure. Vmean was measured in the right middle cerebral artery by a 2-MHz probe, and blood samples were drawn at intervals of 5 mm Hg. RESULTS: MAP values between 122 (range, 110 to 140) and 48 (range, 34 to 75) mm Hg were measured. The lower limit of autoregulation (the blood pressure under which autoregulation is off) as determined by Vmean did not differ significantly from that determined by relative changes in global CBF: 91 (range, 41 to 108) and 79 (range, 53 to 113) mm Hg, respectively. A significant correlation between Vmean and relative changes in global CBF was demonstrated below the lower limit of autoregulation (R2 = .73, P < .001; CBF = -6.3 + 1.0.Vmean). Above the lower limit both values were stable. CONCLUSIONS: TCD is valid for determination of the lower limit of CBF autoregulation, and changes in CBF may be reliably evaluated by TCD during changes in cerebral perfusion pressure in normal subjects.

Adult↗
PubMed1994

Cerebral blood flow velocity during high volume plasmapheresis in fulminant hepatic failure.

High volume plasmapheresis has previously been found to improve neurological statuses in patients with fulminant hepatic failure. We investigated the relationship between the neurological status and cerebral blood flow velocity (Vmean) during high volume plasmapheresis in 18 consecutive patients (ten females and eight males) with fulminant hepatic failure, with a mean age of 43 (range 9 to 57) years. The mean arterial pressure (MAP) and intracranial pressure (ICP) were also recorded. A total of 16% of body weight was exchanged with fresh frozen plasma per day. Thirty-six plasma exchanges wer performed with a median of 2 (range 1 to 8) per patient. Eleven of the patients survived (61%), nine after liver transplantation. Following the first high volume plasmapheresis, the coma score improved from 6 (1-8) to 2 (0-8) (p < 0.05), Vmean increased from 40 (14-152) to 62 (16-186) cm s-1 (p < 0.05), and MAP from 72 (35-118) to 94 (47-138) mmHg (p < 0.05). The intracranial pressure (ICP) was monitored and remained unchanged in nine patients whereas the cerebral perfusion pressure (MAP minus ICP) increased in the surviving group from 55 (40-74) to 80 (50-91) mmHg (p = 0.07) in contrast to no changes in the non survival group. In conclusion this study suggests that the neurological status, may improve during high volume plasmapheresis as MAP and Vmean increase the cerebral oxygen delivery.

Adolescent↗
PubMed1993

[Fulminant hepatic failure].

Fulminant hepatic failure is a rare disorder with a high lethality. It is characterized by the development of acute hepatic symptoms and encephalopathy, in the absence of underlying chronic liver disease. The main causes are viruses, adverse drug effects and toxins. The major causes of death in patients with fulminant hepatic failure are cerebral edema, infections, gastrointestinal hemorrhage and renal failure, or a combination of these. Treatment of fulminant hepatic failure with a variety of medical therapies has hitherto been found to have little overall influence on outcome. With high volume plasmapheresis the clinical condition of the patients improves, and if there is no sign of spontaneous regeneration, emergency liver transplantation is the only solution.

Hepatic Encephalopathy↗
PubMed1993

Glycogen synthase and phosphofructokinase protein and mRNA levels in skeletal muscle from insulin-resistant patients with non-insulin-dependent diabetes mellitus.

In patients with non-insulin-dependent diabetes mellitus (NIDDM) and matched control subjects we examined the interrelationships between in vivo nonoxidative glucose metabolism and glucose oxidation and the muscle activities, as well as the immunoreactive protein and mRNA levels of the rate-limiting enzymes in glycogen synthesis and glycolysis, glycogen synthase (GS) and phosphofructokinase (PFK), respectively. Analysis of biopsies of quadriceps muscle from 19 NIDDM patients and 19 control subjects showed in the basal state a 30% decrease (P < 0.005) in total GS activity and a 38% decrease (P < 0.001) in GS mRNA/microgram DNA in NIDDM patients, whereas the GS protein level was normal. The enzymatic activity and protein and mRNA levels of PFK were all normal in diabetic patients. In subgroups of NIDDM patients and control subjects an insulin-glucose clamp in combination with indirect calorimetry was performed. The rate of insulin-stimulated nonoxidative glucose metabolism was decreased by 47% (P < 0.005) in NIDDM patients, whereas the glucose oxidation rate was normal. The PFK activity, protein level, and mRNA/microgram DNA remained unchanged. The relative activation of GS by glucose-6-phosphate was 33% lower (P < 0.02), whereas GS mRNA/micrograms DNA was 37% lower (P < 0.05) in the diabetic patients after 4 h of hyperinsulinemia. Total GS immunoreactive mass remained normal. In conclusion, qualitative but not quantitative posttranslational abnormalities of the GS protein in muscle determine the reduced insulin-stimulated nonoxidative glucose metabolism in NIDDM.

Adult↗
PubMed1989

Cost-benefit analyses of California family practice residencies.

Several national commissions have recommended that family practice residency training be subsidized, but without stating how much support is needed. Financial studies of graduate medical education have used the methods of cost allocation or joint-products cost analysis. Previous cost-allocation studies indicate that one third of family practice residency costs are met by extramural subsidy. Cost reports of eight California public hospitals with a single family practice residency program were evaluated for the 1984-85 fiscal year. Discrepancies in the education costs reported to Medicare and those reported in state hospital disclosure reports demonstrate the arbitrary nature of the cost-allocation method. The Medicare medical education reimbursement was an average of $20,444 per resident. State and federal grants provided an average of $5,190 per resident. The Medicare payments and grants met an average of 35.7% of the education costs reported to Medicare. A joint-products cost analysis was used to estimate the pure cost of education in an 18-resident family practice residency. Replacing the residency with salaried physicians would have decreased the hospital's net return by $143,534. If neither grants nor Medicare education payments had been received, elimination of the program would have increased hospital net return by $428,083.

California↗
PubMed1987

Seasonal allergic rhinitis treated with a beta-2-adrenostimulant.

The aim of the study was to investigate whether topical application of a beta-2-adrenostimulant (fenoterol) on the mucous membrane has a clinically significant anti-allergic effect. Thirty-three patients with grass pollen hay fever completed the trial which was a double-blind, placebo-controlled cross-over design. After a run-in period the patients received two puffs of 50 micrograms fenoterol 4 times a day or placebo for 21/2 weeks before cross-over. Symptoms were scored on diary cards and there was a moderate, but significant effect of fenoterol on sneezing, but the effect on secretion and blockage was insignificant. It is concluded that beta-2-stimulating agents are not competitors to the very effective topical steroids.

Administration, Topical↗