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E Buchweitz-Milton

Publications and source records attributed to E Buchweitz-Milton.

8 recordsLinked to original sources

Effect of salbutamol on regional cerebral oxygen consumption, flow and capillary and arteriolar perfusion.

This study quantitatively determined the effect of salbutamol (1 microgram kg-1), a beta 2-adrenoceptor agonist, on the perfusion of the brain microvasculature, cerebral O2 consumption, O2 extraction and cerebral blood flow (CBF) in conscious rat. Indices of arteriolar and capillary structure and the percentage of the total cerebral microvascular volume/mm3 (% Vv) and number/mm2 (% Na) perfused were determined. These parameters were obtained from the perfused microvessels, identified by the presence of fluorescein isothiocyanate (FITC) - dextran, and compared with the entire microvascular bed, identified by alkaline phosphatase stain. Cerebral O2 extraction was determined microspectrophotometrically and CBF was determined using 14[C]iodoantipyrine in another group of salbutamol-treated rats. The acute administration of salbutamol did not alter systemic arterial blood pressure. Significant tachycardia was noted in the salbutamol-treated rats. Salbutamol resulted in a significant increase in the percentage of arterioles perfused. Average percentage perfused capillary Na increased significantly from 46 +/- 2 to 88 +/- 1%; %Vv increased significantly and similarly in the arteriolar and capillary beds in all brain regions examined. Average cerebral O2 consumption increased significantly from 3.0 +/- 0.2 to 7.4 +/- 0.7 ml O2 min-1 100 g-1 with salbutamol, while cerebral O2 extraction was unchanged. Average CBF increased from 50 +/- 2 to 142 +/- 9 ml min-1 100 g-1 with salbutamol. Salbutamol may increase the perfusion of the regional microvasculature by increasing cerebral O2 consumption (metabolic vasodilation) and CBF and microvascular perfusion secondarily, although a direct effect of salbutamol on cerebral microvessels cannot be ruled out.

Albuterol↗

Role of alpha-adrenoceptors in the control of the cerebral blood flow response to hypoxia.

This study assessed the role of vascular and central alpha-adrenoceptors in the regional cerebral blood flow response to moderate hypoxia. Studies were conducted in 21 rabbits using radioactive microspheres under normoxic and hypoxic (10% O2 in N2) conditions. Animals were divided into three groups and administered either saline, N-methyl chlorpromazine, or phenoxybenzamine. During normoxia, there were regional differences in cerebral blood flow distribution in the saline- and N-methyl chlorpromazine-treated rabbits which were eliminated by phenoxybenzamine. In control, hypoxia significantly increased average cerebral blood flow from 57 +/- 22 to 132 +/- 52 ml/min per 100 g. Flow to the hindbrain increased to a significantly greater extent than to the mid- or forebrain during hypoxia. The increase in average cerebral blood flow during hypoxia was significantly reduced to 97 +/- 34 ml/min per 100 g by phenoxybenzamine. Both alpha-adrenoceptor antagonists prevented the significantly greater increase in hindbrain flow during hypoxia. The greater flow responsiveness of the hindbrain to hypoxia appears to be related at least in part to alpha-adrenoceptors found in the cerebral vasculature.

Animals↗

Perfused microvascular morphometry during middle cerebral artery occlusion.

This study compared the arteriolar and capillary bed perfusion in the ischemic vs. contralateral cortex 1 h after middle cerebral artery (MCA) ligation in anesthetized rat. Fluorescein isothiocyanate (FITC)-dextran identified the perfused vascular beds. Regional cerebral blood flow (CBF) was monitored with [14C]iodoantipyrine. Morphometric parameters were determined through comparisons of the perfused FITC-labeled vessels with alkaline phosphatase-stained preparations of the total microvascular network. Regional CBF was significantly different when the contralateral cortex (54 +/- 7 ml.min-1.100 g-1) (means +/- SE) and the MCA-occluded cortex (31 +/- 8 ml.min-1.100 g-1) were compared. There were no significant regional differences in any morphometric index of structure in the total microvascular bed. The percentage of the total capillary and arteriolar volume that was perfused in the MCA-ligated cortex was significantly lower than the value obtained from the contralateral cortex. The change in the perfusion pattern of the cerebral microvasculature in the ischemic cortex was not due to vessel blockade. The altered temporal perfusion pattern of capillary and arteriolar vessels in the occluded cortex may be due to an altered microvascular perfusion cycle, longer perfusion pathways, vasoconstriction, or partial vessel obstruction.

Animals↗

Effect of prazosin on microvascular perfusion during middle cerebral artery ligation in the rat.

The purpose of this study was to evaluate the effects of prazosin, an alpha 1-adrenoceptor antagonist, on morphometric indexes of the total and perfused cerebral microvascular bed 1 hour after middle cerebral artery (MCA) ligation in pentobarbital-anesthetized rats. We hypothesized that this agent would prevent catecholamine-induced vasoconstriction in the ischemic brain. Cerebral blood flow (CBF) was determined with 14C-iodoantipyrine, and the perfused microvascular bed was visualized using fluorescein isothiocyanate-dextran. MCA occlusion did not alter systemic hemodynamic or blood gas parameters. CBF averaged 29 +/- 15 (mean +/- SD) ml/min/100 g in the MCA-ligated cortex and 49 +/- 18 in the other examined brain regions. Prazosin did not significantly alter these CBF values, averaging 26 +/- 14 and 48 +/- 10, respectively. There were no significant regional differences in total capillaries/mm2 in either group. The percent of the capillaries/mm2 perfused (51 +/- 6%) was similar in the two groups in all examined regions except the ischemic cortex. In the MCA-ligated cortex, 22 +/- 8% of the capillary volume was perfused in comparison with 49 +/- 8% in the prazosin-treated group. Prazosin-treated rats had an increased percentage of their microvasculature perfused despite a similarly reduced CBF. Prazosin appeared to reduce diffusion distances in the ischemic cortex. This might be due to its alpha 1-adrenoceptor blocking activity.

Animals↗

Effect of MCA occlusion on brain O2 supply and consumption determined microspectrophotometrically.

This study compared oxygen extraction, oxygen consumption, and cerebral blood flow (CBF) in the ischemic and contralateral cortex of middle cerebral artery (MCA)-occluded feline brain using a microspectrophotometric technique. This technique was further validated in several experiments. A transorbital approach exposed the right MCA. After preocclusion blood pressure, heart rate, and blood gas values were determined, radioactively labeled microspheres (15 +/- 3 microns diam) were injected intra-atrially. The right MCA was then occluded. These same measurements were taken 1 h later. Arterial and venous oxygen saturations were determined in the center and surrounding area of the occluded ischemic cortex and other brain regions. Regional cerebral oxygen consumption was determined as the product of CBF and oxygen extraction. CBF decreased significantly from 54.0 +/- 5.0 to 26.6 +/- 4.8 (mean +/- SE) ml X min-1 X 100 g-1 in the center of the ischemic cortex and from 49.6 +/- 7.0 to 30.6 +/- 5.0 ml X min-1 X 100 g-1 in the surrounding ischemic cortex. Oxygen extraction was significantly increased from 3.7 +/- 0.4 ml O2/100 ml blood to 4.6 +/- 0.6 ml O2/100 ml blood in the center of the occluded cortex but was not significantly altered in the surrounding moderately ischemic cortex. Oxygen consumption was not significantly altered in either ischemic cortical region when compared with the contralateral cortices. Unilateral MCA occlusion caused a decreased regional CBF associated with increased brain oxygen extraction in the cortical region directly supplied by the MCA. The feline brain appears to maintain oxygen consumption in the occluded cortex by increasing oxygen extraction.

Animals↗

Perfused capillary morphometry in the senescent brain.

This study compared quantitative indices of capillary morphometry in the perfused vs. total capillary bed of conscious young (8-10 month old) and senescent (28-33 month old) rat brains. The total capillary bed was identified through alkaline phosphatase staining of tissue sections cut from specific brain regions. The perfused capillary bed was identified by the presence of fluorescein isothiocyanate (FITC) dextran in the microvessels. Average capillary volume fraction, VV (mm3/mm3, mean +/- S.E.M.) was 0.040 +/- 0.002 and 0.033 +/- 0.001 in the total capillary bed of the young and old animals, respectively. These values were not statistically different. Perfused VV averaged 0.020 +/- 0.001 and 0.017 +/- 0.001 mm3/mm3 in the young and old animals, respectively. Average perfused VV was 50% in the young and 49% in the senescent rat brains. Young and senescent brains utilize similar proportions of their "capillary reserves." In the areas examined in the brains of young animals, differences were found in the percentage of capillary volume/mm3, VV, and surface area/mm3, SV, perfused which were not present in old animals. The structural and neurochemical changes noted by others in the brain during aging were not related to alterations in indices of average and regional total or perfused cerebral capillary bed morphometry. However, differences in percent perfused VV, SV, length, LV, and number, Na, present in the younger rat brains were not present in the senescent rat brains.

Aging↗

Effect of AF64A on cerebral oxygen consumption in young and old rats.

Regional brain O2 consumption was determined in conscious Fischer-344 rats 3- and 33-months of age after intrahippocampal injection of the selective presynaptic cholinergic neurotoxin AF64A to investigate the influence of acetylcholine on this parameter. Regional cerebral blood flow (rCBF) was determined with 14[C]-iodoantipyrine. Regional arterial and venous oxygen saturation was measured microspectrophotometrically. Regional cerebral oxygen consumption was calculated by multiplying rCBF and cerebral oxygen extraction. Systemic hemodynamic and blood gas parameters were not altered by aging or AF64A. Aging or sham injection per se did not have any significant effect on rCBF, oxygen extraction and cerebral oxygen consumption. In 3-month-old AF64A-treated rats, rCBF, oxygen extraction or cerebral oxygen consumption were significantly lower than in the control group of the same age. Old AF64A-treated animals demonstrated a significant decrease in rCBF and cerebral oxygen consumption but not in cerebral oxygen extraction when compared to the sham-lesioned group of the same age. Oxygen consumption was significantly decreased by AF64A in each examined region of both young and old groups of rats, although the decreases were less severe in the older rats. This may be related to the lesser influence of the cholinergic system on cerebral oxygen consumption in old animals or a decreased toxicity of AF64A in older animals.

Aging↗

Cerebral oxygen consumption and blood flow in Fischer-344 rats of different ages.

Regional cerebral oxygen consumption and blood flow were determined and compared in conscious male Fischer-344 rats at 3, 12, 24 and 33 months of age to correlate the reported regional neurochemical and morphological changes which occur in these parameters during development, maturation, aging and senescence. Cerebral blood flow was determined with 14[C]-labelled iodoantipyrine and regional cerebral arterial and venous oxygen saturation was measured microspectrophotometrically. Oxygen consumption was obtained by multiplying cerebral blood flow and oxygen extraction. Systolic and diastolic blood pressure and heart rate decreased significantly with age. Average cerebral blood flow, oxygen extraction and oxygen consumption/100 g did not differ significantly between the four age groups examined. Oxygen consumption averaged 2.9 +/- 0.1 ml O2/min/100 g (mean +/- S.E.M.) in the 3-month-old group and 3.6 +/- 0.1 ml O2/min/100 g in the 33-month-old group. Differences in flow among the examined brain regions, which were present in the mature, 12-month-old brain, were not present in the developing, aging or senescent rat brain. Compensatory alterations in the efficiency or organization of neurochemical activity which occur during development, aging and senescence may modify the inter-regional differences in cerebral blood flow and oxygen consumption noted during maturation. There was no correlation found between the neurochemical and morphological changes which have been reported during maturation, aging or senescence and regional cerebral oxygen consumption.

Aging↗