Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of infusion of arginine vasopressin (20 mU.kg-1.min-1) on coronary blood flow and the proportion of the coronary microvasculature perfused was studied in rabbit myocardium. Fluorescein isothiocyanate--dextran was injected into anesthetized open-chest rabbits to identify the perfused vessels and an alkaline phosphatase stain was employed to locate the total microvasculature. Coronary blood flow (radioactive microspheres) was studied in separate groups of rabbits. Vasopressin infusion caused bradycardia (243 +/- 19 to 165 +/- 22 beats/min, mean +/- SD) and an increase in mean blood pressure (92 +/- 18 to 104 +/- 12 mmHg) (1 mmHg = 133.32 Pa). Coronary blood flow decreased significantly with vasopressin from 209 +/- 68 to 97 +/- 36 mL.min-1.100 g-1. The proportion of the arteriolar bed per millimeter squared perfused decreased significantly after vasopressin from 54 +/- 13 to 44 +/- 21%, while the percentage of capillaries per millimeter squared increased significantly from 57 +/- 6 to 67 +/- 11%. There were no subepicardial versus subendocardial differences in any measured parameter. Thus, both coronary blood flow and the proportion of the arteriolar bed perfused decreased with vasopressin. However, compensation occurred in that the proportion of capillaries perfused increased. This indicated an independent level of control of the coronary arteriolar and capillary beds. These microvascular changes may help to maintain oxygen supply-demand balance with vasopressin in the heart.
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PMID:Effect of vasopressin on myocardial capillary recruitment and coronary blood flow in the anesthetized rabbit. 171 7

The effects of selective alpha 1-adrenoceptor blockade with prazosin were investigated in ischemic rabbit heart. Using labeled microspheres, regional coronary blood flow was measured before and 1 hr after occlusion of the circumflex coronary artery in controls and animals given 1 mg/kg of prazosin 10 min after ligation. Small artery and vein O2 saturations were obtained microspectrophotometrically from hearts of anesthetized rabbits. Fluorescein isothiocyanate-dextran (150 mg/kg) was administered to mark the perfused microvessels and alkaline phosphatase stain was used to locate the total microvasculature. Prazosin depressed the arterial blood pressure. Coronary flow and O2 consumption (10.9 +/- 4.5 and 6.1 +/- 1.8 ml O2/min/100 g, nonoccluded and occluded) were significantly lower in the occluded region in the control group, while O2 extraction (4.9 +/- 1.4 and 6.8 +/- 2.6 ml O2/100 ml) was locally elevated. The results of occlusion in the prazosin-treated group were similar for flow, O2 consumption (9.9 +/- 4.5 and 6.7 +/- 5.3 ml O2/min/100 g, nonoccluded and occluded) and O2 extraction (6.6 +/- 2.3 and 8.2 +/- 2.3 ml O2/100 ml). The per cent of perfused microvessels was not significantly altered by occlusion in the control group. In the prazosin group, the percentage of occluded region subendocardial capillaries and arterioles perfused was significantly greater than in the control group, e.g., 65 +/- 9% perfused capillaries/mm2 in control occluded subendocardium vs 78 +/- 9% perfused capillaries/mm2 in prazosin-treated occluded subendocardium. Thus, the slight increase in microvessel utilization with prazosin was not sufficient to improve the flow or the O2 consumption in the ischemic myocardium.
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PMID:Microvascular, flow and O2 consumption responses of ischemic myocardium to prazosin. 172 45

The aim of this study was to identify the percentage of the capillary and arteriolar beds that was perfused at a given time or that was capable of being perfused within subepicardium and subendocardium of ischemic and nonischemic myocardium of anesthetized, open-chest rabbits. Fluorescein isothiocyanate-dextran (150,000 MW) was injected intravenously to label perfused microvessels of rabbits that were subjected to 60 min of coronary artery occlusion. Fluorescent microscopy was used to identify the perfused vessels and an alkaline phosphatase stain was employed to locate the total microvasculature. Stereological principles were utilized to determine various morphometric parameters. After 14 sec of dextran injection, approximately 66 +/- 2% (mean +/- SEM) of the capillaries and 65 +/- 5% of the arterioles (19-50 microns) were perfused within ischemic myocardium. Two minutes after dextran injection, 72 +/- 3% of the capillaries and 94 +/- 4% of the arterioles were perfused within the ischemic myocardium. In the nonischemic myocardium, 64 +/- 2% of the capillaries and 59 +/- 5% of the arterioles were perfused 14 sec after dextran injection, while 94 +/- 1% and 96 +/- 2% of the capillaries and arterioles, respectively, were perfused 2 min after dextran injection. It is concluded that a significant unperfused reserve of arterioles exists, but a significant portion of the capillary bed is incapable of being perfused within ischemic rabbit myocardium.
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PMID:Quantitative morphometric determination of arteriolar and capillary perfusion within ischemic rabbit left ventricle. 242 63

The effects of adenosine on regional cerebral blood flow and indexes of the total and perfused microvascular bed were studied after 1 h of middle cerebral artery occlusion in the anesthetized rat. Iodo[14C]antipyrine was used to determine cerebral blood flow. Fluorescein isothiocyanate-dextran was used to study the perfused microvasculature, and an alkaline phosphatase stain was used to identify the total bed. Mean arterial blood pressure was significantly reduced by adenosine. Cerebral blood flow increased significantly by 75%, except in the flow-restricted cortex where flow averaged 28 +/- 15 (SD) ml.min-1.100 g-1 in control and 34 +/- 33 ml.min-1.100 g-1 in adenosine-treated animals. No significant regional structural differences were observed within the microvascular beds of the two groups. The percentage of the microvascular volume perfused increased significantly in all brain regions in the adenosine-treated rats, including the flow-restricted cortex. The percent perfused arteriolar volume in the flow-restricted cortex was 30 +/- 12% in control and 95 +/- 3% in adenosine-treated animals. Similar values for the capillary bed were 22 +/- 10% in control and 54 +/- 3% in adenosine-treated rats. These results indicate a maintenance of flow with a reduction in diffusion distances in the flow-restricted cortex after treatment with adenosine.
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PMID:Adenosine and cerebral capillary perfusion and blood flow during middle cerebral artery occlusion. 258 18

The effect of chronic propranolol administration (2 mg.kg-1.d-1 for 14d) and withdrawal on microvascular perfusion was studied in rabbit myocardium. Fluorescein isothiocyanate-dextran was injected into four groups of anaesthetised open chest rabbits. Fluorescent microscopy was used to identify the perfused vessels and alkaline phosphatase stain was employed to locate the total microvasculature. Beta adrenoceptor density (Bmax), measured using 125I-iodopindolol, increased from 20.3(SD 6.3) fmol.mg-1 protein in control to 52.4(8.9) in chronically treated rabbits. The proportion of the capillary bed which was perfused, 61.4(4.3)% was significantly decreased by acute injection of propranolol to 51.1(5.1)%, but not affected by chronic administration, remaining at 57.0(4.0)%. The percentage of the capillary bed perfused increased significantly after cessation of chronic propranolol treatment to 69.1(6.5)%. Similar results were seen for myocardial arterioles. Thus, while diffusion distances are increased by acute adrenoceptor blockade, this effect is not seen in the chronic condition. Diffusion distance decreased significantly after withdrawal of chronic propranolol treatment. We conclude that the percentage of perfused capillaries is strongly influenced by the number of beta adrenoceptors or their effect.
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PMID:Effect of prolonged propranolol administration and withdrawal on perfusion of the myocardial capillary bed. 285 20

The purpose of the present investigation was to determine the effects of thyroxine (T4), which induces myocardial hypertrophy, on the number per square millimetre and volume per cubic millimetre of both the total and perfused portions of the arteriolar and capillary beds of the heart. Studies were conducted in the subendocardial and subepicardial regions of the left ventricle of anesthetized open-chest rabbits. Fluorescein isothiocyanate-dextran (i.v.) or radioactive microspheres (intra-atrial) were injected to label the perfused microvessels or to determine coronary flow in three groups of rabbits: controls, and rabbits given 0.5 mg/kg T4 for 3 days and for 16 days. Fluorescent photography was used to identify the perfused microvessels. An alkaline phosphatase stain was employed to locate the total microvascular bed. There were 2369 +/- 638 (SD) capillaries/mm2 and 4 +/- 3 arterioles/mm2 in control hearts. These decreased significantly to 1380 +/- 199/mm2 and 1 +/- 1/mm2, respectively, after 16 days of T4. In controls, 60 +/- 5% of the capillaries and 59 +/- 21% of the arterioles were perfused. This increased significantly to 90 +/- 5 and 86 +/- 18%, respectively, by 16 days of T4 treatment. Similar changes, although smaller, were observed after 3 days of T4. Coronary blood flow increased to 1.7 times control after 3 days and 2.9 times after 16 days of T4. No significant subepicardial versus subendocardial differences were observed in any condition or measurement. Thus, the physiological response to the increased work and increase in anatomic minimum diffusion distance is to increase flow and the proportion of the capillary bed perfused to at least maintain physiological diffusion distances.
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PMID:T4-induced cardiac hypertrophy and the perfused and total microvasculature of the heart. 296 28

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.
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PMID:Perfused microvascular morphometry during middle cerebral artery occlusion. 313 28

Fluorescein (Fl) and tetramethyl rhodamine (Rh) were evaluated as possible candidates for a double hapten sandwich system in enzyme immunohistology. Monoclonal antibodies were raised against Fl and Rh. Their fine-specificity was tested with a competition-like assay. A pair of Mab's was selected for immunohistology in which they functioned as a bridge between Fl/Rh conjugated antibodies and Fl/Rh labeled peroxidase and alkaline phosphatase, respectively. The binding of fluorescein labeled antibodies could be successfully demonstrated in histological slides. A large variability in the efficacy of staining was observed in the case of rhodamine labeled antibodies. The phenomenon is explained by assuming that tetramethyl rhodamine isothiocyanate reacts preferentially with lysine residues near to, or embedded in, hydrophobic regions in a protein. This condition may reduce the accessibility of the Rh moiety for anti-Rh antibodies.
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PMID:Fluorescein and tetramethyl rhodamine as haptens in enzyme immunohistochemistry. 352 96

The aim of this study was to determine the effect of blood coagulation and platelet aggregation on the perfusability of arterioles (19-50 micron) and capillaries in subepicardial and subendocardial ischemic and nonischemic myocardium of anesthetized open-chest rabbits. Fluorescein isothiocynate-dextran (MW 150,000) was injected intravenously to label perfusable myocardial microvessels of rabbits that were subjected to 60 min of coronary artery occlusion. Fluorescent microscopy was used to identify the perfusable vessels and an alkaline phosphatase stain was employed to locate the total microvasculature of the heart. Stereological principles were utilized to determine various morphometric parameters. About 25% of the capillaries were incapable of being perfused but virtually all arterioles were perfusable in occluded myocardium of the control group. Essentially all capillaries and arterioles were perfusable in nonoccluded myocardium. Collagen infusion produced a perfusion defect in 14% of the capillaries and arterioles in nonoccluded myocardium and in 33% of the capillaries and arterioles in occluded myocardium. Heparin, prostaglandin E1 (PGE1), or PGE1 + heparin did not prevent the perfusion defect in capillaries of occluded myocardium. It is concluded that while promotion of blood coagulation and platelet aggregation was able to produce microvessel obstruction, these hemostatic mechanisms were not primarily responsible for the capillary obstruction observed during myocardial ischemia in the rabbit heart.
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PMID:Effect of blood coagulation and platelet aggregation on perfusable capillaries and arterioles in ischemic and nonischemic myocardium. 365 5

The effects of moderate and severe hypoxia on quantitative regional morphometric indexes of the total and perfused arteriolar and capillary network were studied in the rat brain to determine whether diffusion distances were reduced in hypoxia. Fluorescein isothiocyanate (FITC)-labeled dextran was injected into the femoral vein of conscious control and hypoxic rats. After 20 s, the animal was decapitated and the head was frozen in liquid N2. Sections from eight brain regions were photographed to detect the perfused microvessels and then stained for alkaline phosphatase to visualize the total vascular network. There were significant increases in percent perfused arteriolar and capillary morphology between the two groups of hypoxic animals and control animals. In control rats, the percent of capillaries perfused averaged 45.6 +/- 0.6% (mean +/- SE). In moderate hypoxia 63.4 +/- 1.8% of the vessels were perfused and in severe hypoxia 89.4 +/- 0.1% were perfused. The percentage of arterioles perfused changed similarly. There were no significant differences in any index of total or percent perfused arteriolar or capillary morphometry among the regions within any group. During severe hypoxia, a greater percentage of the capillary reserves was utilized. These results demonstrate a uniform response to hypoxia in the capillary and arteriolar network of the conscious rat brain.
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PMID:Effect of hypoxia on percent of arteriolar and capillary beds perfused in the rat brain. 394 37


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