Journal articles on the topic 'Microsphere infusion'
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1
Carter, A. M., J. R. G. Challis, and P. Svendsen. "Regional adrenal blood flow responses to adrenocorticotropic hormone after chronic embolization of the fetal placental circulation in sheep." Journal of Endocrinology 148, no. 3 (March 1996): 517–22. http://dx.doi.org/10.1677/joe.0.1480517.
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Abstract To ascertain whether repeated hypoxic stress would alter the response of the adrenal cortex to adrenocorticotropic hormone (ACTH), by premature activation of the hypothalamic–pituitary–adrenal axis, we studied fetal sheep subjected to daily reduction of arterial oxygen content by embolization of the fetal placental circulation with 15 μm microspheres for 8 days from about day 124 of gestation (term ∼147 days) and sham-embolized controls. Starting before the final embolization (or shamembolization) on day 8, and continuing for 24 h, the fetus was given an intravenous infusion of ACTH1–24 (0·5 μg/h) or vehicle. Fetal and maternal blood samples were taken for determination of immunoreactive cortisol, and regional adrenal and fetal placental blood flows were measured by the microsphere technique at three time points: 1 h before infusion, 3 h after the start of the infusion (1 h after embolization), and after 24 h of infusion. Prior to infusion of ACTH or vehicle, fetal placental blood flow was lower in microsphere-embolized fetuses than in sham-embolized controls (199 ± 15 vs 292 ± 25 ml/min per 100 g tissue; mean ± s.e.; P<0·01). However, plasma cortisol and adrenal cortical blood flow did not differ between embolized fetuses and controls. Adrenal vascular responses to the 24-h infusion of ACTH were similar in embolized and shamembolized fetuses. Adrenal cortical blood flow increased 3-fold (P<0·05) due to decreased vascular resistance (P<0·01), with no change in adrenal medullary blood flow. Thus, while daily embolization of the fetal placental circulation caused a sustained decrease in cotyledonary blood flow, no evidence of altered responsiveness of the adrenal cortex to ACTH was found in these experiments. Journal of Endocrinology (1996) 148, 517–522
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Pearse, David B., Thomas E. Dahms, and Elizabeth M. Wagner. "Microsphere-induced bronchial artery vasodilation: role of adenosine, prostacyclin, and nitric oxide." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 3 (March 1, 1998): H760—H768. http://dx.doi.org/10.1152/ajpheart.1998.274.3.h760.
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We previously found that injection of 15-μm microspheres into the bronchial artery of sheep decreased bronchial artery resistance. This effect was inhibited partially by indomethacin or 8-phenyltheophylline, suggesting that microspheres caused release of a dilating prostaglandin and adenosine. To identify the prostaglandin and confirm adenosine release, we perfused the bronchial artery in anesthetized sheep. In 12 sheep, bronchial artery blood samples were obtained before and after the infusion of 1 × 106microspheres or microsphere diluent into the bronchial artery. Microspheres, but not diluent, decreased bronchial artery resistance by 40% and increased bronchial artery plasma 6-ketoprostaglandin F1α (194.7 ± 45.0 to 496.5 ± 101.3 pg/ml), the stable metabolite of prostacyclin, and prostaglandin (PG) F2α (28.1 ± 4.4 to 46.2 ± 9.7 pg/ml). There were no changes in PGD2, PGE2, thromboxane B2, adenosine, inosine, or hypoxanthine. Pretreatment with dipyridamole, an adenosine uptake inhibitor, did not affect bronchial artery nucleoside concentrations ( n = 7). Microsphere-induced vasodilation was not enhanced by dipyridamole ( n = 9) and was not inhibited by either the adenosine receptor antagonist xanthine amine congener ( n = 4) or the nitric oxide (NO) synthase inhibitor N G-monomethyl-l-arginine ( n = 8). These results do not support a role for either adenosine or NO and suggest that microspheres caused bronchial artery vasodilation through release of prostacylin and an unidentified vasodilator.
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Geffin, G. A., D. D. O'Keefe, A. G. Denenberg, and W. M. Daggett. "Microsphere reference flow samples during systemic flow adjustment." American Journal of Physiology-Heart and Circulatory Physiology 252, no. 4 (April 1, 1987): H851—H856. http://dx.doi.org/10.1152/ajpheart.1987.252.4.h851.
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Regional myocardial blood flow measurements in the right heart bypass preparation can be particularly valuable, since this preparation provides control of the main hemodynamic determinants of coronary blood flow. We examined the validity of aortic reference flow samples in relation to coronary samples during continuous systemic flow adjustment for aortic pressure control in six dogs on right heart bypass, anesthetized with chloralose and urethan. Microsphere concentrations were compared in paired reference flow samples drawn from the aortic arch and from a coronary artery for 119 left atrial microsphere injections. During left subclavian artery infusion and during femoral artery infusion at rates above 2,000 ml/min, there were high percentage errors in microsphere concentration between paired samples, consistent with aortic sample dilution by systemically infused blood. In 52 injections during withdrawal or femoral infusion below 2,000 ml/min, at cardiac outputs of 390-4,800 ml/min, the percentage error was 0.001 +/- 1.18% (SE); the absolute value of this error was below 20% in 96%, and below 10% in 77% of these injections. Linear regression related these coronary to aortic microsphere concentrations by the equation Y = 1.005X - 1.64, r = 0.997, Sy.x = 13.2 (5.9%). (Sy.x represents the standard deviation from regression.) These data indicate that valid aortic reference flow samples can be obtained within specific hemodynamic conditions during systemic flow adjustment in the right heart bypass preparation.
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Janssen, W. M., H. Beekhuis, R. de Bruin, P. E. de Jong, and D. de Zeeuw. "Noninvasive measurement of intrarenal blood flow distribution: kinetic model of renal 123I-hippuran handling." American Journal of Physiology-Renal Physiology 269, no. 4 (October 1, 1995): F571—F580. http://dx.doi.org/10.1152/ajprenal.1995.269.4.f571.
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A new technique for noninvasive measurement of intrarenal blood flow distribution over cortex and medulla is proposed. The technique involves analysis of 123I-labeled hippuran renography, according to a kinetic model that describes the flow of 123I-hippuran from the heart (input) through the renal cortex and medulla to the bladder (output). The method is validated and compared with the standard microsphere injection technique in anesthetized dogs. Changes in intrarenal blood flow distribution were induced by infusion of placebo (n = 6), angiotensin I (n = 5), or atrial natriuretic factor (n = 5). Baseline percentage medullary blood flow in the left kidney was 12 +/- 1% of total renal blood flow measured with microspheres and 15 +/- 1% with renography. During infusion of the placebo, medullary blood flow decreased slightly compared with baseline, as measured with both methods, by 2 +/- 6 (microspheres) and 1 +/- 8% (renography). Infusion of angiotensin I caused a marked fall in medullary blood flow by 42 +/- 11 (microspheres) and 57 +/- 8% (renography). In contrast, infusion of atrial natriuretic factor caused a small rise in medullary blood flow as measured with both methods (9 +/- 3 and 12 +/- 11%, respectively). The absolute and percent changes in medullary blood flow measured with renography correlated with those measured with microspheres (left kidney: r = 0.67, P = 0.005; r = 0.71, P = 0.003, respectively; right kidney: r = 0.62, P = 0.01; r = 0.68, P = 0.004, respectively). We conclude that the proposed kinetic model of renal 123I-hippuran handling can be used to measure changes in intrarenal blood flow distribution and, because of its noninvasive character, may be of use in clinical studies.
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Fischman, Alan J., Hongbing Hsu, Edward A. Carter, Yong M. Yu, Ronald G. Tompkins, J. Luis Guerrero, Vernon R. Young, and Nathaniel M. Alpert. "Regional measurement of canine skeletal muscle blood flow by positron emission tomography with H2 15O." Journal of Applied Physiology 92, no. 4 (April 1, 2002): 1709–16. http://dx.doi.org/10.1152/japplphysiol.00445.2001.
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Positron emission tomography (PET) with H2 15O was used as an in vivo, relatively noninvasive, quantitative method for measuring regional blood flow to hindlimb skeletal muscle of anesthetized dogs. A hydrooccluder positioned on the femoral artery was used to reduce flow, and high-flow states were produced by local infusion of adenosine. Three to four measurements were made in each animal. Approximately 40 mCi of H2 15O were injected intravenously, and serial images and arterial blood samples were acquired over 2.5 min. Data analysis was performed by fitting tissue and arterial blood time-activity curves to a modified, single-compartment Kety model. The model equation was also solved on a pixel-by-pixel basis to yield maps of regional skeletal muscle blood flow. After each PET determination, flow was measured with radioactive microspheres. Results of the PET measurements demonstrated that basal flow to hindlimb skeletal muscle was 3.83 ± 0.36 ml · min−1 · 100 g−1(mean ± SE). This value was in excellent agreement with the microsphere data, 3.73 ± 0.32 ml · min−1 · 100 g−1( P = 0.69, not significant). Adenosine infusion resulted in flows as high as 30 ml · min−1 · 100 g−1, and the PET and microsphere data were highly correlated over the entire range of flows ( r 2 = 0.98, P < 0.0001). We conclude that muscle blood flow can be accurately measured in vivo by PET with H2 15O and that this approach offers promise for application in human studies of muscle metabolism under varying pathophysiological states.
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Laptook, Abbot R., Janet Peterson, and A. Michael Porter. "Effects of Lactic Acid Infusions and pH on Cerebral Blood Flow and Metabolism." Journal of Cerebral Blood Flow & Metabolism 8, no. 2 (April 1988): 193–200. http://dx.doi.org/10.1038/jcbfm.1988.49.
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To determine the effects of lactic acidemia versus lactate on CBF, we infused lactic acid, either buffered with NaOH (L + NaOH) or with added NaCl (L + NaCl), to attain similar osmolalities in 18 piglets. CBF (microsphere technique), pH, blood gases, plasma osmolality, and cerebral arteriovenous differences of O2 content and lactic acid concentrations were measured prior to, at 30 min of a lactic acid infusion, and 15 and 90 min after completion of the infusion. Control arterial pH was comparable between groups (7.50 ± 0.02 vs. 7.49 ± 0.02, X̄ ± SE); during and following L + NaCl and L + NaOH, values were (p < 0.05) 7.09 ± 0.03, 7.35 ± 0.02, and 7.46 ± 0.02 vs. 7.58 ± 0.03,7.61 ± 0.01, and 7.57 ± 0.03, respectively. PaCO2 remained unchanged and osmolality rose by 15% in both groups during infusions and persisted throughout the study period. For L + NaCl piglets, CBF (ml/min · 100 g) rose from 136 ± 15 to 198 ±26 (p < 0.05) at 30 min of infusion and remained elevated at 201 ± 25 and 207 ± 28 at 15 and 90 min following the infusion, respectively. Similarly, for L + NaOH piglets, CBF rose from 130 ± 25 to 196 ±31 (p < 0.05) with the infusion and was 174 ± 17 and 166 ± 21 at 15 and 90 min afterward, respectively. Although lactic acid infusion increases CBF, the associated metabolic acidemia is not responsible for changes in CBF.
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Muhonen, Michael G., Scott C. Robertson, Jeffrey S. Gerdes, and Christopher M. Loftus. "Effects of serotonin on cerebral circulation after middle cerebral artery occlusion." Journal of Neurosurgery 87, no. 2 (August 1997): 301–6. http://dx.doi.org/10.3171/jns.1997.87.2.0301.
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✓ Serotonin (5-HT) produces constriction of peripheral collateral blood vessels. Using an animal model, the authors tested the hypothesis that 5-HT constricts collateral vessels in the cerebrum. A branch of the middle cerebral artery (MCA) was occluded proximally and cannulated distally in anesthetized dogs. Blood flow to the area at risk for infarction was detected by perfusing the cannulated MCA branch with microsphere-free blood during systemic injection of radioactive microspheres (shadow flow technique). Blood flow to collateral-dependent and normal cerebrum was measured during intravenous infusion of 5-HT (10 and 40 mg/kg/minute). Serotonin produced a dose-related reduction of blood flow to collateral-dependent cerebrum, increased collateral vessel resistance in large cerebral arteries and collateral vessels, and decreased cerebral artery perfusion pressure. In contrast, blood flow to normal cerebrum was not altered because a decrease in small vessel resistance effectively compensated for a decrease in MCA perfusion pressure. These findings indicate that 5-HT produces constriction of collateral vessels in the cerebrum. This response is clearly different from normal small cerebral vessels, which dilate during 5-HT infusion.
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Miura, T., S. Yoshida, O. Iimura, and J. M. Downey. "Dobutamine modifies myocardial infarct size through supply-demand balance." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 5 (May 1, 1988): H855—H861. http://dx.doi.org/10.1152/ajpheart.1988.254.5.h855.
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We investigated dobutamine effect on infarct size during permanent coronary artery occlusion in dogs. The coronary artery of closed-chest dog was embolized by a 2.5-mm Teflon bead. Regional flow was measured 8 min after embolization with microspheres and, in drug-treated animals, again 20 min after starting dobutamine infusion (10 micrograms.kg-1.min-1 for 5 h immediately after the first microsphere measurement). The percent of the ischemic region progressing to infarct was determined 48 h later in each animal. Percent necrosis in the control group correlated closely with collateral flow to the epicardial one-third of the ischemic zone normalized against flow to the corresponding layer in the nonischemic zone. This flow should reflect an index of supply (collateral flow) and demand (flow to the nonischemic region determined by autoregulation). Percent necrosis in the drug-treated group did not correlate with normalized collateral flow measurement made before drug infusion, indicating that dobutamine had modified the course of infarction. Percent necrosis correlated well with normalized collateral flow measured during drug infusion, and that relationship was not different from that in the control group. Dobutamine increased infarct size over that expected from the predrug flow measurement in some dogs and reduced it in others. In all cases, however, the drug effect on infarct size was clearly reflected in normalized collateral flow measurement during drug infusion. Percent necrosis correlated with absolute collateral flow but less closely than with the normalized one.(ABSTRACT TRUNCATED AT 250 WORDS)
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Kuznetsova, Larisa V., Nicole Tomasek, Gisli H. Sigurdsson, Andrej Banic, Dominique Erni, and Anthony M. Wheatley. "Dissociation between volume blood flow and laser-Doppler signal from rat muscle during changes in vascular tone." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 4 (April 1, 1998): H1248—H1254. http://dx.doi.org/10.1152/ajpheart.1998.274.4.h1248.
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Although the laser-Doppler flowmetry (LDF) signal from skeletal muscle has been shown to provide a good measure of blood flow under some conditions, its behavior during administration of vasoactive substances has never been addressed. The aims of this study were to compare 1) changes in LDF signal with those in total muscle blood flow measured with radioactive microspheres after ganglionic blockade (chlorisondamine) and during administration of angiotensin II (ANG II), phenylephrine (PE), and isoproterenol (Iso) and 2) changes in vascular resistance estimated by the two techniques. The LDF signal from the biceps femoris muscle was investigated in anesthetized male Wistar rats. Ganglionic blockade led to a significant ( P < 0.05) fall in mean arterial pressure (MAP) [medians (lower, upper quartiles): 78 (72, 83) vs. 127 (114, 138) mmHg under basal conditions], muscle blood flow (MBF, microsphere technique; 61%), and the LDF signal (29%). Muscle vascular resistance (MVR = MAP/MBF) was increased (64%, P < 0.05), but vascular resistance estimated as MAP/LDF signal (MVRLDF) was unchanged. During ANG II and PE infusions, MAP rose ( P< 0.05) to 178 (155, 194) and 127 (124, 142) mmHg, respectively; MBF did not change compared with the preinfusion (postganglionic blockade) level and remained significantly ( P< 0.05) lower than baseline, whereas the LDF signal increased up to a level not different from baseline. MVR rose and was significantly ( P < 0.05) higher than baseline, whereas MVRLDF did not differ significantly from baseline. During Iso infusion, MAP fell [58 (56, 60) vs. 94 (92, 102) mmHg, P < 0.05], the LDF signal was reduced (49%, P < 0.05) despite a large increase in MBF (139%, P < 0.05), and MVR fell (74%, P < 0.05), whereas MVRLDF did not change vs. preinfusion level. Our results suggest that 1) changes in the LDF signal from muscle may not correlate with changes in total muscle blood flow measured by the microsphere technique during infusion of vasoactive substances and 2) the use of LDF data for estimation of MVR during changes in vascular tone in rat skeletal muscle is probably not appropriate.
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Lertxundi, Unai, Jorge Aramburu, Julio Ortega, Macarena Rodríguez-Fraile, Bruno Sangro, José Ignacio Bilbao, and Raúl Antón. "CFD Simulations of Radioembolization: A Proof-of-Concept Study on the Impact of the Hepatic Artery Tree Truncation." Mathematics 9, no. 8 (April 12, 2021): 839. http://dx.doi.org/10.3390/math9080839.
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Radioembolization (RE) is a treatment for patients with liver cancer, one of the leading cause of cancer-related deaths worldwide. RE consists of the transcatheter intraarterial infusion of radioactive microspheres, which are injected at the hepatic artery level and are transported in the bloodstream, aiming to target tumors and spare healthy liver parenchyma. In paving the way towards a computer platform that allows for a treatment planning based on computational fluid dynamics (CFD) simulations, the current simulation (model preprocess, model solving, model postprocess) times (of the order of days) make the CFD-based assessment non-viable. One of the approaches to reduce the simulation time includes the reduction in size of the simulated truncated hepatic artery. In this study, we analyze for three patient-specific hepatic arteries the impact of reducing the geometry of the hepatic artery on the simulation time. Results show that geometries can be efficiently shortened without impacting greatly on the microsphere distribution.
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SHANG, Q., X. WANG, M. APLEY, S. B. KUKANICH, and C. BERKLAND. "PPF microsphere depot sustains NSAID blood levels with infusion-like kinetics without ‘burst’." Journal of Veterinary Pharmacology and Therapeutics 35, no. 3 (June 23, 2011): 231–38. http://dx.doi.org/10.1111/j.1365-2885.2011.01317.x.
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VINCENT, RATTIGAN, and CLARK. "Microsphere infusion reverses vasoconstrictor‐mediated change in hindlimb oxygen uptake and energy status." Acta Physiologica Scandinavica 164, no. 1 (September 1998): 61–69. http://dx.doi.org/10.1046/j.1365-201x.1998.00408.x.
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Dhaliwal, Parneet, Sidra Ibad, Diana Losak, and Clay Cockerell. "A Case of Granulomatous Hypersensitivity Reactions to a Dermal Filler Precipitated by PD-1 Checkpoint Inhibitor Therapy." SKIN The Journal of Cutaneous Medicine 5, no. 1 (January 1, 2021): 41–45. http://dx.doi.org/10.25251/skin.5.1.10.
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Injection of filler material has become routine in dermatology in improving the appearance of rhytides and increasing skin volume associated with aging. While the vast majority of injections are accomplished without complications, foreign body reactions may develop in a certain percentage of individuals. We recently encountered a 65-year-old woman with recurrent malignant melanoma who presented with marked thickening along the sides of her face for approximately 2 months. She recently received nivolumab infusions for recurrent malignant melanoma and noted that symptoms worsened after each infusion. She reported having had cosmetic procedures done three years prior, one of which was an injection of a long-lasting dermal filler, polymethylmethacrylate microsphere enhanced bovine collagen (Bellafill). A biopsy of two areas revealed nodular infiltrates of histiocytes with small round lobules recognizable as polymethylmethacrylate microspheres. Based on clinical and histopathologic findings, a diagnosis of granulomatous dermatitis filler reaction was rendered. Nivolumab is a PD-1 checkpoint inhibitor that disrupts T-cell inhibitory pathways leading to increased immune activation. In this case, the immune activation triggered a florid granulomatous reaction to the filler the patient had been injected with 3 years previously. We present this case as the second report of this phenomenon and the first in the dermatologic literature. This is a newly recognized side effect of PD-1 checkpoint immunotherapy and patients who are about to initiate such therapy who have had filler injections should be warned about this potential complication.
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Dhaliwal, Parneet, Sidra Ibad, Diana Losak, and Clay Cockerell. "A Case of Granulomatous Hypersensitivity Reactions to a Dermal Filler Precipitated by PD-1 Checkpoint Inhibitor Therapy." SKIN The Journal of Cutaneous Medicine 5, no. 1 (January 1, 2021): 41–45. http://dx.doi.org/10.25251/skin.5.1.10.
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Injection of filler material has become routine in dermatology in improving the appearance of rhytides and increasing skin volume associated with aging. While the vast majority of injections are accomplished without complications, foreign body reactions may develop in a certain percentage of individuals. We recently encountered a 65-year-old woman with recurrent malignant melanoma who presented with marked thickening along the sides of her face for approximately 2 months. She recently received nivolumab infusions for recurrent malignant melanoma and noted that symptoms worsened after each infusion. She reported having had cosmetic procedures done three years prior, one of which was an injection of a long-lasting dermal filler, polymethylmethacrylate microsphere enhanced bovine collagen (Bellafill). A biopsy of two areas revealed nodular infiltrates of histiocytes with small round lobules recognizable as polymethylmethacrylate microspheres. Based on clinical and histopathologic findings, a diagnosis of granulomatous dermatitis filler reaction was rendered. Nivolumab is a PD-1 checkpoint inhibitor that disrupts T-cell inhibitory pathways leading to increased immune activation. In this case, the immune activation triggered a florid granulomatous reaction to the filler the patient had been injected with 3 years previously. We present this case as the second report of this phenomenon and the first in the dermatologic literature. This is a newly recognized side effect of PD-1 checkpoint immunotherapy and patients who are about to initiate such therapy who have had filler injections should be warned about this potential complication.
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Parisi, V. M., and S. W. Walsh. "Fetal placental vascular responses to prostacyclin after angiotensin II-induced vasoconstriction." American Journal of Physiology-Endocrinology and Metabolism 257, no. 1 (July 1, 1989): E102—E107. http://dx.doi.org/10.1152/ajpendo.1989.257.1.e102.
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The vasodilator prostacyclin is produced by many fetal tissues and may serve to protect umbilical placental blood flow. We hypothesized that prostacyclin could reverse fetoplacental vasoconstriction produced by angiotensin II (ANG II). Studies were done in eight unanesthetized near-term ovine fetuses. After a control period, ANG II was infused into the fetal inferior vena cava at a rate of 0.5 microgram/min for 40 min. Twenty minutes after starting the ANG II infusion, an infusion of prostacyclin at a rate of 5 micrograms/min was added to the ANG II infusion. Blood flows were measured by the radioactive microsphere technique. Blood flow measurements were made during the control period, 20 min after starting the ANG II infusion, and 20 min after adding prostacyclin to the ANG II infusion. ANG II produced significant fetal hypertension and renal, intestinal, and placental vasoconstriction. Placental vascular resistance rose from 0.14 +/- 0.01 to 0.18 +/- 0.01 mmHg.min.kg fetal wt.ml-1 during the ANG II infusion period (P less than 0.05). The addition of prostacyclin to the ANG II infusion resulted in a return to control values for fetal blood pressure and renal and intestinal resistance. However, placental vasoconstriction was not reversed by addition of prostacyclin as placental vascular resistance remained significantly elevated over the control value (0.17 +/- 0.01 mmHg.min.kg fetal wt.ml-1). Although unchanged by ANG II infusion, fetal pH decreased significantly during the ANG II plus prostacyclin infusion period. We conclude that ANG II causes fetal hypertension and renal and intestinal vasoconstriction, which are reversed by prostacyclin.(ABSTRACT TRUNCATED AT 250 WORDS)
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Richardson, B. S., J. E. Patrick, J. Bousquet, J. Homan, and J. F. Brien. "Cerebral metabolism in fetal lamb after maternal infusion of ethanol." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 249, no. 5 (November 1, 1985): R505—R509. http://dx.doi.org/10.1152/ajpregu.1985.249.5.r505.
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Cerebral uptake of glucose and O2 (VCO2) was measured in 10 chronically catheterized fetal lambs during a control period, after a 1-h maternal infusion of ethanol (1.0 g X kg-1 X h-1) and 1-h postethanol infusion, to determine if alterations in cerebral metabolism might occur. Brachiocephalic artery and sagittal vein blood samples were analyzed for glucose, O2 content, blood gases, pH, and ethanol. Cerebral blood flow (Qc) was measured with a radioactive microsphere technique. VCO2 decreased significantly, from 140 +/- 13 mumol X 100 g-1 X min-1 during the control period to 91 +/- 8 (P less than 0.05) with the ethanol infusion, with a related fall in Qc, 177 +/- 12 to 104 +/- 9 ml X 100 g-1 X min-1 (P less than 0.001), the cerebral arteriovenous O2 difference being little changed. Cerebral glucose uptake, although decreased, was not significantly changed with the ethanol infusion, because the cerebral arteriovenous difference for glucose increased with the related fall in Qc. We conclude that maternal infusion of ethanol results in a decreased fetal VCO2 with a related fall in Qc. If prolonged, this decrease in cerebral oxidative metabolism might well affect cerebral development and provide a mechanism whereby chronic alcohol intake contributes to central nervous system growth anomalies and dysfunction of infants exposed to alcohol in utero.
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Koerfer, J., P. Bauerfeind, D. Armstrong, and A. L. Blum. "Continuous measurement of rat gastric blood flow using Doppler flowmeter." American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no. 4 (April 1, 1993): G686—G692. http://dx.doi.org/10.1152/ajpgi.1993.264.4.g686.
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We describe the use of pulsed Doppler flowmetry to permit continuous measurement of gastric blood flow in the anesthetized rat. The aims of this study were: 1) to assess the stability of blood flow during Doppler flowmetry; 2) to assess the ability of Doppler flowmetry to record rapid, transient blood flow changes; and 3) to validate Doppler flowmetry against an established blood flow measurement technique using labeled microspheres. Measurements over 3-h periods with a Doppler probe placed on the left gastric artery showed that there was an initial 30-min stabilization period; after this the mean percentage coefficient of variation, indicating intraindividual variability for blood flow, was < 10% for the remaining 150 min. The infusion of norepinephrine produced rapid, transient blood flow changes, including the typical "autoregulatory escape" and "postinfusion hyperemia," both of which were detected by Doppler flowmetry. The accuracy of pulsed Doppler flowmetry in measuring gastric blood flow was established by the demonstration of a highly significant agreement between blood flow measured by the Doppler flowmetry and microsphere techniques. These data indicate that pulsed Doppler flowmetry is an accurate method for the continuous measurement of left gastric artery blood flow in the rat.
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Zhao, Rui, Shan Gao, Haiqi He, Jia Zhang, Guangjian Zhang, and Xiaopeng Wen. "Targeting Pulmonary Artery Infusion of Nuclear-Targeted Plasmid-Based Short Hairpin RNA (ShRNA) to Hypoxia Inducible Factor-1α3 (pshHIF-1α3) Nano-Microspheres for Treatment of Implanted Lung Cancer in Rats." Journal of Biomedical Nanotechnology 18, no. 3 (March 1, 2022): 740–46. http://dx.doi.org/10.1166/jbn.2022.3277.
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The pshHIF-1α3 stealth nanospheres have been studied if they have the function of arterial targeted drug delivery to provide a new arterial targeted drug delivery method for interventional therapy of lung cancer. The study is also aimed at exploring therapeutic effect of the checked drug delivery on lung cancer. The tested groups were designed as follows: Group I: blank control group (pulmonary artery perfusion of 0.5 mL 0.9% saline); group II: tail vein injection of pshHIF-1α3 nano-microsphere; group III: pshHIF-1α3 nano-microsphere pulmonary artery perfusion group. In vitro experiment assessed the effects of pulmonary artery perfusion of pshHIF-1α3 nanospheres on proliferation, apoptosis and colony forming ability of lung cancer A549 cells, which were all evaluated by using MTT method, flow cytometry and colony formation experiments, respectively. In vivo experiment tumor xenotransplantation was used to observe the effect of pulmonary artery perfusion of pshHIF-1α3 nanospheres on treatment of lung cancer. Both the In vivo pulmonary artery perfusion experiment and In vitro experiments in A549 cells confirmed that the pulmonary artery perfusion of pshHIF-1α3 nano-microspheres can inhibit the proliferation of lung cancer tissues and cells, promoting apoptosis and inhibiting migration, leading to enhanced therapeutic effect of lung cancer. One of characteristics of nanomaterials is their large surface area, high dispersion, specific adhesion, tumor-specific affinity and adhesion, thereby prolonging their circulation time in the body. Through aggregation of nanodrug delivery system in tumor cells, the local concentration of the drug is increased, thereby improving selectivity of chemotherapeutic drugs. The results from this study therefore suggest that pulmonary artery perfusion of pshHIF-1α3 may be used in arterial targeted drug delivery for treatment of lung cancer, providing a new and efficient targeted drug delivery arterial route for interventional therapy of lung cancer.
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Burchfield, DJ, A. Pena, AJ Peters, RM Abrams, and D. Phillips. "Cocaine does not compromise cerebral or myocardial oxygen delivery in fetal sheep." Reproduction, Fertility and Development 8, no. 3 (1996): 383. http://dx.doi.org/10.1071/rd9960383.
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Eight time-dated pregnant ewes at 125 days' gestation (145 days = term) underwent surgery for placement of fetal vascular catheters, electrodes for recording fetal behavioural state, and maternal venous catheters. Three days later, fetal cerebral and myocardial blood flow were determined by the coloured microsphere technique under four conditions: (1) during rapid-eye movement (REM) sleep, before fetal cocaine infusion, (2) 30 min after initiation of a cocaine infusion to the fetus at 0.2 mg/kg per min, (3) during REM sleep, before maternal cocaine infusion, and (4) 30 min after initiation of a cocaine infusion to the ewe at 0.3 mg/kg per min. Cocaine infusion directly to the fetal lamb did not cause hypoxaemia or significantly change cerebral or myocardial blood flow or oxygen delivery. Cocaine administered to the ewe led to a drop in fetal oxygen tension from 3.0 +/- 0.5 to 2.5 +/- 0.3 kPa (P < 0.0001) and in fetal oxygen content from 3.8 +/- 0.7 to 2.8 +/- 0.4 mmol O2/L (P < 0.0001). Prior to maternal cocaine administration, fetal cerebral blood flow was 146 +/- 103 mL/100 g per min and during maternal cocaine infusion it went to 184 +/- 147 mL/100 g per min (P = NS) while myocardial blood flow increased from 156 +/- 92 to 333 +/- 178 mL/100 g per min (P < 0.002). This increase in blood flow negated the effects of hypoxaemia so that cerebral oxygen delivery was unaffected while myocardial oxygen delivery increased an average of 67%. It is concluded that cocaine administration to pregnant sheep does not impede fetal cerebral or myocardial oxygen delivery.
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Sawmiller, D. R., and C. C. Chou. "Adenosine is a vasodilator in the intestinal mucosa." American Journal of Physiology-Gastrointestinal and Liver Physiology 261, no. 1 (July 1, 1991): G9—G15. http://dx.doi.org/10.1152/ajpgi.1991.261.1.g9.
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The vasoactivity of adenosine in the intestinal mucosa of anesthetized dogs was determined using two experimental techniques. By use of the microsphere technique, infusion of adenosine (1 mumol/min ia) was found to increase significantly venous outflow and mucosal and muscularis blood flows in both jejunum (+77, +72, and +78%) and ileum (+111, +146, and +71%). In constant flow jejunal preparations, intra-arterial adenosine significantly decreased perfusion pressure (-32%), an index of vascular resistance, but did not significantly alter the blood flow distribution between the mucosa and muscularis as determined by microspheres. Thus adenosine equally dilated the mucosal and muscularis vasculatures. Using the second experimental technique, we found that local mucosal application of adenosine or non-metabolizable adenosine analogues [N6-cyclohexyladenosine or 5'-(N-ethylcarboxamido)-adenosine] dose dependently increased jejunal venous outflow. Almost all of the adenosine absorbed from the lumen was localized in the mucosal tissue, suggesting that the above hyperemia resulted from exposure of the mucosal vasculature to these compounds. The hyperemia produced by the luminal placement was not mediated by stimulation of the mucosal nerves, because the hyperemia was unaltered after treating the mucosal surface with a local anesthetic. The present results demonstrate therefore that adenosine is a vasodilator in the canine intestinal mucosa.
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Wagerle, L. C., S. P. Kumar, J. Belik, and M. Delivoria-Papadopoulos. "Blood-brain barrier to hydrogen ion during acute metabolic acidosis in piglets." Journal of Applied Physiology 65, no. 2 (August 1, 1988): 776–81. http://dx.doi.org/10.1152/jappl.1988.65.2.776.
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The present study investigates the integrity of the blood-brain barrier to H+ or HCO3- during acute plasma acidosis in 35 newborn piglets anesthetized with pentobarbital sodium. Cerebrospinal fluid acid-base balance, cerebral blood flow (CBF), and cerebral oxygenation were measured after infusion of HCl (0.6 N, 0.191-0.388 ml/min) for a period of 1 h at a constant arterial PCO2 of 35-40 Torr. HCl infusion resulted in decreased arterial pH from 7.38 +/- 0.01 to 7.00 +/- 0.02 (P less than 0.01). CBF measured by the tracer microsphere technique was decreased by 12% from 69 +/- 6 to 61 +/- 4 ml.min-1.100 g-1 (P less than 0.05). Infusion of 0.6 N NaCl as a hypertonic control had no effect on CBF. Cerebral metabolic rate for O2 and O2 extraction was not significantly changed from control (3.83 +/- 0.20 ml.min-1.100 g-1 and 5.7 +/- 0.6 ml/100 ml, respectively) during acid infusion. Cerebral venous PO2 was increased from 41.6 +/- 2.1 to 53.8 +/- 4.0 Torr by HCl infusion (P less than 0.02) associated with a shift in O2-hemoglobin affinity of blood in vivo from 38 +/- 2 to 50 +/- 1 Torr. Cisternal cerebrospinal fluid pH decreased from 7.336 +/- 0.014 to 7.226 +/- 0.027 (P less than 0.005), but cerebrospinal fluid HCO3- concentration was not changed from control (25.4 +/- 1.0 meq/l). These data suggest that there is a functional blood-brain barrier in newborn piglets, that is relatively impermeable to HCO3- or H+ and maintains cerebral perivascular pH constant in the face of acute severe arterial acidosis. (ABSTRACT TRUNCATED AT 250 WORDS)
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Weigle, C. G., R. C. Koehler, S. W. Brusilow, and R. J. Traystman. "Arterial pH modulation of regional cerebral blood flow during hyperammonemia in dogs." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 1 (July 1, 1990): H34—H41. http://dx.doi.org/10.1152/ajpheart.1990.259.1.h34.
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Acute hyperammonemia at normal arterial pH causes selective increases in midbrain blood flow in dogs. Unexpectedly, further increases occur with hypocapnia. We investigated whether metabolic acidemia and alkalemia modulate the distribution of ammonium across the blood-brain barrier and if, in turn, midbrain blood flow is effectively modulated. In dogs anesthetized with pentobarbital sodium, hyperammonemia (approximately 940 microM) was produced by a 210-min infusion of ammonium acetate. Concurrent infusion of NaHCO3 increased arterial pH to 7.53 +/- 0.02 (SE), whereas HCl infusion decreased pH to 7.11 +/- 0.01. Normocapnia was maintained. Cerebrospinal fluid [HCO3-] increased 5 mM with alkalemia (one-half of the increase in blood) and was unchanged with acidemia. Thus cerebrospinal fluid [H+]/blood [H+] was greater with alkalemia than acidemia. The corresponding ratio for ammonium was likewise greater with alkalemia (0.70 +/- 0.06) than acidemia (0.44 +/- 0.08). Microsphere-determined blood flow to midbrain more than doubled in the alkalemic group but was unchanged in the acidemic group. No other region along the neuraxis or in cerebrum showed increased blood flow in either hyperammonemic group. Alkalemia without hyperammonemia did not increase midbrain blood flow. Thus metabolic acidemia-alkalemia significantly alters ammonium partitioning into cerebrospinal fluid, and this alteration is sufficiently great to exert a specific physiological effect manifested by changes in midbrain blood flow.
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Martin, Robert C. G., Lisa Rustein, Daniel Pérez Enguix, Julio Palmero, Victor Carvalheiro, Jose Urbano, Alessandro Valdata, Ivan Kralj, Petar Bosnjakovic, and Cliff Tatum. "Hepatic Arterial Infusion of Doxorubicin-Loaded Microsphere for Treatment of Hepatocellular Cancer: A Multi-Institutional Registry." Journal of the American College of Surgeons 213, no. 4 (October 2011): 493–500. http://dx.doi.org/10.1016/j.jamcollsurg.2011.07.010.
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Eberlein, T. J. "Hepatic Arterial Infusion of Doxorubicin-Loaded Microsphere for Treatment of Hepatocellular Cancer: A Multi-Institutional Registry." Yearbook of Surgery 2012 (January 2012): 337–39. http://dx.doi.org/10.1016/j.ysur.2012.01.010.
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Tabrizchi, Reza, and Catherine Cheuk Ying Pang. "Comparative effects of rauwolscine, prazosin, and phentolamine on blood pressure and cardiac output in anesthetized rats." Canadian Journal of Physiology and Pharmacology 65, no. 7 (July 1, 1987): 1421–27. http://dx.doi.org/10.1139/y87-223.
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The endogenous role of the α-adrenergic system in the maintenance of mean arterial pressure (MAP), total peripheral resistance (TPR), cardiac output (CO) and its distribution, and plasma norepinephrine and epinephrine release was investigated by the administration of selective α-adrenoceptor antagonists to halothane-anesthetized rats. The blockade of α1, α2-, and both α1 and α2-receptors was accomplished by i.v. infusions of prazosin, rauwolscine, and phentolamine, respectively. The microsphere technique was used for the determination of CO and its distribution. Since the infusions of the three antagonists caused similar decreases of MAP and heart rate, the results suggest that postjunctional α1 and α2-receptors are both important in the control of MAP. During the infusion of prazosin, TPR was decreased but CO was not changed. In contrast, CO was decreased but TPR was not changed during the infusions of rauwolscine and phentolamine. Thus, CO was reduced after the blockade of α2-but not α1 receptors. All three antagonists caused an increase in percent distribution of CO to the lungs and muscle, suggesting that the sympathetic nervous system plays the greatest vasoconstrictor influence in the lungs and muscle via stimulations of both subtypes of α-adrenoceptors. The administration of either prazosin or rauwolscine caused little change in plasma catecholamine levels. In contrast, phentolamine caused large increases in both epinephrine and norepinephrine levels. Therefore catecholamine release was only increased after concurrent blockade of both α1 and α2-adrenoceptors.
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Thurlby, Peter L., and Rodney D. M. Ellis. "Differences between the effects of noradrenaline and the β-adrenoceptor agonist BRL 28410 in brown adipose tissue and hind limb of the anaesthetized rat." Canadian Journal of Physiology and Pharmacology 64, no. 8 (August 1, 1986): 1111–14. http://dx.doi.org/10.1139/y86-189.
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In mature (450–600 g) 21 °C-acclimated male rats, anaesthetized with urethane, blood flow (measured by the radioactive microsphere technique) to brown adipose tissue (BAT) was determined during the infusion of the β-adrenoceptor agonist BRL 28410 or noradrenaline bitartrate at doses chosen to give similar increases in whole body oxygen uptake. Blood flow to BAT during BRL 28410 infusion was only about one third of that found during noradrenaline infusion although increases in whole body thermogenesis were similar (55 and 77% for BRL 28410 and noradrenaline, respectively). This suggests that BAT may be less involved in the thermogenic response to BRL 28410 than to noradrenaline. In a separate experiment using slightly smaller rats (350–500 g) hind limb oxygen uptake was measured in situ using a venous bypass preparation. BRL 28410, at a dose having a maximum effect on whole body thermogenesis (53% increase), had no effect on oxygen delivery to the hind limb but significantly increased oxygen extraction by 33% (p < 0.001). In contrast, noradrenaline, also at a dose that maximally increased whole body thermogenesis, led to a 35% decrease in oxygen delivery to the hind limb and no change in oxygen extraction. For the thermogenic β-agonist BRL 28410 the hind limb, and presumably muscular tissue in general, may be contributing to thermogenesis.
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Bere, Zsófia, Tihomir P. Obrenovitch, Gábor Kozák, Ferenc Bari, and Eszter Farkas. "Imaging Reveals the Focal Area of Spreading Depolarizations and a Variety of Hemodynamic Responses in a Rat Microembolic Stroke Model." Journal of Cerebral Blood Flow & Metabolism 34, no. 10 (July 30, 2014): 1695–705. http://dx.doi.org/10.1038/jcbfm.2014.136.
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Spreading depolarizations (SDs) occur in stroke, but the spatial association between SDs and the corresponding hemodynamic changes is incompletely understood. We applied multimodal imaging to visualize the focal area of selected SDs, and hemodynamic responses with SDs propagating over the ischemic cortex. The intracarotid infusion of polyethylene microspheres ( d = 45 to 53 μm) produced multifocal ischemia in anesthetized rats ( n = 7). Synchronous image sequences captured through a cranial window above the frontoparietal cortex revealed: Changes in membrane potential (voltage-sensitive (VS) dye method); cerebral blood flow (CBF; laser speckle contrast (LSC) imaging); and hemoglobin (Hb) deoxygenation (red intrinsic optical signal (IOS) at 620 to 640 nm). A total of 31 SD events were identified. The foci of five SDs were seen in the cranial window, originating where CBF was the lowest (56.9 ± 9%), but without evident signs of infarcts. The hyperemic CBF responses to propagating SDs were coupled with three types of Hb saturation kinetics. More accentuated Hb desaturation was related to a larger decrease in CBF shortly after ischemia induction. Microsphere-induced embolization triggers SDs in the rat brain, relevant for small embolic infarcts in patients. The SD occurrence during the early phase of ischemia is not tightly associated with immediate infarct evolution. Various kinetics of Hb saturation may determine the metabolic consequences of individual SDs.
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Yang, H. T., Robert W. Ogilvie, and Ronald L. Terjung. "Exercise training enhances basic fibroblast growth factor-induced collateral blood flow." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 6 (June 1, 1998): H2053—H2061. http://dx.doi.org/10.1152/ajpheart.1998.274.6.h2053.
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This study evaluated whether daily exercise would enhance the peripheral collateral vessel development found in response to exogenous basic fibroblast growth factor (bFGF) infusion. After bilateral femoral occlusion, male Sprague-Dawley rats (∼325 g) received intra-arterial infusions of either bFGF (1 μg/day; n = 15) or carrier solution ( n = 13) via osmotic pumps for 2 wk. Subgroups of each treatment were kept sedentary (cage activity) or trained by walking at 20 m/min at 15% grade, two times a day, 5 days/wk for 4 wk. Training markedly increased citrate synthase activity in the active muscle ( P < 0.001). Muscle function and blood flows (85Sr microsphere) were evaluated using an isolated hindquarter perfused at 100 mmHg via the abdominal aorta. The significant increase in blood flow to the entire hindlimb in the sedentary animals, caused by bFGF infusion ( P < 0.05), was further increased ( P < 0.01) in the bFGF-trained group. The quantitatively largest increases in blood flows were observed in the collateral-dependent tissues of the distal hindlimb. Blood flows to the entire calf muscle group increased ∼140% in carrier-trained ( P < 0.001), ∼180% in bFGF sedentary ( P< 0.001), and ∼240% in the bFGF-trained ( P < 0.001) groups compared with the carrier sedentary group. The increases in collateral blood flow were functionally important, as improvements in calf muscle performance correlated with measured blood flows. Our results demonstrate that exogenous bFGF administration in combination with a moderate-intensity exercise program greatly increases collateral-dependent blood flow and improves muscle performance. That physical activity enriched the bFGF response is consistent with the hypothesis that hemodynamic factors are important contributors to collateral vessel enlargement.
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Hussain, S. N., F. Rutledge, R. Graham, S. Magder, and C. Roussos. "Effects of norepinephrine and fluid administration on diaphragmatic O2 consumption in septic shock." Journal of Applied Physiology 62, no. 4 (April 1, 1987): 1368–76. http://dx.doi.org/10.1152/jappl.1987.62.4.1368.
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The effects of norepinephrine infusion and fluid administration on diaphragmatic O2 consumption during endotoxic shock were assessed in spontaneously breathing anesthetized dogs. Blood flow was measured with the microsphere technique, and diaphragmatic venous blood was obtained via a catheter inserted into the left inferior phrenic vein. One group of dogs (n = 6) received 10 mg/kg Escherichia coli endotoxin intravenously (E group). In the second and third groups, blood pressure after endotoxin injection was restored by continuous infusion of norepinephrine tartrate (N group) or by infusion of normal saline and dextran infusion (F group). The animals were observed for 2 h after endotoxin injection. Cardiac output fell significantly in the E and N group, whereas it was restored in the F group. Minute ventilation and diaphragmatic pressure-time index rose twofold in the three groups of dogs. Diaphragmatic O2 consumption (VO2 di) increased substantially in the E group to a mean value of 3.46 ml X 100 g-1 X min-1, which was achieved by higher blood flow and by an increase in O2 extraction. In the N group, VO2 di was higher than control but was lower than that of the E group (mean value of 1.43 ml X 100 g-1 X min-1), which was achieved solely by increasing O2 extraction. In the F group, VO2 di was also lower than that of the E group (mean value of 1.51 ml X 100 g-1 X min-1), which was achieved by high diaphragmatic blood flow. Thus, at any given diaphragmatic task, the diaphragm consumed less O2 in the N and F group than in the E group.
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Gorman, M. W., R. D. Wangler, and H. V. Sparks. "Distribution of perfusate flow during vasodilation in isolated guinea pig heart." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 1 (January 1, 1989): H297—H301. http://dx.doi.org/10.1152/ajpheart.1989.256.1.h297.
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The purpose of this study was to determine the effect of vasodilation on the distribution of perfusate flow in the isolated guinea pig heart. Hearts were perfused retrogradely through the aorta with oxygenated Krebs-Henseleit buffer solution at 37 degrees C. Regional myocardial flows were measured with 15-micron radioactive microspheres. Each heart was subdivided into 45 pieces (average size 44 mg), and heterogeneity of flow was quantified as the relative dispersion (standard deviation/mean). Under control conditions at a perfusion pressure of 46 mmHg (60 cm water), the relative dispersion of left ventricular (LV) flow was 30 +/- 2% (n = 8). Vasodilation was induced via infusion of dipyridamole (10(-5) M). When flow was held constant at the resting value, relative flow dispersion increased to 43 +/- 6% (n = 8). When perfusion pressure was held constant and flow allowed to increase, relative dispersion fell to 20 +/- 5% (n = 5). Heterogeneity for the heart as a whole was higher than for the left ventricle but followed the same pattern with vasodilation. In a separate series of hearts (n = 5) equipped with LV balloons but without microsphere flow measurements, vasodilation at constant flow decreased LV pressure development, dP/dt, and O2 consumption. Vasodilation at constant pressure increased O2 consumption, but did not increase LV pressure or dP/dt. We conclude that vasodilation in this preparation will increase flow heterogeneity during constant-flow perfusion but decrease heterogeneity during constant-pressure perfusion. Furthermore, increased flow heterogeneity can compromise ventricular function.
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Harris, W. H., D. O. Foster, and B. E. Nadeau. "The relationship between the thermogenic response of brown adipose tissue and age during noradrenaline infusion in the young rabbit." Canadian Journal of Physiology and Pharmacology 63, no. 10 (October 1, 1985): 1215–20. http://dx.doi.org/10.1139/y85-201.
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This work was undertaken to determine if the thermogenic activity of brown fat decreased with age in young rabbits despite the morphological evidence indicating persistence of the brown adipocytes at 4 weeks of age. Data obtained by infusing five doses of noradrenaline and measuring oxygen consumption were used to construct cumulative dose–response curves for five age groups between 3 and 32 days of age. Blood flow to brown fat and other tissues was measured by the microsphere method at 1 and 3 weeks of age. The noradrenaline-induced increase in oxygen consumption when expressed as a percentage of resting oxygen consumption in millilitres per 100 g of body weight decreased (p < 0.05) with age. However, the absolute noradrenaline-induced increase in metabolic rate (millilitres per minute) increased with age. Total blood flow to brown fat (millilitres per minute) during noradrenaline infusion was unchanged between 1 and 3 weeks of age, but when the blood flow was expressed in millilitres per minute per gram of tissue flow decreased significantly (p < 0.05) probably because of infiltration of brown fat with white fat. These data suggest that the amount of brown fat and its thermogenic capacity remain relatively constant between 1 and 3 weeks of age, but as a thermogenic organ, brown fat becomes proportionally less effective with age because of the large increase in body mass.
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Kingma Jr., J. G., Y. Qiu, and D. J. Hearse. "Influence of low-flow infusion and magnesium on tissue necrosis during regional ischemia in the canine myocardium." Canadian Journal of Physiology and Pharmacology 70, no. 7 (July 1, 1992): 1004–10. http://dx.doi.org/10.1139/y92-138.
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Passive intracoronary perfusion of therapeutic agents has been used in the clinical setting to attenuate the effects of brief episodes of myocardial ischemia. The objective of this study was to assess the effects of low-flow coronary infusion with or without Mg2+ on tissue necrosis and cardiac hemodynamics after prolonged regional ischemia. In 33 anesthetized dogs (5 excluded during study), the left anterior descending coronary artery was occluded for 6 h. Dogs were assigned to three groups: the first group (n = 8) was subjected to 6 h coronary occlusion without low-flow perfusion (controls), the second group (n = 10) received a low-flow coronary infusion of Ringer's lactate (Mg2+-free), and the third group (n = 10) received a low-flow coronary infusion of Ringer's lactate plus Mg2+ sulfate (15 mM). Tissue necrosis was evaluated using tetrazolium staining and was normalized to the principal baseline predictors of infarct size including anatomic risk zone (microsphere autoradiography) and coronary collateral flow. In control hearts, infarct size comprised 51.1 ± 4.1% of the risk zone (40.8 ± 5.1% left ventricular cross-sectional area (LV)). In the Mg2+-free and Mg2+ groups, risk zone size was 17.3 ± 2.2 and 16.8 ± 1.8% LV (p < 0.05 vs. controls), while infarct size was 23.1 ± 3.1 and 24.9 ± 8.1% (p < 0.05 vs. controls), respectively. Coronary collateral flow in the endocardium was similar for all of the experimental groups; however, hearts subjected to ischemia with low-flow perfusion of Ringer's lactate demonstrated significantly higher epicardial coronary collateral flow levels compared with controls. Our findings demonstrate that low-flow infusion of Ringer's solution (with or without Mg2+) into the ischemic zone produced significantly smaller infarcts; however, after 6 h of ischemia we could not demonstrate an additional beneficial effect of Mg2+.Key words: myocardial ischemia, infarct size, low-flow passive perfusion, Mg2+.
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Bersten, A. D., W. J. Sibbald, M. Hersch, H. Cheung, and F. S. Rutledge. "Interaction of sepsis and sepsis plus sympathomimetics on myocardial oxygen availability." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 4 (April 1, 1992): H1164—H1173. http://dx.doi.org/10.1152/ajpheart.1992.262.4.h1164.
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The ability to regulate myocardial blood flows (Q) in accord with changing myocardial O2 needs may be depressed in sepsis. This could be an important concern when sympathomimetics are used to augment systemic oxygen delivery (QO2) in this syndrome as increased myocardial O2 needs may accompany an infusion of this class of drugs. Therefore after measuring the effect of sepsis on myocardial O2 metabolism, we then infused various sympathomimetics to evaluate the sepsis+sympathomimetic interaction on myocardial QO2. We measured Q to the left (LV) and right (RV) ventricles by the radioactive microsphere technique in 36 unanesthetized mature sheep, before and during the infusion of dopamine, dobutamine, dopexamine, norepinephrine, salbutamol, or placebo. Randomly selected for infusion, these drugs were titrated to augment the thermodilution-derived cardiac index (CI) by greater than 20%. This study was repeated 24-48 h after cecal ligation and perforation had resulted in a hyperdynamic septic state [change (delta) in CI = sepsis - baseline = +54%; P less than 0.01]. During the septic study, both Q-LV (delta = +80%; P less than 0.01) and Q-RV (delta = +84%; P less than 0.01) were increased above baseline values; the augmented Q to both LV and RV was directly correlated with the arterial perfusion pressure (PA) x CI product and the mean pulmonary artery pressure (PPA) x CI product, respectively. Only 23% of study animals demonstrated net transmyocardial lactate production during the septic study. When the infusion of sympathomimetics was accompanied by an increase in the PPA x CI and PA x CI products, a further increase in both Q-RV and Q-LV, respectively, occurred. Also, neither the ventricular endocardial-to-epicardial flow ratios nor transmyocardial lactate extraction were modified by the sympathomimetics infusion. We conclude that the septic response to infection in this animal model was not accompanied by significant abnormalities in the metabolic regulation of myocardial QO2 (R. E. Cunnion, G. L. Scher, and M. M. Parker, Circulation 73: 637-644, 1986).
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Zhang, Xiao-Jun, Øivind Irtun, Yaoqing Zheng, and Robert R. Wolfe. "Methysergide reduces nonnutritive blood flow in normal and scalded skin." American Journal of Physiology-Endocrinology and Metabolism 278, no. 3 (March 1, 2000): E452—E461. http://dx.doi.org/10.1152/ajpendo.2000.278.3.e452.
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Methysergide is a serotonin antagonist and has been demonstrated to reduce wound blood flow and edema formation. We have determined the effect of methysergide on protein kinetics in normal and scalded skin of anesthetized rabbits.l-[ ring-13C6]- orl-[ ring-2H5]phenylalanine was used to reflect skin protein kinetics by use of an ear model, andl-[1-13C]leucine was used to reflect whole body protein kinetics. The results were that infusion of methysergide (2–3 mg ⋅ kg− 1 ⋅ h− 1) reduced the blood flow rate in normal skin by 50% without changing skin or whole body protein kinetics. After scald injury on the ear, administration of methysergide for 48 h reduced the weight of scalded ears (43 ± 4 vs. 30 ± 5 g, P < 0.01) and ear blood flow rate (42.6 ± 4.9 vs. 5.8 ± 1.0 ml ⋅ 100 g− 1 ⋅ min− 1, P < 0.0001) and did not change wound protein kinetics. Methysergide reduced arteriovenous shunting and maintained inward phenylalanine transport from the blood to the skin pool. Using the microsphere technique, we found that the infusion of methysergide decreased blood perfusion by 33–36% in both normal and scalded ear skin. We conclude that methysergide administration reduces nonnutritive, as opposed to nutritive, blood flow in normal and scalded skin.
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Murakami, H., S. J. Kim, and H. F. Downey. "Persistent right coronary flow reserve at low perfusion pressure." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 4 (April 1, 1989): H1176—H1184. http://dx.doi.org/10.1152/ajpheart.1989.256.4.h1176.
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To determine whether right coronary (RC) flow reserve persists at perfusion pressures below the apparent autoregulatory range, the RC artery of 18 anesthetized dogs was cannulated and perfused at controlled pressures. RC blood flow (RCBF) fell from 65.3 +/- 6.1 to 33.7 +/- 2.3 ml.min-1.100 g-1 as RC perfusion pressure (RCPP) was reduced from 80 to 40 mmHg. At 40 mmHg, intracoronary adenosine increased RCBF by 97.9 +/- 10.6 ml.min-1.100 g-1 (P less than 0.001). RCBF fell to 9.5 +/- 1.7 ml.min-1.100 g-1 at 20 mmHg, and RCBF did not significantly increase during adenosine, although RC vasodilation was observed in four dogs. Regional right ventricular (RV) blood flows at RCPP of 80 and 40 mmHg were measured by radioactive microsphere technique. Before adenosine infusion, RCBF was distributed uniformly across the RV free wall at normal and low perfusion pressures. During adenosine infusion, blood flow in both regions increased significantly, but the flow reserve was greater in the subendocardial region at both normal and reduced pressures. RV myocardial O2 consumption (MVo2) was decreased significantly at 40 mmHg, however, there was no evidence of ischemia at this pressure, since the RV lactate extraction ratio was normal (n = 8). Thus RV O2 demand fell when RC O2 supply was reduced, although a flow reserve was available. RV MVo2 was restored to normal when right coronary flow reserve was mobilized by adenosine infusion. For RCBF from 65 to 365 ml.min-1.100 g-1, RC venous O2 content rose and RV MVo2 was essentially constant.(ABSTRACT TRUNCATED AT 250 WORDS)
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Tamaki, N., C. A. Rabito, N. M. Alpert, T. Yasuda, J. A. Correia, M. Barlai-Kovach, M. Kanke, S. C. Dragotakes, and H. W. Strauss. "Serial analysis of renal blood flow by positron tomography with rubidium-82." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 5 (November 1, 1986): H1024—H1030. http://dx.doi.org/10.1152/ajpheart.1986.251.5.h1024.
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To determine whether renal blood flow can be measured by positron-emission tomography (PET) during constant infusion of rubidium-82 (82Rb) using a steady-state kinetic model, studies were performed in 10 dogs at control (n = 10), during mild flow reduction (n = 7), during severe flow reduction (n = 10), and after reperfusion of the kidney (n = 3). PET data were quantified to determine mean concentration of 82Rb (Ct) in each transverse section of the kidney. The arterial concentration (Ca) of 82Rb was measured by well counting of arterial blood samples during the equilibrium scan. 82Rb renal uptake (Ct/Ca) correlated nonlinearly with microsphere renal blood flow according to a steady-state kinetic model (r = 0.90). 82Rb estimated flow was 3.16 +/- 1.36 ml X min-1 X g-1 at control and 1.56 +/- 0.57 and 0.37 +/- 0.59 during mild and severe flow reductions, respectively. Microsphere determined flow was 2.89 +/- 0.77 ml X min-1 X g-1 at control, 1.58 +/- 0.42 at mild reduction, and 0.27 +/- 0.49 at severe reduction. In the occlusion and reperfusion model, the 82Rb estimated flow during occlusion was 0.21 +/- 0.15 ml X min-1 X g-1 and on reperfusion went up to 2.13 +/- 1.08. The contralateral kidney demonstrated reductions in the 82Rb estimated flow of 3.02 +/- 1.62 ml X min-1 X g-1 (63%) and 2.92 +/- 0.89 (61%) during mild and severe flow reductions, respectively. We conclude that PET with 82Rb permits serial quantitative assessment of renal flood flow.
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Lamm, Wayne J. E., Susan L. Bernard, Wiltz W. Wagner, and Robb W. Glenny. "Intravital microscopic observations of 15-μm microspheres lodging in the pulmonary microcirculation." Journal of Applied Physiology 98, no. 6 (June 2005): 2242–48. http://dx.doi.org/10.1152/japplphysiol.01199.2004.
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Vascular infusions of 15-μm-diameter microspheres are used to study pulmonary blood flow distribution. The sites of microsphere lodging and their effects on microvascular perfusion are debated but unknown. Using intravital microscopy of the subpleural surface of rat lungs, we directly observed deposition of fluorescent microspheres. In a pump-perfused lung model, ∼0.5 million microspheres were infused over 30 s into the pulmonary artery of seven rats. Microsphere lodging was analyzed for the location in the microvasculature and the effect on local flow after lodging. On average, we observed 3.2 microspheres per 160 alveolar facets. The microspheres always entered the arterioles as singlets and lodged at the inlets to capillaries, either in alveolar corner vessels or small arterioles. In all cases, blood flow continued either around the microspheres or into the capillaries via adjacent pathways. We conclude that 15-μm-diameter microspheres, in doses in excess of those used in typical studies, have no significant impact on pulmonary capillary blood flow distribution.
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Drescher, Robert, Falk Gühne, Philipp Seifert, Christian Kühnel, and Martin Freesmeyer. "Ex Vivo Evaluation of Residual Activity and Infusion Dynamics in a Commercially Available Yttrium-90 Resin Microsphere Administration System." Journal of Vascular and Interventional Radiology 30, no. 9 (September 2019): 1504–11. http://dx.doi.org/10.1016/j.jvir.2018.10.019.
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Grindstaff, Ryan J., Regina R. Grindstaff, Margaret J. Sullivan, and J. Thomas Cunningham. "Role of the locus ceruleus in baroreceptor regulation of supraoptic vasopressin neurons in the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 1 (July 1, 2000): R306—R319. http://dx.doi.org/10.1152/ajpregu.2000.279.1.r306.
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The goal of this study was to identify the source of baroreceptor-related noradrenergic innervation of the diagonal band of Broca (DBB). Male Sprague-Dawley rats underwent sinoaortic denervation (SAD, n = 13) or sham SAD surgery ( n = 13). We examined Fos expression produced by baroreceptor activation and dopamine-β-hydroxylase immunofluorescence in hindbrain regions that contain noradrenergic neurons. Baroreceptors were stimulated by increasing blood pressure >40 mmHg with phenylephrine (10 μg · kg−1· min−1 iv) in sham SAD and SAD rats. Controls were infused with 0.9% saline. Only the locus ceruleus (LC) demonstrated a baroreceptor-dependent increase in Fos immunoreactivity in dopamine-β-hydroxylase-positive neurons. In a second experiment, normal rats received rhodamine-labeled microsphere injections in the DBB ( n = 12) before phenylephrine or vehicle infusion. In these experiments, only the LC consistently contained Fos-positive cells after phenylephrine infusion that were retrogradely labeled from the DBB. Finally, we lesioned the LC with ibotenic acid and obtained extracellular recordings from identified vasopressin neurons in the supraoptic nucleus. LC lesions significantly reduced the number of vasopressin neurons that were inhibited by acute baroreceptor stimulation. Together, these results suggest that noradrenergic neurons in the LC participate in the baroreflex activation of the DBB and may thus be important in the baroreflex inhibition of vasopressin-releasing neurons in the supraoptic nucleus.
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Mazer, C. D., B. A. Cason, W. C. Stanley, C. B. Shnier, J. A. Wisneski, and R. F. Hickey. "Dichloroacetate stimulates carbohydrate metabolism but does not improve systolic function in ischemic pig heart." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 2 (February 1, 1995): H879—H885. http://dx.doi.org/10.1152/ajpheart.1995.268.2.h879.
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Increased carbohydrate utilization may protect the heart during ischemia and reperfusion. Dichloroacetate (DCA) stimulates pyruvate dehydrogenase, which is the rate-limiting step in oxidation of lactate and pyruvate. The purpose of this study was to determine if the myocardial metabolic changes induced by intracoronary DCA during myocardial ischemia were accompanied by improvement in systolic function. A perfusion circuit was created from the carotid to left anterior descending coronary artery (LAD) in 11 anesthetized Yorkshire swine. Data were obtained under strict hemodynamic control at baseline, after 15 min of moderate (30%) LAD flow reduction, and after an additional 15 min of ischemia with either intracoronary DCA (3 mM, n = 6) or saline (n = 5) infusion. DCA decreased lactate release and increased lactate uptake during ischemia as measured by glucose and lactate carbon-labeled tracers. Despite these metabolic changes, no improvement in systolic shortening, microsphere blood flow, or oxygen consumption occurred. Thus, although DCA stimulated carbohydrate metabolism during myocardial ischemia, it did not directly improve systolic function.
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Jansson, L., and C. Hellerstrom. "Glucose-induced changes in pancreatic islet blood flow mediated by central nervous system." American Journal of Physiology-Endocrinology and Metabolism 251, no. 6 (December 1, 1986): E644—E647. http://dx.doi.org/10.1152/ajpendo.1986.251.6.e644.
Full textAbstract:
Earlier experiments with the microsphere technique suggested that a heightened serum glucose concentration consistently leads to an increase in islet blood flow (IBF). Several lines of evidence suggest that this glucose-sensitive control mechanism is located at an extrapancreatic site. The purpose of this study was to define the possible role of the central nervous system in such a mechanism. D-glucose, L-glucose, 3-O-methylglucose, or saline were therefore infused into the carotid artery, each at a dose of 1 mg X kg body wt-1 X min-1 for 3 min, and the pancreatic and islet blood flows were measured. None of these substances affected the systemic serum glucose level. The intracarotid infusion of D-glucose, however, caused a rapid increase in both the serum insulin concentration and IBF. The blood flow to the whole pancreas nevertheless remained unchanged, indicating a redistribution of flow within the gland. Carotid infusion of the other test substances or a similar amount of D-glucose given in a femoral vein did not affect these parameters. Both the increase in serum insulin concentration and the increase in IBF caused by D-glucose could be abolished by vagotomy or administration of atropine. When the systemic blood glucose concentration was increased by intraperitoneal glucose administration (2 g/kg body wt), vagotomy blocked the increase in islet blood flow but not the concomitant insulin release. These observations suggest that the glucose-induced increase in IBF is mediated by vagal cholinergic influences.
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Fiorentini, G., C. Aliberti, P. Giovanis, M. Tilli, S. Rossi, and G. Benea. "Trans-arterial chemoembolization (TACE) of liver metastases (LM) from colorectal cancer (CRC) adopting irinotecan-eluting beads: Results of a phase II clinical study." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 14525. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.14525.
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14525 Background: Patients with LM from CRC have a poor prognosis with survival rates of 31% at 1 year and 2.6% at 3 years. Surgery is feasible in a minority of patients and most them received systemic chemotherapy. Irinotecan (IRI) is an active drug in the treatment of advanced CRC. The advantage of delivering chemotherapy by hepatic arterial infusion is the achievement of high-dose of the drug in the target . TACE is a combination of local drug infusion with selective embolization of the feeding arteries of the liver metastases. DC bead is a new embolic microsphere product that can be loaded with IRI before administration in TACE. The purpose of this study is to assess the safety and efficacy of this new embolic microspheres IRI loaded and administered as TACE in patients with LM from CRC. Methods: 35 patients with LM from CRC Stage II-III Pettavel Classification pretreated were observed from Nov 2005 to Dec 2006. 25 gave their written consent to be treated with one o more cycles of TACE. Imaging was performed before, immediately and 4 weeks after TACE to determine response and the need for further treatment. Each patient received i.v hydration, antibiotics, analgesics and medications against nausea before TACE. Survival was calculated with Kaplan-Meier method. Results: 60 cycles were administered. We observed a Response Rate of 80% by RECIST criteria. A month after TACE we had a reduction of +50% of CEA in 60% of patients. A reduction of the lesional contrast enhancement of the metastases was observed in 80% of patients. 22 patients are alive, with a median survival of 9.5 months (range 6–13). Median duration response was 16 weeks (range 12–25). 14 cases experienced WHO Grade 2 right upper quadrant pain (RUQP) and 11 cases Grade 3 lasting 12 hours (range 3–30). All patients had 2 days Grade 2 fever (range 1–7), ten had 3 days Grade 3. 20 have had Grade 2 nausea and vomiting for 6 hours (range 4–29). No alopecia or marrow toxicity was reported. Conclusions: DC bead -TACE was feasible and effective in patients with LM from CRC. RUQP seems the most significant toxic event and needs analgesic therapy. No survival data are conclusive because the follow up is short. DC bead of IRI 100 mgr-TACE myght be an appropriate palliative therapy for these patients. No significant financial relationships to disclose.
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Bouder, T. G., L. J. Huffman, and G. A. Hedge. "Effects of vasoactive intestinal peptide on vascular conductance are unaffected by anesthesia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255, no. 6 (December 1, 1988): R968—R973. http://dx.doi.org/10.1152/ajpregu.1988.255.6.r968.
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In rats anesthetized with ketamine and pentobarbital (KET/PB), vasoactive intestinal peptide (VIP) increases vascular conductance (VC) in the salivary gland, pancreas, and thyroid gland, whereas no changes in VC are observed in a number of other organs. Because anesthesia may alter the responsiveness of physiological systems, we compared the effects of VIP on organ VC in conscious or anesthetized rats. Chronically catheterized rats were studied in the conscious state or 30 min after induction of anesthesia with KET/PB, isoflurane, or Inactin. Blood flows were measured by the reference sample version of the radioactive microsphere (MS) technique using two MS injections (141Ce-MS/85Sr-MS). Mean arterial blood pressure was monitored and used in the calculation of VC. Organ VCs were similar under basal conditions in conscious and anesthetized rats. VIP infusion caused systemic hypotension and increased VCs in the salivary gland, pancreas, and thyroid gland, and these responses were largely unaffected by anesthesia. These results indicate that the anesthetics used do not alter basal VC or the responsiveness of the vasculature to exogenous VIP.
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Meyer, J., F. Hinder, J. Stothert, L. D. Traber, D. N. Herndon, J. T. Flynn, and D. L. Traber. "Increased organ blood flow in chronic endotoxemia is reversed by nitric oxide synthase inhibition." Journal of Applied Physiology 76, no. 6 (June 1, 1994): 2785–93. http://dx.doi.org/10.1152/jappl.1994.76.6.2785.
Full textAbstract:
We evaluated regional blood flows in a hyperdynamic sepsis model and the reversal of increased flows by blockade of nitric oxide (NO) synthase. Seven awake sheep were continuously infused with Escherichia coli endotoxin [lipopolysaccharide (LPS), 10 ng.kg-1.min-1] for 48 h. The NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 25 mg/kg) was injected after 24 h. Blood flows to systemic organs were determined with the radioactive microsphere technique. LPS induced elevation of cardiac index by 36% (P < 0.05) and a fall in systemic vascular resistance index by 37% (P < 0.05) at 0 h [time of L-NAME administration, 24 h after infusion of LPS had begun] L-NAME administration normalized cardiac index [6.1 +/- 0.5 at 4 h posttreatment, 6.1 +/- 0.5 l.min-1.m-2 at -24 h (baseline)] and systemic vascular resistance index (1,333 +/- 105 at 4 h posttreatment, 1,280 +/- 163 dyn.s.cm-5.m2 at -24 h) and reduced all regional blood flows to near-baseline levels for the remainder of the study period (24 h). O2 consumption was unaffected by treatment.
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Wu, Lin, Anna Olverling, Zhen Huang, Leif Jansson, Hongfen Chao, Xin Gao, and Åke Sjöholm. "GLP-1, exendin-4 and C-peptide regulate pancreatic islet microcirculation, insulin secretion and glucose tolerance in rats." Clinical Science 122, no. 8 (December 14, 2011): 375–84. http://dx.doi.org/10.1042/cs20090464.
Full textAbstract:
GLP-1 (glucagon-like peptide 1) and its mimetic exendin-4 are used against Type 2 diabetes. C-peptide has also proven promising to enhance insulin action. Since insulin secretion in vivo can be rapidly tuned by changes in islet microcirculation, we evaluated the influence of GLP-1, exendin-4 and C-peptide on pancreatic IBF (islet blood flow), and dynamic changes in insulin secretion and glycaemia in the rat. Adult male Wistar rats were divided into four groups given intravenous saline, GLP-1, exendin-4 or C-peptide respectively and administered either saline or 30% glucose. Furthermore, we investigated the effect of intravenous infusion of different doses of exendin-4 into either the femoral vein or the portal vein on islet microcirculation. A non-radioactive microsphere technique was adopted to measure the regional blood flow. Both GLP-1 and exendin-4 prevented the glucose-induced PBF (pancreatic blood flow) redistribution into the islets. Infusion of exendin-4 into the portal vein did not alter pancreatic islet microcirculation, while infusion of exendin-4 into femoral vein significantly decreased basal IBF. C-peptide increased basal IBF and the proportion of IBF out of total PBF, but did not affect the islet microcirculation after glucose administration. GLP-1, exendin-4 and C-peptide stimulated insulin secretion and significantly decreased glycaemia. Blocking NO formation did not prevent the decreased IBF and post-load glycaemia evoked by exendin-4, but further decreased IBF and KBF (kidney blood flow) and increased basal glycaemia. Blocking the vagus nerve enhanced pancreatic IBF and further decreased post-load glycaemia and KBF and increased basal glycaemia. The vascular modulatory effect on pancreatic islet microcirculation described herein, with subsequent effects on in vivo insulin secretion and glycaemia, might be one of the mechanisms underlying the anti-diabetic actions of GLP-1 and its long acting mimetic exendin-4, as well as that of C-peptide.
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Stephens, John, Barbara Stoll, Jeremy Cottrell, Xiaoyan Chang, Michael Helmrath, and Douglas G. Burrin. "Glucagon-like peptide-2 acutely increases proximal small intestinal blood flow in TPN-fed neonatal piglets." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 2 (February 2006): R283—R289. http://dx.doi.org/10.1152/ajpregu.00588.2005.
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Glucagon-like peptide-2 (GLP-2) is a gut hormone that is secreted in response to enteral feeding and stimulates small intestinal mucosal growth. We have previously shown that GLP-2 infusion acutely increases portal venous blood flow in TPN-fed piglets. The aim of this study was to localize the vasoactive effect of GLP-2 within the gastrointestinal tissues and other visceral organs in TPN-fed piglets. Tissue blood flow rates were quantified using fluorescent microsphere deposition in anesthetized TPN-fed piglets given intravenous infusion of GLP-2 at either 500 pmol·kg−1·h−1 (low GLP-2, n = 7 pigs) or 2,000 pmol·kg−1·h−1 (high GLP-2, n = 8 pigs) for 2 h. Compared with baseline, the low and the high GLP-2 treatment significantly increased the blood flow rate in the duodenum (+77%) and jejunum (+40% and 80%), respectively, but blood flow to the distal small intestine and colon (−15%) was unchanged or slightly decreased. Baseline mucosal blood flow was five-fold higher than serosal blood flow; however, high GLP-2 treatment increased serosal (+140%) to a larger degree than mucosal blood flow (+73%). The high GLP-2 dose increased pancreatic flow (+34%) but decreased blood flow in the kidneys (−14%) and stomach (−12%), whereas the spleen and brain were unaffected. These findings suggest that the acute GLP-2-mediated stimulation of portal blood flow in TPN-fed piglets occurs principally via increased blood flow through the superior mesenteric artery to the proximal small intestine, a tissue region where the GLP-2R mRNA abundance and trophic GLP-2 effects are greatest.
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Morisaki, H., F. Bloos, J. Keys, C. Martin, A. Neal, and W. J. Sibbald. "Compared with crystalloid, colloid therapy slows progression of extrapulmonary tissue injury in septic sheep." Journal of Applied Physiology 77, no. 3 (September 1, 1994): 1507–18. http://dx.doi.org/10.1152/jappl.1994.77.3.1507.
Full textAbstract:
We tested the hypothesis that the type of fluid infused to chronically maintain intravascular volumes would modify both microvascular integrity and cellular structure in extrapulmonary organs in hyperdynamic sepsis. After cecal ligation and perforation, awake sheep were treated for 48 h with 10% pentastarch (n = 9), 10% pentafraction (Du Pont Critical Care; n = 8), or Ringer lactate (n = 8) titrated to maintain a constant left atrial pressure. After 48 h of fluid therapy, biopsy samples were taken from the left ventricle and gastrocnemius for electron microscopy. At this time, all groups demonstrated a similar hyperdynamic circulatory response, increased systemic O2 utilization and organ blood flows, measured by radioactive microsphere injection. However, greater capillary luminal areas with less endothelial swelling and less parenchymal injury were found in septic sheep treated with pentastarch vs. Ringer lactate infusion in both muscle types. Pentafraction showed few benefits in study end points over pentastarch. Thus, we conclude that chronic intravascular volume resuscitation of hyperdynamic sepsis with pentastarch ameliorated the progression of both microvascular and parenchymal injury. These findings indicate that microvascular surface area for tissue O2 exchange in sepsis may be better preserved with chronically infused colloid, resulting in less parenchymal injury.
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Carmichael, F. J., V. Saldivia, G. A. Varghese, Y. Israel, and H. Orrego. "Ethanol-induced increase in portal blood flow: role of acetate and A1- and A2-adenosine receptors." American Journal of Physiology-Gastrointestinal and Liver Physiology 255, no. 4 (October 1, 1988): G417—G423. http://dx.doi.org/10.1152/ajpgi.1988.255.4.g417.
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The increase in portal blood flow induced by ethanol appears to be adenosine mediated. Acetate, which is released by the liver during ethanol metabolism, is known to increase adenosine levels in tissues and in blood. The effects of acetate on portal blood flow were investigated in rats using the microsphere technique. The intravenous infusion of acetate (7-250 mumol.kg-1.min-1) resulted in vasodilation of the preportal vasculature and in a dose-dependent increase in portal blood flow [control, 39.1 +/- 2.6 ml.kg-1.min-1; acetate (250 mumol.kg-1. min-1), 68.7 +/- 4.0 ml.kg-1.min-1]. This acetate-induced increase in portal blood flow was suppressed by the adenosine receptor blocker, 8-phenyltheophylline. Using the A1-adenosine receptor agonist N-6-cyclohexyl adenosine and the A2-agonist 5'-N-ethylcarboxamido adenosine, we demonstrate that the effect of adenosine on the preportal vasculature is mediated by the A2-subtype of adenosine receptors. In conclusion, these data support the hypothesis that the increase in portal blood flow after ethanol administration results from a preportal vasodilatory effect of adenosine formed from acetate metabolism in extrahepatic tissues.
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Drescher, Wolf R., Karen P. Weigert, Mathias H. Bünger, Ebbe S. Hansen, and Cody E. Bünger. "Spinal blood flow in 24-hour megadose glucocorticoid treatment in awake pigs." Journal of Neurosurgery: Spine 99, no. 3 (October 2003): 286–90. http://dx.doi.org/10.3171/spi.2003.99.3.0286.
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Object. Because of the controversy regarding the benefits of 24-hour administration of methylprednisolone in patients with spinal cord injury (SCI), it is important to investigate its mechanism of action and side effects. This study was conducted to determine if high-dose methylprednisolone modulates neural and vertebral blood flow in an awake large-sized animal model without SCI. Methods. From a group of 18 immature female domestic pigs born to nine different litters, nine animals were randomly allocated to receive methylprednisolone treatment, whereas their nine female siblings served as controls. Drug or placebo was applied in a blinded fashion by a third person not involved in the study. The following treatment for SCI, as suggested by the North American Spinal Cord Injury Study, was administered to the awake pig: methylprednisolone (30 mg/kg of body weight) was infused into the jugular vein during a 15-minute period, followed by a 45-minute pause, and the infusion was maintained over a 23-hour period at a dose of 5.4 mg/kg body weight/hour. By means of the radioactive tracer microsphere technique, spinal cord blood flow (SCBF) was measured in the awake standing pig in the cerebrum, and in spinal gray and white matter, nerve roots, endplates, cancellous bone, cortical shell, and T12—L2 discs. Blood flow was measured before, 1 hour after initiation of infusion, and 24 hours postinfusion. Examination of blood flow in the neural and vertebral tissue samples, as well as of central hemodynamics, revealed no significant difference between the experimental and control groups, and this parity was maintained throughout the experimental phases. Conclusions. In the awake pig model, 24-hour methylprednisolone treatment does not modulate cerebral or SCBF, nor does it increase the risk for vertebral osteonecrosis by producing vertebral ischemia.
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Ulatowski, J. A., J. R. Kirsch, and R. J. Traystman. "Hypoxic reperfusion after ischemia in swine does not improve acute brain recovery." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 5 (November 1, 1994): H1880—H1887. http://dx.doi.org/10.1152/ajpheart.1994.267.5.h1880.
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We tested the hypothesis that transient hypoxic reperfusion after 15 min of global cerebral ischemia would improve acute recovery of electrical function. We also determined the changes in cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2) during transient hypoxic reperfusion. Pentobarbital-anesthetized pigs were exposed to cerebral ischemia by raising intracranial pressure to 100 mmHg above arterial pressure with rapid infusion of artificial cerebral spinal fluid into a lateral ventricle. During the reperfusion period, normoxia was maintained at an arterial oxygen partial pressure (PaO2) of 80–120 mmHg for 120 min of reperfusion and hypoxia at a PaO2 of 35–45 mmHg for the first 30 min of reperfusion in another group. The postischemic hypoxia group showed persistent elevation in microsphere-determined CBF at 30 min of reperfusion in all brain regions and lack of delayed hypoperfusion through 120 min of reperfusion. The normoxic group demonstrated transient postischemic hyperemia and hypoperfusion. CMRO2 was not significantly different between groups at any time point. In both groups, the somatosensory-evoked potential amplitude reached only 10% recovery by the end of 120 min of reperfusion. We conclude that hypoxemia during reperfusion after cerebral ischemia in this model does not improve acute brain electrical function and prolongs postischemic hyperemia.