Effects of hypoxia and ischemia on autoregulation in postnatal intestine

1991 ◽  
Vol 261 (1) ◽  
pp. G152-G157 ◽  
Author(s):  
P. T. Nowicki ◽  
C. E. Miller ◽  
R. C. Edwards
Keyword(s):  
Blood Flow ◽  
Pressure Reduction ◽  
Experimental Conditions ◽  
Hypoxic Conditions ◽  
Significant Relationships ◽  
Norepinephrine Infusion ◽  
Before And After ◽  
Age Appropriate ◽  
Arterial Po2

Pressure-flow autoregulation was quantified within in vitro intestine from 3- and 35-day-old swine before and after lowering arterial PO2 (hypoxia) or lowering baseline blood flow by means of norepinephrine infusion (ischemia). Autoregulation was elicited by reducing arterial pressure approximately 33% from an age-appropriate baseline pressure. In 3-day-old intestine, autoregulation was unaffected by hypoxia or ischemia: vascular resistance was unchanged after pressure reduction, while Gf averaged -0.33 +/- 0.15 vs. -0.26 +/- 0.05 under control vs. hypoxic conditions, and -0.48 +/- 0.15 vs. -0.46 +/- 0.11 under control vs. ischemic conditions, respectively. In 35-day-old intestine, autoregulation was enhanced by hypoxia and ischemia. Under both experimental conditions, vasodilation was noted in response to pressure reduction: Gf averaged -0.04 +/- 0.14 vs. 0.38 +/- 0.08 under control vs. hypoxic conditions, and -0.12 +/- 0.10 vs. 0.28 +/- 0.08 under control vs. ischemic conditions, respectively. Regression analysis revealed a significant inverse linear correlation between Gf and venous PO2 in older, but not younger, subjects. Significant relationships between Gf and blood flow were not demonstrated in either group under any experimental condition. We conclude that autoregulation is enhanced within in vitro intestine from 35-, but not 3-day-old, swine during hypoxia or ischemia, and that reduction of venous PO2 is the principal factor responsible for the effect noted in older subjects.

THE USE OF POLYSTYRENE–ALLERGEN CONJUGATES FOR THE REMOVAL OF ANTIBODIES FROM SERA OF ALLERGIC INDIVIDUALS

1960 ◽  
Vol 38 (1) ◽  
pp. 1249-1253
Author(s):  
L. Gyenes ◽  
A. H. Sehon
Keyword(s):  
Hydrochloric Acid ◽  
Protein Concentration ◽  
Complete Removal ◽  
Experimental Conditions ◽  
Comparative Analyses ◽  
Before And After

Polystyrene–ragweed conjugates were shown to remove specifically antibodies from sera of individuals allergic to ragweed. This observation is considered evidence that firm combination occurs in vitro between allergic antibodies and the homologous allergens. Comparative analyses of allergic sera before and after exposure to immunosorbents indicated that complete removal of skin-sensitizing, blocking, and hemagglutinating antibodies did not result in a measurable decrease in protein concentration, thus demonstrating that these factors are present only in minute amounts.Attempts to eîute allergic antibodies from the homologous immunosorbents under various experimental conditions did not lead to their recovery in significant yields; these antibodies could be recovered in small amounts by dissociation with hydrochloric acid at pH 3.

Urinary excretion of prostacyclin in a rat model of uteroplacental vasculature occlusion: implications for fetal growth retardation

1996 ◽  
Vol 8 (5) ◽  
pp. 895 ◽  
Author(s):  
M Hophy ◽  
S Harel ◽  
E Yavin
Keyword(s):  
Blood Flow ◽  
Urinary Concentration ◽  
Fetal Blood ◽  
Experimental Conditions ◽  
Pregnant Rat ◽  
Flow Interruption ◽  
Lower Ability ◽  
Wet Weight ◽  
High Concentrations

An experimental model was devised in the pregnant rat to study by a combined high pressure liquid chromatography and radioimmunoassay technique the accumulation of prostanoids (PNs) in the urine after transient-complete or permanent-partial interruption of the maternal-fetal blood flow. After 8 min of complete restriction of the blood flow in the pregnant rat at 18 days of gestation, the urinary concentration of 6-keto-prostaglandin F1 alpha (6k-PGF1 alpha, the stable prostacyclin metabolite) increased from 4.97 +/- 1.27 ng mg-1 creatinine to 8.09 +/- 2.47 ng mg-1 creatinine and 13.02 +/- 4.5 ng mg-1 creatinine after the second and third post-operative day respectively. The urinary concentration of the 2,3-dinor derivative of prostacyclin reached 12.35 +/- 5.44 ng mg-1 creatinine after the second post-operative day and was reduced to 4.71 +/- 1.94 ng mg-1 creatinine after the third post-operative day. The concentration of thromboxane B2 (TxB2, the stable thromboxane A2 metabolite) increased approximately 7-fold and 13-fold over that of the control after the second and third post-operative day respectively. The urinary concentration of the 2,3-dinor derivative of TxB2 (d-TxB2) increased from about 1.42 +/- 0.3 ng mg-1 creatinine to 4.49 +/- 0.9 ng mg-1 creatinine and 7.76 +/- 2.63 ng mg-1 creatinine under the same experimental conditions. Increases in the urinary concentrations of 6k-PGF1 alpha and d-TxB2 to 94 +/- 27.76 ng mg-1 creatinine and 12.05 +/- 2.26 ng mg-1 creatinine, respectively, were observed on the second post-operative day, after the restriction time was increased to 30 min. Permanent-partial occlusion of the maternal fetal circulation resulted in excretion of PNs in the urine to similar levels produced after transient-complete restriction. High concentrations of prostacyclin (range, 0.8 ng min-1 mg-1 wet weight) were produced in vitro by uterine preparations from restricted animals after the second post-operative day. Placenta preparations from restricted animals generally exhibited a lower ability to synthesize PNS (up to 0.006 ng min-1 mg-1 wet weight) compared with uterine tissue but produced more thromboxane than their sham counterparts. The data suggest that the uterus constitutes the main source for urinary PN excretion following short episodes of maternal-fetal blood flow interruption.

Hemodynamic and renal effects of cross-linked hemoglobin infusion

1997 ◽  
Vol 272 (3) ◽  
pp. R793-R799 ◽  
Author(s):  
A. Cases ◽  
J. M. Stulak ◽  
Z. Katusic ◽  
E. Villa ◽  
J. C. Romero
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Sodium Excretion ◽  
Calcium Ionophore ◽  
Urinary Flow ◽  
Binding Effect ◽  
Scavenging Effect ◽  
Before And After ◽  
Vascular Beds

It is well known that hemoglobin binds nitric oxide (NO) and produces a pronounced vasoconstriction in isolated arteries. However, it is debatable whether such an effect takes place in whole animals, because hemoglobin also catalyzes the formation of prostaglandins from arachidonic acid. Short-term studies were performed to evaluate the effects induced by intravenous infusion of cross-linked hemoglobin (XL-Hb) on blood pressure (BP) and renal, iliac, and mesenteric flows, and on renal function in six anesthetized dogs. A similar volume-matched expansion with 6% dextran was used as a control (n = 6). Glomerular filtration rate (GFR), urinary flow, and total and fractional sodium excretion were measured before and after XL-Hb or dextran infusion to evaluate possible renal function changes. XL-Hb administration resulted in a 29% elevation in BP and a significant decrease of blood flow (30-37%) to the three vascular beds. XL-Hb did not alter GFR or sodium excretion, despite the increase in BP. In contrast, the administration of dextran did not significantly alter BP but induced a significant increase (6-13%) of blood flow in the three vascular beds. These changes were accompanied by threefold increases in urinary flow and sodium excretion without alterations in GFR. The binding effect of XL-Hb on NO was studied in isolated renal arteries in organ chambers. These in vitro studies showed that XL-Hb blunted the endothelium-mediated vasodilator response to calcium ionophore A-23187 and to acetylcholine. Our results demonstrate that XL-Hb administration is followed by hypertension, vasoconstriction, and blunted natriuresis. All these effects are compatible with the scavenging effect on NO attributed to XL-Hb.

Remineralization Potential of a New Toothpaste Formulation: An In-Vitro Study

2004 ◽  
Vol 5 (1) ◽  
pp. 18-30 ◽  
Author(s):  
Carlos A. Muñoz ◽  
Anna Torrado ◽  
Manuel Valiente ◽  
Wu Zhang ◽  
Yiming Li
Keyword(s):  
Ion Exchange ◽  
In Vitro Study ◽  
Ion Exchange Resin ◽  
Ion Exchange Resins ◽  
Experimental Conditions ◽  
Human Enamel ◽  
Before And After ◽  
Ph Cycling ◽  
Exchange Resins

Abstract The aim of the present study was to determine the ability of a dentifrice containing a mixture of ion-exchange resins (named NMTD), which supplies calcium, fluoride, phosphate, and zinc ions, to promote remineralization and/or inhibit demineralization of dental human enamel in a pH cycling model in vitro. A fluoride toothpaste was used as the control. The enamel specimens were tested for microhardness before and after 10 days and 16 days of the demineralizing and remineralizing treatments. The results of this study showed both dentifrices were effective in limiting in vitro enamel demineralization although the effects were not significantly different from each other. Inclusion of calcium and phosphate ion-exchange resins in the dentifrice containing a fluoride ion-exchange resin maintained a similar net outcome of the conventional dentifrice in the demineralization/ remineralization process under the experimental conditions employed. Citation Torrado A, Valiente M, Zhang W, et. al. Remineralization Potential of a New Toothpaste Formulation: An In-Vitro Study. J Contemp Dent Pract 2004 February;(5)1:018-030.

Effects of increased pulmonary vascular tone on gas exchange in canine oleic acid pulmonary edema

1988 ◽  
Vol 65 (2) ◽  
pp. 662-668 ◽  
Author(s):  
M. Leeman ◽  
P. Lejeune ◽  
R. Hallemans ◽  
C. Melot ◽  
R. Naeije
Keyword(s):  
Oleic Acid ◽  
Gas Exchange ◽  
Cardiac Index ◽  
Vascular Tone ◽  
Pulmonary Arterial Pressure ◽  
Intrapulmonary Shunt ◽  
Experimental Conditions ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Arterial Po2

Pulmonary gas exchange was investigated before and after an increase in pulmonary vascular tone induced by administration of acetylsalicylic acid (ASA), indomethacin, or almitrine in 32 pentobarbital-anesthetized and ventilated (fraction of inspired O2 0.4) dogs with oleic acid lung injury. Pulmonary vascular tone was evaluated by five-point pulmonary arterial pressure (PAP)/cardiac index (Q) plots and intrapulmonary shunt was measured using a SF6 infusion. PAP/Q plots were rectilinear in all experimental conditions. In control dogs (n = 8), oleic acid (0.09 ml/kg iv) increased PAP over the range of Q studied (1-5 l.min-1.m-2). At the same Q, arterial PO2 fell from 186 +/- 11 to 65 +/- 8 (SE) Torr and intrapulmonary shunt rose from 5 +/- 1 to 50 +/- 6% 90 min after oleic acid injection. These changes remained stable during the generation of two consecutive PAP/Q plots. ASA (1 g iv, n = 8), indomethacin (2 mg/kg iv, n = 8), and almitrine (8 micrograms.kg-1.min-1 iv, n = 8) produced a further increase in PAP at each level of Q. ASA and indomethacin, respectively, increased arterial PO2 from 61 +/- 4 to 70 +/- 3 Torr (P less than 0.05) and from 70 +/- 6 to 86 +/- 6 Torr (P less than 0.05) and decreased intrapulmonary shunt from 61 +/- 5 to 44 +/- 4% (P less than 0.05) and from 44 +/- 5 to 29 +/- 4% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Cerebral Blood Flow and Brain Oxygenation in Rats Breathing Oxygen under Pressure

2005 ◽  
Vol 25 (10) ◽  
pp. 1288-1300 ◽  
Author(s):  
Ivan T Demchenko ◽  
Yuriy I Luchakov ◽  
Alexander N Moskvin ◽  
Diana R Gutsaeva ◽  
Barry W Allen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Platinum Electrodes ◽  
Brain Oxygenation ◽  
Before And After ◽  
Scatter Plots ◽  
Opposing Effects ◽  
Breathing Room

Hyperbaric oxygen (HBO2) increases oxygen tension (PO2) in blood but reduces blood flow by means of O2-induced vasoconstriction. Here we report the first quantitative evaluation of these opposing effects on tissue PO2 in brain, using anesthetized rats exposed to HBO2 at 2 to 6 atmospheres absolute (ATA). We assessed the contribution of regional cerebral blood flow (rCBF) to brain PO2 as inspired PO2 (PiO2) exceeds 1 ATA. We measured rCBF and local PO2 simultaneously in striatum using collocated platinum electrodes. Cerebral blood flow was computed from H2 clearance curves in vivo and PO2 from electrodes calibrated in vitro, before and after insertion. Arterial PCO2 was controlled, and body temperature, blood pressure, and EEG were monitored. Scatter plots of rCBF versus pO2 were nonlinear ( R2 = 0.75) for rats breathing room air but nearly linear ( R2 = 0.88–0.91) for O2 at 2 to 6 ATA. The contribution of rCBF to brain PO2 was estimated at constant inspired PO2, by increasing rCBF with acetazolamide (AZA) or decreasing it with N-nitro-l-arginine methyl ester (l-NAME). At basal rCBF (78 mL/100 g min), local PO2 increased 7- to 33-fold at 2 to 6 ATA, compared with room air. A doubling of rCBF increased striatal PO2 not quite two-fold in rats breathing room air but 13- to 64-fold in those breathing HBO2 at 2 to 6 ATA. These findings support our hypothesis that HBO2 increases PO2 in brain in direct proportion to rCBF.

scholarly journals Microelectrode Sensor for Real-Time Measurements of Nitrite in the Living Brain, in the Presence of Ascorbate

Biosensors ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 277
Author(s):  
Tiago Monteiro ◽  
Cândida Dias ◽  
Cátia F. Lourenço ◽  
Ana Ledo ◽  
Rui M. Barbosa ◽  
...  
Keyword(s):  
Blood Flow ◽  
Real Time ◽  
Brain Research ◽  
Electrochemical Techniques ◽  
Spatial Dynamics ◽  
Fast Scan Cyclic Voltammetry ◽  
Hypoxic Conditions ◽  
The Brain

The impaired blood flow to the brain causes a decrease in the supply of oxygen that can result in cerebral ischemia; if the blood flow is not restored quickly, neuronal injury or death will occur. Under hypoxic conditions, the production of nitric oxide (●NO), via the classical L-arginine–●NO synthase pathway, is reduced, which can compromise ●NO-dependent vasodilation. However, the alternative nitrite (NO2−) reduction to ●NO, under neuronal hypoxia and ischemia conditions, has been viewed as an in vivo storage pool of ●NO, complementing its enzymatic synthesis. Brain research is thus demanding suitable tools to probe nitrite’s temporal and spatial dynamics in vivo. In this work, we propose a new method for the real-time measurement of nitrite concentration in the brain extracellular space, using fast-scan cyclic voltammetry (FSCV) and carbon microfiber electrodes as sensing probes. In this way, nitrite was detected anodically and in vitro, in the 5–500 µM range, in the presence of increasing physiological concentrations of ascorbate (100–500 µM). These sensors were then tested for real-time and in vivo recordings in the anesthetized rat hippocampus; using fast electrochemical techniques, local and reproducible transients of nitrite oxidation signals were observed, upon pressure ejection of an exogenous nitrite solution into the brain tissue. Nitrite microsensors are thus a valuable tool for investigating the role of this inorganic anion in brain redox signaling.

scholarly journals Obesity decreases the contribution of Kv channels to hypoxic coronary vasodilation

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Hannah E. Clark ◽  
Hana E. Baker ◽  
Adam G. Goodwill ◽  
Bianca S. Blaettner ◽  
Michael C. Kozlowski ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Functional Expression ◽  
K Channel ◽  
Coronary Vasodilation ◽  
Kv Channels ◽  
Arterial Blood ◽  
Before And After ◽  
Arterial Po2

Background and Hypothesis: Our group previously demonstrated that reductions in the functional expression of voltage-dependent K+ (Kv) channels contribute to impaired metabolic control of coronary blood flow in the setting of obesity. This study tested the hypothesis that obesity diminishes the contribution of Kv channels to coronary vasodilation in response to hypoxemia. Experimental Design or Project Methods: Control lean (n = 7) and obese (n = 5) swine were anesthetized and the heart exposed via left lateral thoracotomy. Coronary blood flow was measured in response to hypoxemia, before and after inhibition of Kv channels by 4-aminopyridine (4-AP; 0.3 mg/kg, iv), by a flow probe placed about the left anterior descending coronary artery. Hypoxemia was induced by progressive increases in the amount of nitrogen introduced into the ventilator. Arterial blood samples were obtained at each reduction in arterial oxygenation via a catheter placed in the femoral artery. Results: Blood pressure decreased from ~88 ± 5 mmHg to ~68 ± 6 mmHg (P = 0.01) as arterial PO2 was reduced below 50 mmHg in both lean and obese swine (P = 0.51). In lean swine, coronary flow progressively increased from ~0.6 to >3.0 ml/min/g as arterial PO2 was reduced. This response was decreased by ~40% in obese swine and by ~30% in lean swine treated with 4-AP. Administration of 4AP had no effect on coronary flow in obese swine. Conclusion and Potential Impact: These data support that Kv channels contribute to increases in coronary flow in response to hypoxemia in lean swine and that reductions in Kv channel function contribute to impaired hypoxic coronary vasodilation in obese swine. We propose that therapeutic targeting of obesity associated pathways (angiotensin-aldosterone system) known to influence K+ channel expression could improve coronary microvascular function and cardiovascular outcomes in subjects with obesity. Supported by R01 HL136386; T35 HL 110854.

Effect of polycythemia on gastrointestinal blood flow and oxygenation in piglets

1984 ◽  
Vol 247 (3) ◽  
pp. G220-G225 ◽  
Author(s):  
P. T. Nowicki ◽  
W. Oh ◽  
A. Yao ◽  
N. B. Hansen ◽  
B. S. Stonestreet
Keyword(s):  
Blood Flow ◽  
Small Bowel ◽  
Exchange Transfusion ◽  
Similar Degree ◽  
Packed Red Blood Cells ◽  
Blood Flows ◽  
Newborn Piglets ◽  
Before And After ◽  
Gastrointestinal Blood Flow

Gastrointestinal blood flow and oxygenation were measured before and after the induction of polycythemia in newborn piglets. Sixty minutes after exchange transfusion with age-matched packed red blood cells, hematocrit and in vitro whole blood viscosity increased, while 51Cr-measured blood volume did not change. Cardiac output and total gastrointestinal blood flow (the sum of stomach, jejunum, ileum, and colon blood flows) decreased a similar degree after exchange transfusion, although the reduction in total gastrointestinal blood flow was not uniform in all regions of the gastrointestinal tract. Specifically, blood flow to the stomach and mucosa-submucosa layer of the small bowel decreased, whereas that to the colon and muscularis-serosa layer of the small bowel remained unchanged. Gastrointestinal O2 delivery increased after exchange transfusion because of the increase in arterial O2 content consequent to polycythemia. The arteriovenous O2 content difference remained unchanged following exchange transfusion, and gastrointestinal O2 consumption thus decreased 49 +/- 2%. After a test meal, postprandial values for gastrointestinal blood flow and oxygenation in polycythemic piglets increased to levels similar to postprandial values reported previously in normal newborn piglets.

Autoregulatory escape from norepinephrine infusion: roles of adenosine and histamine

1988 ◽  
Vol 254 (4) ◽  
pp. G560-G565 ◽  
Author(s):  
K. D. Crissinger ◽  
P. R. Kvietys ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Adenosine Deaminase ◽  
Intestinal Blood Flow ◽  
Base Line ◽  
Norepinephrine Infusion ◽  
Before And After ◽  
Autoregulatory Escape ◽  
Escape Responses ◽  
High Concentrations ◽  
Infusion Of Norepinephrine

Stimulation of sympathetic fibers or infusion of norepinephrine (NE) into the superior mesenteric artery (SMA) leads to an initial decrease in intestinal blood flow, which is followed by a return of flow toward the base-line value (autoregulatory escape) despite continued nerve stimulation or NE infusion. Although the mechanisms responsible for “autoregulatory escape” have not been defined, accumulation of vasodilator metabolites is frequently invoked to explain this phenomenon. Inasmuch as histamine and adenosine exist in high concentrations in the intestinal mucosa and both are potent vasodilators, we examined the effects of chlorpheniramine (an H1 blocker) and adenosine deaminase (degrades adenosine) on autoregulatory escape from NE infusion. In autoperfused piglet intestinal preparations, we measured SMA blood flow and the arteriovenous oxygen difference during intra-arterial NE infusion before and after blockade with chlorpheniramine or adenosine deaminase. Adenosine deaminase pretreatment increased the peak vasoconstrictor and reduced the steady-state escape responses to NE infusion. Chlorpheniramine did not affect either the vasoconstrictor or escape responses. The oxygen uptake changes induced by NE infusion were not dramatically modified by either treatment. These results indicate that adenosine but not histamine is responsible for at least part of the escape of intestinal blood flow from NE infusion.

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