Pentoxifylline: cerebral blood flow and glucose utilization in conscious spontaneously hypertensive rats.

Johansson, Barbro

doi:10.1161/01.str.17.4.744

Cited by 17 publications

(6 citation statements)

References 25 publications

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“…Johansson 18 reported glucose utilization rates in 22-week-old SHR that resemble our results for 26-30-week-old SHR. Relative to the data in Table 2, the values of LCGU for 22-week-old SHR reported by Johansson were slightly but not significantly greater for the inferior colliculus, approximately equal for the hippocampus, and slightly but not significantly less in 11 other areas (uncorrected t tests).…”

Section: Comparisons Of Local Cerebral Glucose Utilization Findings Isupporting

confidence: 87%

Cerebral glucose utilization and blood flow in adult spontaneously hypertensive rats.

et al. 1992

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Not only blood pressure but also behavioral activity, brain morphology, and cerebral ventricular size differ between young spontaneously hypertensive rats (SHR) and nonnotensive Wistar-Kyoto (WKY) rats. This suggests that cerebral blood flow and cerebral metabolism may vary between these two rat strains. To test this hypothesis, we measured local cerebral glucose utilization in 31 brain areas of 26-30 -week-old rats. Local cerebral blood flow was also assessed in these same areas. Cerebral glucose utilization was measured by the 2-deoxyglucose method; cerebral blood flow was determined by the iodoantipyrene method. In virtually all gray matter structures, the apparent rate of glucose utilization was lower in SHR than in nonnotensive WKY rats; the interstrain differences varied significantly among structures and were statistically significant (uncorrected t tests) in 14 of 28 gray matter areas. Local cerebral blood flow was fairly similar in the two rat strains. The coupling of blood flow to glucose utilization varied significantly among brain areas in nonnotensive WKY rats as well as in SHR. In a number of gray matter structures, the coupling of flow to metabolism differed between hypertensive and nonnotensive animals. These data suggest that for many brain areas, either glucose utilization or glucose partitioning differs between WKY rats and SHR. A number of years ago, Sokoloff and coworkers 2 developed the carbon-14-labeled 2-deoxyglucose (2DG) method of measuring glucose metabolism and, by use of quantitative autoradiography, assessed local cerebral glucose utilization (LCGU) in more than 30 areas of the rat brain. Subsequently, the 2DG technique has been used extensively to measure changes and differences in brain metabolism in a variety of studies and has provided considerable information on local alterations in cerebral activity. Using the 2DG technique, Kadekaro et al 3 determined that LCGU was very similar in 41 of 44 brain areas of 11-12-week-old spontaneously hypertensive rats (SHR) and their normotensive, genetically related control, the Wistar-Kyoto (WKY) rat. This suggested that metabolism is relatively normal in the brain of juvenile SHR. Differences in mean arterial blood pres- sure (MABP) and behavior 4 -3 as well as in brain weight and structure and ventricular size 6 -9 between SHR and WKY rats, however, have been reported at this and other stages of development.In view of these physiological, behavioral, and morphological observations, we have postulated that cerebral glucose utilization is altered in adult SHR and have tested this hypothesis by measuring LCGU in 26-30-week-old SHR and WKY rats by the 2DG technique of Sokoloff et al. 2 In addition, because of the purported coupling between LCGU and local cerebral blood flow (LCBF) and of the possible change in this coupling in chronically hypertensive animals, LCBF was determined in age-matched SHR and WKY rats by the radiolabeled iodoantipyrine (IAP) technique of Sakurada et al. 10 In both the LCGU and the LCBF experiments, quantitative autor...

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Section: Comparisons Of Local Cerebral Glucose Utilization Findings Isupporting

confidence: 87%

Cerebral glucose utilization and blood flow in adult spontaneously hypertensive rats.

et al. 1992

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“…The other study of intravenous oxpentifylline to report an increase in CBF used a similar method of measuring CBF to the current study, but the trial was uncontrolled and oxpentifylline was given with other medication, leading to uncertainty about the conclusions (Gabaschwili et al, 1979). In contrast to previous human studies, the results of the current study are more consistent with two carefully controlled animal studies which showed that acute administration of oxpentifylline did not alter CBF in the anaesthetised dog (Steen et al, 1981) and reduced CBF in hypertensive rats (Johansson, 1986).…”

Section: Discussionsupporting

confidence: 71%

Effect of oxpentifylline on blood viscosity and cerebral blood flow in man.

Brown

1989

Brit J Clinical Pharma

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The effects of intravenous oxpentifylline on blood viscosity and cerebral blood flow were studied in eight patients with cerebrovascular disease using a double‐blind placebo controlled design. A single dose of 200 mg oxpentifylline in 10 ml saline was given by intravenous injection over 10 min and compared with 10 ml saline alone. Whole blood and plasma viscosity were measured in a Contraves LS 30 coaxial viscometer at shear rates of 0.7 and 94.5 s‐1. Cerebral blood flow was measured by the non‐invasive intravenous xenon133 clearance method. The measurements were made before and then 30 min after the start of the injection of drug or saline alone. Oxpentifylline was found to have no significant effect on blood viscosity or cerebral blood flow.

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“…in the pathogenesis of focal cerebral ischemia is unknown. The lack of a beneficial hemodynamic effect of PTX on experimental cerebral ischemia 38 - 39 and the recent observation of the lack of efficacy of hemodilution in acute ischemic stroke in community hospitals 40 raise questions about the therapeutic potential of hemorheologic modification in ischemic stroke. Additional experimental and clinical studies are needed to define further the potential efficacy of hemorheologic therapeutics in acute cerebral ischemia.…”

Section: Discussionmentioning

confidence: 99%

Pentoxifylline in acute nonhemorrhagic stroke. A randomized, placebo-controlled double-blind trial.

Hsu

Norris

Hogan

et al. 1988

Stroke

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The efficacy and safety of pentoxifylline were assessed in 297 adult patients with ischemic stroke in a molticenter, doable-blind, randomized and placebo-controlled trial. Treatment was started within 12 hoars after the stroke onset Study medication was administered intravenously continuously (16 mg/kg/day, maximum 1,200 mg/day) for 3 days and per os (400 mg ti.d.) for the remainder of 28 days. Demographic data were comparable, and functional impairment and mortality (pentoxifylline 12%, placebo 10%) were not different between the two groups. Neurologic deficit scores Improved from baseline admission scores during the 4-week study in both groups but did not differ between groups at admission or throughout the study except during the first few days when the consciousness level (Days 1 and 2), motor function (Days 1 and 2), cranial nerve function (Days 1-4), and total neurologic deficit scores (Days 1 and 2) were better in the pentoxifylline group than in the placebo group, especially in a subset of patients with severe deficits at admission. Laboratory values and side effects were also comparable between groups. Our study indicates that pentoxifylline can be given safely in patients with acute ischemic stroke. Although pharmacologk effects were present during the first few days, the clinical benefits were small and not sustained.

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Pentoxifylline: cerebral blood flow and glucose utilization in conscious spontaneously hypertensive rats.

Cited by 17 publications

References 25 publications

Cerebral glucose utilization and blood flow in adult spontaneously hypertensive rats.

Cerebral glucose utilization and blood flow in adult spontaneously hypertensive rats.

Effect of oxpentifylline on blood viscosity and cerebral blood flow in man.

Pentoxifylline in acute nonhemorrhagic stroke. A randomized, placebo-controlled double-blind trial.

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