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Biomedical subjects

H R Weiss

Publications and source records attributed to H R Weiss.

At least 163 records · Page 9Linked to original sources

Blood flow, O2 extraction and O2 consumption along the rat small intestine.

Differences in O2 delivery and consumption along the fed and fasted small intestine are described. Total wall blood flow was determined in sequential segments of small intestine from 5 to 6-month-old male, anesthetized Fischer 344 rats either 75-80 min before or after feeding, using radioactive microspheres. Oxygen saturation in submucosal arterioles and venules (50-60 micron diam) was determined throughout the intestine, using a microspectrophotometric technique. Venous O2 saturations showed considerable heterogeneity in all regions, and ranged from 0 to 77%. Arterial-venous O2 content differences (CaO2-CvO2) did not change along the fasted rat intestine, and averaged 8.2 ml O2/100 ml blood. However, CaO2-CvO2 followed a small proximal to distal gradient (proximal greater than distal) in the fed rats. Larger proximal to distal gradients (proximal greater than distal) occurred in both blood flow and O2 consumption in both groups. Feeding did not change intestinal average CaO2-CvO2. However, feeding induced a 53% increase in average O2 consumption, with the greatest increase (130%) occurring in the middle third of the intestine. Feeding induced a 42% increase in average blood flow, with the greatest increase (70%) occurring in the distal third of the intestine. The increased O2 used by the fed intestine was primarily provided by the increased blood flow. The O2 consumption gradient is assumed to reflect differences in mucosal mass along the intestine and/or differences in metabolic activity.

Animals↗

Oxygen diffusion distance in thyroxine-induced hypertrophic rabbit myocardium.

We studied the oxygen diffusion distance in the rabbit myocardium in untreated animals and in animals treated with thyroxine (T4) for 3 days and 16 days. The subepicardial and subendocardial regions were studied separately. Sixteen days of T4 treatment results in significant cardiac hypertrophy. After 16 days, the percentage of the myocardium occupied by myocytes decreases as the volume of extracellular matrix increases. After 3 days, the number of myocyte mitochondria per unit volume of myocardium increases without an increase in mitochondrial volume. After 16 days the volume density of the myocyte mitochondria increases. Oxygen diffusion distance was determined by measuring the distance between the myocardial capillaries and the cardiomyocyte mitochondria. The deposition of extracellular matrix results in an increase in the distance between the myocardial capillaries and the myocytes. The distribution of the mitochondria within the myocytes remains unchanged resulting in an increased distance between the capillaries and the mitochondria, hence, an increased oxygen diffusion distance. There is some evidence that the mitochondria most distant from the capillaries are the mitochondria in which division is most frequent with T4 stimulation. This may be related to the relative deprivation of oxygen of these mitochondria.

Animals↗

Effect of prolonged propranolol administration and withdrawal on perfusion of the myocardial capillary bed.

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.

Animals↗

Effect of nifedipine on regional O2 consumption in ischemic myocardial tissue.

The effect of intravenous (i.v.) nifedipine (5 micrograms/kg/min) on regional O2 supply/consumption variables was determined in 14 anesthetized open-chest dogs subjected to left anterior descending coronary artery (LAD) stenosis sufficient to reduce blood flow 50%. Myocardial blood flow was measured using radioactive microspheres, and regional arterial and venous O2 saturations were determined using microspectrophotometry. During LAD occlusion, blood flow and O2 consumption were decreased in the ischemic region while O2 extraction was increased. With nifedipine treatment, LAD flow (flow probe) was increased 44% as compared with the initial occluded value, with most of this increase going to the subepicardium (microspheres). Flow to the ischemic subendocardium was not changed with nifedipine treatment. Ischemic subepicardial O2 consumption increased slightly in nifedipine-treated animals as compared with saline values, whereas O2 extraction decreased slightly. In the subendocardial region, nifedipine resulted in a significant decrease in O2 extraction, with a slight decrease in O2 consumption as compared with saline controls. The O2 supply/demand ratio was significantly improved with nifedipine only in the subendocardium of the ischemic region. This suggested that nifedipine could increase O2 consumption in the ischemic subepicardium through proportional increase in O2 supply while it decreased O2 consumption in the subendocardium relative to O2 supply.

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↗

Microvascular morphometry and perfusion in renal hypertension-induced cardiac hypertrophy.

This study examined alterations in microvascular morphometry and perfusion occurring concomitantly with changes in coronary blood flow (CBF), flow reserves, and coronary vascular resistance (CVR) in myocardial hypertrophy. New Zealand White rabbits (n = 28) with one-kidney, one-clip hypertension (1K,1C) or uninephrectomy (control) were examined 4 wk after surgery in anesthetized open-chest preparations. Animals were divided into two experimental series. In the first series, flows were determined with radioactive microspheres during rest and adenosine-induced vasodilation. In a second series, fluorescein isothiocyanate dextran (FITC-dextran) was injected to visualize the perfused arteriolar and capillary beds. The total vasculature was marked with an alkaline phosphatase stain. Mean arterial pressure was elevated in 1K,1C animals (110 +/- 7 mmHg, means +/- SE) when compared with controls (77 + 4 mmHg), and the myocardial weight was greater. Resting CBF was higher in 1K,1C animals compared with controls (227 +/- 21 vs. 168 +/- 12 ml.min-1.100 g-1), and the flow reserve was reduced. Minimal CVR was higher in 1K,1C compared with controls (0.190 +/- 0.035 vs. 0.091 +/- 0.018 mmHg.ml-1.min.100 g). The number of capillaries per squared millimeter was not different from control (2,448 + 121 vs. 2,216 +/- 132/mm2) and the percent perfused was similar (56 +/- 2 vs. 61 +/- 3%). The arteriolar density in cardiac hypertrophy was lower (1.2 +/- 0.2 vs. 2.1 +/- 0.3/mm2), and the percent perfused was higher (86 +/- 5 vs. 63 + 6%) compared with controls. Thus, in myocardial hypertrophy, the anatomical density and volume fraction of arterioles appears to be reduced, and the percentage of arterioles perfused increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗

Myocardial oxygen consumption, oxygen supply/demand heterogeneity, and microvascular patency in regionally stunned myocardium.

Although oxygen consumption closely parallels mechanical work in the normal heart, previous studies have found that stunned myocardium may have normal or even increased oxygen consumption despite depressed function. In this study we used microspectrophotometry to measure the oxygen saturations within arteries and veins of less than 100 micron diameter in quick-frozen biopsy samples from normal and regionally stunned myocardium of 10 open-chest anesthetized dogs. Regional myocardial blood flow, measured by radioactive microspheres, was similar in stunned and normal regions, as was mean arteriolar oxygen saturation. However, mean venous oxygen saturation was lower in the stunned region (epicardium 38.0% vs 43.8%, p less than .02; endocardium 36.2% vs 39.5%, p = .12), indicating increased oxygen extraction and consumption, despite a marked reduction in mean systolic segmental shortening from 14.4% to 0.5%. In addition, there was greater vein-to-vein heterogeneity of oxygen saturation in the stunned region, with an excess of veins having low saturations (statistically significant in epicardium, nonsignificant trend in endocardium). Microvascular injections studies with Microfil or drafting ink revealed filling of over 95% of arterioles and 85% of capillaries in the stunned region, similar to the findings in the normal region. Our results are consistent with an inefficient transfer of energy into myocyte contraction or an increased use of energy for noncontractile activities in stunned myocardium. In addition, the finding of increased heterogeneity of oxygen extraction suggests that the injury to stunned myocardium may not be uniform to all contractile elements, but instead may be focally and irregularly distributed.

Animals↗

Improved distribution of regional oxygenation in denervated ischemic dog myocardium.

The role of the adrenergic nervous system in the response to coronary artery occlusion has been examined using surgical and chemical denervation techniques. Experiments were conducted on four groups of dogs (n = 18): 1) untreated controls; 2) intrapericardial denervation immediately prior to coronary ligation; 3) surgical denervation 2 weeks prior to the experiment; and 4) chemical sympathectomy 5 days prior to the experiment with 6-hydroxydopamine (50 mg/kg). Small artery and vein O2 saturations were obtained microspectrophotometrically and combined with radioactive microsphere blood flow determinations to calculate regional myocardial O2 consumption in open chest dogs. Denervation significantly reduced the preocclusion heart rate from 165 +/- 16 beats/min in the control to 114 +/- 13 in the chronic surgically denervated and to 137 +/- 15 in the chemically sympathectomized groups. After 2 hours of occlusion, the O2 consumption and flow were similar in the nonischemic area except for lower values in the surgically denervated group. Total coronary blood flow and O2 consumption in the occluded regions were not significantly affected by chronic denervation. However, significant elimination of areas with low venous O2 saturation (less than 20%) were found in the ischemic myocardium of the chronically denervated groups as compared with the control or with the acutely denervated dogs. The mean venous O2 saturation was found to be significantly higher in all regions of these two groups as compared with the control. The O2 extraction was also lowered. Thus, chronic denervation reduced microregional heterogeneity of oxygenation in the ischemic myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

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↗

Beta-adrenoceptor stimulation and blockade during myocardial ischemia in dogs: effect on cardiac O2 supply and consumption.

The effect of beta-adrenoceptor blockade and activation on ischemic regional and microregional myocardial O2 supply/consumption parameters was assessed in 28 open chest, anesthetized dogs. Ten minutes after LAD occlusion, dogs were given i.v. saline, 2 mg/kg propranolol, 0.2 mg/kg pindolol, or 1 microgram/kg per min isoproterenol. Coronary blood flow was determined using radioactive microspheres before and 2 h after LAD occlusion while O2 supply/consumption parameters were determined using microspectrophotometry. Ischemia resulted in a 66% reduction in subendocardial flow in controls in the ischemic zone and no experimental treatment significantly altered this flow. Pindolol resulted in a significant improvement in the ischemic regional subendocardial/subepicardial flow ratio (from 0.69 in the control ischemic region to 0.88 during pindolol treatment). O2 extractions were significantly increased and O2 consumptions were significantly depressed in the ischemic regions of all groups. O2 extractions were increased to a lesser degree in the ischemic region with the use of pindolol and propranolol. Propranolol and pindolol both significantly decreased the proportion of veins with low (0-20%) O2 saturations in the ischemic region indicating an improved microregional distribution of blood flow and/or O2 consumption within the ischemic region.

Adrenergic beta-Agonists↗

Effect of blood coagulation and platelet aggregation on perfusable capillaries and arterioles in ischemic and nonischemic myocardium.

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.

Alprostadil↗

Effect of aortic stenosis on oxygen balance in partially ischemic myocardium.

Valvar aortic stenosis can result in myocardial underperfusion with or without coronary obstruction. The purpose of this study was to determine how hearts with valvar aortic stenosis without hypertrophy can maintain their oxygen supply/consumption balance with partial left anterior descending coronary artery (LAD) occlusion. Open-chested, anesthetized dogs (n = 9) were subjected to mild valvar aortic stenosis and then to a reduction of LAD flow to 50% of baseline, while controls (n = 9) received partial LAD occlusion without aortic stenosis. Blood flows were determined before and after aortic stenosis and after LAD occlusion using radioactive microspheres. The hearts were then removed for microspectrophotometric analysis of regional venous and arterial oxygen saturation. Aortic stenosis resulted in a pressure gradient of approximately 50 mm Hg, representing mild aortic stenosis. Only a slight increase in myocardial blood flow was seen with aortic stenosis. Ischemia resulted in a significant drop in blood flow in control (40%) and aortic stenosis (55%) animals compared with their own preocclusion values. These ischemic region flows were not different from each other. Aortic stenosis itself did not alter oxygen extraction, although partial occlusion similarly increased extraction for all groups in the ischemic zone. The LAD occlusion resulted in a decreased oxygen consumption in the occluded region of all groups, with no differences noted between control and aortic stenosed animals. Thus, mild, acute aortic stenosis without hypertrophy does not appear to significantly increase the severity of an ischemic episode precipitated by partial LAD occlusion.

Acute Disease↗

T4-induced cardiac hypertrophy and the perfused and total microvasculature of the heart.

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.

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↗

Effects of propranolol on regional O2 supply and O2 consumption in reperfused dog myocardium.

This study was designed to assess whether propranolol would improve the relationship between O2 supply and O2 consumption in the reperfused ischemic dog myocardium. In 14 dogs, the left anterior descending coronary artery was occluded for 2 hr, followed by a 4-hr period of reperfusion. In 7 of the 14 dogs, 1 mg/kg of propranolol was administered 10 min before and again 2 hr after reperfusion. Small artery and vein O2 saturations obtained microspectrophotometrically were combined with regional blood flow measurements using radioactive microspheres to determine regional myocardial O2 consumption. In both groups, 2 hr of occlusion lowered the regional flow to a similar level. In the control group, 4 hr of reperfusion returned the blood flow toward normal levels, from 17 +/- 20 ml/min/100 g (mean +/- S.D.) at the end of occlusion to 60 +/- 42 ml/min/100 g in the affected area compared with 84 +/- 28 ml/min/100 g in the nonischemic area. In the propranolol-treated animals, the flow increase with reperfusion was not significant (25 +/- 30 ml/min/100 g to 45 +/- 26 ml/min/100 g). O2 extraction was greater in the ischemic than in the unaffected area in both groups. However, ischemic region O2 extraction was lower in the propranolol-treated group than in the control group. There were a greater number of arteries and veins with reduced O2 saturations in the control group reperfused area compared with the nonischemic area. Propranolol decreased the number of low O2 saturation vessels in the ischemic area.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Coronary adjustments to graded hypotension in rabbits.

The purpose of this study was to determine how the myocardium can compensate (change O2 supply/consumption parameters) regionally during acute hemorrhagic hypotension. Twenty-one open chest, anesthetized rabbits were subjected to one of three treatments: (1) control (nonhemorrhaged), (2) hemorrhage to 70 mm Hg, (3) hemorrhage to 50 mm Hg. Myocardial blood flows were determined by using radioactive microspheres before and during hemorrhage. At the end of the experiment the hearts were removed and stored in liquid N2 and analyzed for subepicardial and subendocardial arterial and venous O2 saturation by using microspectrophotometry, and from this, O2 consumption was determined. During hemorrhage, blood pressures were significantly depressed for all groups compared to the control group. Myocardial blood flow was depressed 20% in the 70 mm Hg group and coronary resistance fell 15% compared to control. In the 50 mm Hg group, flow was reduced 38% and resistance decreased 31% compared to the 70 mm Hg group. No regional (subepicardial-subendocardial) differences in flow or resistance occurred during hypotension. These decreases in resistance were observed despite a 32% drop in O2 consumption in the 70 mm Hg group and 44% in the 50 mm Hg group compared to the control. O2 extraction remained unchanged for all groups as did the O2 supply/consumption balance. Thus, despite decreases in O2 consumption during acute hemorrhage, rabbit hearts decreased coronary resistance so as to maintain the O2 regional supply/consumption balance constant. Since O2 extraction did not change, these hearts were not ischemic, even in the subendocardium.

Animals↗

Effect of withdrawal from chronic naltrexone on regional cerebral oxygen consumption in the cat.

This investigation determined the effects of withdrawal from chronic naltrexone administration on average and regional cerebral blood flow, oxygen extraction and oxygen consumption. The relationship between the effects of withdrawal from chronic administration of this opiate receptor antagonist, which may increase the numbers of postsynaptic opiate receptors, and these parameters was investigated. Fourteen adult mongrel cats were administered subcutaneous injections of 1 mg/kg naltrexone HCl or 1 ml 0.9% saline twice daily for 21 days. Two days later, regional cerebral blood flow was monitored using radioactively tagged microspheres. The animals were sacrificed and prepared for microspectrophotometric analysis of regional cerebral venous and arterial oxygen saturation. Regional cerebral oxygen consumption was calculated as the product of cerebral blood flow and oxygen extraction for each area examined. After 2 days of withdrawal from chronic naltrexone treatment, the blood pressure, heart rate and blood gas parameters did not change significantly when compared to saline-treated animals. Average cerebral blood flow was significantly increased from 47.9 +/- 3.4 ml/min/100 g (mean +/- S.E.M.) in the control group to 80.3 +/- 6.5 (ml/min/100 g) in the chronic naltrexone-treated group. Flow was significantly increased in the cortex, lenticulate nuclei, thalamus and pons. Neither average cerebral oxygen consumption, which increased slightly, nor cerebral oxygen extraction, which decreased slightly, were significantly altered by treatment. The distribution of flow among the examined regions was, however, significantly altered in the animals 2 days after receiving chronic naltrexone injections. These changes were not restricted to brain regions dense in neuronal opiate receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Alterations in perfused capillary morphometry in awake vs anesthetized brain.

This study quantitatively compared various indices of perfused capillary morphometry in pentobarbital-anesthetized and awake rat brains. We hypothesized that barbiturate anesthesia would reduce intraregional differences in percent perfused capillary volume and surface area. A high-molecular-weight FITC-labeled Dextran was injected intravenously into awake or barbiturate-anesthetized (50 mg/kg i.p.) rats. After 20 s, the animal was decapitated and the head frozen in liquid N2. Nine brain regions were isolated and mounted in a microtome cryostat. Sections, 2 microns thick, were photographed with a fluorescent microscope to detect the perfused capillaries. The sections were stained for alkaline phosphatase to visualize the total capillary network. Standard morphometric techniques were employed to determine the total and perfused volume (Vv), surface area (Sv) per mm3 and diameter (D) from the photographs. There were no significant differences in any index of total capillary morphometry among the regions in the anesthetized brain. Approximately half of the average total capillary bed was perfused and there were no significant differences in percent perfused Vv or Sv between awake and anesthetized brains. There were significant differences among the various brain regions in the perfused capillary bed of the awake rat. The percent perfused capillary Vv and Sv in the awake rat was significantly greater in the thalamus and anterior cortex than in other brain regions. In awake rats, the percent perfused capillary Vv ranged from 67.9 +/- 4.7% (mean +/- S.E.M.) in the thalamus to 26.1 +/- 4.3% in the posterior cortex. Thus, while the average percent perfused indices of capillary morphometry were not altered by anesthesia, regional differences in these indices among the examined regions were abolished with anesthesia.

Anesthesia, General↗