Quantification of in vitro and in vivo energy metabolism of the gastrointestinal tract of fed or fasted sheep

1993 ◽  
Vol 73 (4) ◽  
pp. 855-868 ◽  
Author(s):  
J. M. Kelly ◽  
B. G. Southorn ◽  
C. E. Kelly ◽  
L. P. Milligan ◽  
B. W. McBride

The effect of level of nutrition on in vitro and in vivo O2 consumption by the gastrointestinal tract in four nonlactating, nonpregnant ewes catheterized in the anterior mesenteric vein, hepatic portal vein and mesenteric artery with duodenal cannulae was investigated. Animals were fed a pelleted ration at maintenance (M) or twice maintenance (2M) or fasted (F) subsequent to the M measurement. Duodenal in vitro O2, ouabain-sensitive O2 (OSO2) and cycloheximide-sensitive O2 (CSO2) consumption was determined polarographically using a YSI O2 monitor; whole-gut O2 consumption was determined as (arterio-venous difference of O2 concentration) × (blood flow through the PV). Whole-body O2 consumption was determined using indirect calorimetry. Ewes fed 2M exhibited higher (P < 0.10) whole-body O2 consumption than either M or F ewes. Ewes fed M and 2M had higher (P < 0.10) duodenal in vitro O2 and ouabain-insensitive O2 (OIO2) consumption than F ewes. Hepatic portal blood flow was directly proportional to level of intake (P < 0.10): it was lowest for F ewes (81.0 L h−1), intermediate for M ewes (97.7 L h−1) and highest for 2M ewes (122.5 L h−1). Ouabain inhibition of O2 consumption by portal-drained viscera (PDV) was highest in M ewes and lowest in 2M ewes (P < 0.10). CSO2 consumption by the entire PDV was not affected by level of intake, corresponding to no change in OIO2 consumption by the PDV. As a proportion of whole-body O2 consumption, total O2, OSO2 and cycloheximide-insensitive O2 consumption by the PDV was higher in F ewes than in 2M ewes (P < 0.10). Fasted ewes expended a greater proportion of whole-body O2 consumption on gastrointestinal energetics than did 2M ewes. Key words: Sheep, gastrointestinal oxygen consumption, sodium–potassium ATPase, protein synthesis

2020 ◽  
Vol 40 (04) ◽  
pp. 365-372
Author(s):  
Scott H. Freeburg ◽  
Wolfram Goessling

AbstractHepatocytes and biliary epithelial cells (BECs), the two endodermal cell types of the liver, originate from progenitor cells called hepatoblasts. Based principally on in vitro data, hepatoblasts are thought to be bipotent stem cells with the potential to produce both hepatocytes and BECs. However, robust in vivo evidence for this model has only recently emerged. We examine the molecular mechanisms that stimulate hepatoblast differentiation into hepatocytes or BECs. In the absence of extrinsic cues, the default fate of hepatoblasts is hepatocyte differentiation. Inductive cues from the hepatic portal vein, however, initiate transcription factor expression in hepatoblasts, driving biliary specification. Defining the mechanisms of hepatobiliary differentiation provides important insights into congenital disorders, such as Alagille syndrome, and may help to better characterize the poorly understood hepatic lineage relationships observed during regeneration from liver injury.


1990 ◽  
Vol 125 (1) ◽  
pp. 81-88 ◽  
Author(s):  
R. J. Madon ◽  
D. M. Ensor ◽  
D. J. Flint

ABSTRACT An in-vitro perifusion system was devised in order to examine the secretory profiles of isolated islets of Langerhans, derived from different physiological states, when subjected to various stimuli relevant to lactation. Islets from pregnant rats secreted more insulin than did those from virgin animals; however, islets from lactating and virgin animals secreted similar amounts of insulin with all stimuli, including glucose, amino acids, cations and neurotransmitters. When virgin rats were pretreated for 5 days in vivo with GH or prolactin, insulin responses in vitro were unchanged. Cannulation of the hepatic portal vein and inferior vena cava in vivo revealed that both insulin and glucose concentrations were lower in the portal vein of the lactating rat compared with the virgin animal. It was therefore concluded that insulin concentrations are depressed during lactation as a consequence of the pancreas receiving a diminished glycaemic stimulus rather than because of any change in β-cell sensitivity. Journal of Endocrinology (1990) 125, 81–88


2011 ◽  
Vol 120 (12) ◽  
pp. 537-548 ◽  
Author(s):  
Nicholas M. Hurren ◽  
George M. Balanos ◽  
Andrew K. Blannin

Preprandial aerobic exercise lowers postprandial lipaemia (a risk factor for coronary heart disease); however, the mechanisms responsible are still not clear. The present study investigated whether blood flow to skeletal muscle and/or the liver was increased in the postprandial period after exercise, relative to a control trial, and whether this resulted from increased cardiac output or redistribution of flow. Eight overweight inactive males, aged 49.4±10.5 years (mean±S.D.), acted as their own controls in a counterbalanced design, either walking briskly for 90 min at 60% V̇O2max (maximal oxygen uptake), or resting in the lab, on the evening of day 1. The following morning, a fasting blood sample was collected, participants consumed a high-fat breakfast, and further venous blood samples were drawn hourly for 6 h. Immediately after blood sampling, Doppler ultrasound was used to measure cardiac output and blood flow through both the femoral artery of one leg and the hepatic portal vein, with the ultrasonographer blinded to trial order. The total postprandial triacylglycerol response was 22% lower after exercise (P=0.001). Blood flow through the femoral artery and the hepatic portal vein was increased by 19% (P<0.001) and 16% (P=0.033), respectively, during the 6-h postprandial period following exercise; however, postprandial cardiac output did not differ between trials (P=0.065). Redistribution of blood flow, to both exercised skeletal muscle and the liver, may therefore play a role in reducing the plasma triacylglycerol response to a high-fat meal on the day after an exercise bout.


2020 ◽  
Author(s):  
GengQiang Shi ◽  
Shuai S. Yin

Abstract Laparoscopic surgery has been gradually promoted by people because of its advantages of small trauma and quick recovery. However, the operation is difficult, the first hepatic portal should be completely fastened during the operation. In this paper, through the study of the existing structure of the blocker, a kind of blood flow blocker for the first hepatic hilum blocking under laparoscope is designed. All kinds of parameters were calibrated through equation calculation, and the pressure guiding the blood flow blocking of hepatic portal during operation was calculated. The dynamic analysis was carried out with ANSYS software, and it was found that the fluid movement state was most uniform when the airflow velocity reached 8m/s. The experimental apparatus was set up to simulate the process of hepatic portal vein being blocked in vitro, then the feasibility of blocking effect was evaluated. Finally, it is concluded that the designed blood flow blocking device can have good blocking effect on blood vessels.


1966 ◽  
Vol 51 (4) ◽  
pp. 609-618 ◽  
Author(s):  
P. A. Desaulles ◽  
P. Barthe ◽  
B. Schär ◽  
M. Staehelin

ABSTRACT The adrenocorticotrophic activity of synthetic α-melanophore-stimulating hormone (α-MSH) has been evaluated on the basis of its effects on corticosteroid production in vitro, on its action on corticosteroid secretion in vivo in hypophysectomised rats as well as on its effect on the ascorbic acid output, and on the blood flow through the adrenals. These actions have been compared with those of synthetic β1–24 corticotrophin and of synthetic β1–39 corticotrophin. The results of these investigations show that α-MSH has a stimulating effect on corticosteroid secretion both in vitro and in vivo. These effects are compared with those obtained with synthetic corticotrophins, and the results discussed.


2021 ◽  
Vol 12 ◽  
Author(s):  
Longlong Tu ◽  
Julia Y. H. Liu ◽  
Zengbing Lu ◽  
Dexuan Cui ◽  
Man P. Ngan ◽  
...  

Purpose: Cancer patients receiving cisplatin therapy often experience side-effects such as nausea and emesis, but current anti-emetic regimens are suboptimal. Thus, to enable the development of efficacious anti-emetic treatments, the mechanisms of cisplatin-induced emesis must be determined. We therefore investigated these mechanisms in Suncus murinus, an insectivore that is capable of vomiting.Methods: We used a microelectrode array system to examine the effect of cisplatin on the spatiotemporal properties of slow waves in stomach antrum, duodenum, ileum and colon tissues isolated from S. murinus. In addition, we used a multi-wire radiotelemetry system to record conscious animals’ gastric myoelectric activity, core body temperature, blood pressure (BP) and heart rate viability over 96-h periods. Furthermore, we used whole-body plethysmography to simultaneously monitor animals’ respiratory activity. At the end of in vivo experiments, the stomach antrum was collected and immunohistochemistry was performed to identify c-Kit and cluster of differentiation 45 (CD45)-positive cells.Results: Our acute in vitro studies revealed that cisplatin (1–10 μM) treatment had acute region-dependent effects on pacemaking activity along the gastrointestinal tract, such that the stomach and colon responded oppositely to the duodenum and ileum. S. murinus treated with cisplatin for 90 min had a significantly lower dominant frequency (DF) in the ileum and a longer waveform period in the ileum and colon. Our 96-h recordings showed that cisplatin inhibited food and water intake and caused weight loss during the early and delayed phases. Moreover, cisplatin decreased the DF, increased the percentage power of bradygastria, and evoked a hypothermic response during the acute and delayed phases. Reductions in BP and respiratory rate were also observed. Finally, we demonstrated that treatment with cisplatin caused inflammation in the antrum of the stomach and reduced the density of the interstitial cells of Cajal (ICC).Conclusion: These studies indicate that cisplatin treatment of S. murinus disrupted ICC networking and viability and also affected general homeostatic mechanisms of the cardiovascular system and gastrointestinal tract. The effect on the gastrointestinal tract appeared to be region-specific. Further investigations are required to comprehensively understand these mechanistic effects of cisplatin and their relationship to emesis.


2018 ◽  
Vol 115 (15) ◽  
pp. E3569-E3577 ◽  
Author(s):  
Osama F. Harraz ◽  
Thomas A. Longden ◽  
Fabrice Dabertrand ◽  
David Hill-Eubanks ◽  
Mark T. Nelson

Brain capillaries play a critical role in sensing neural activity and translating it into dynamic changes in cerebral blood flow to serve the metabolic needs of the brain. The molecular cornerstone of this mechanism is the capillary endothelial cell inward rectifier K+ (Kir2.1) channel, which is activated by neuronal activity–dependent increases in external K+ concentration, producing a propagating hyperpolarizing electrical signal that dilates upstream arterioles. Here, we identify a key regulator of this process, demonstrating that phosphatidylinositol 4,5-bisphosphate (PIP2) is an intrinsic modulator of capillary Kir2.1-mediated signaling. We further show that PIP2 depletion through activation of Gq protein-coupled receptors (GqPCRs) cripples capillary-to-arteriole signal transduction in vitro and in vivo, highlighting the potential regulatory linkage between GqPCR-dependent and electrical neurovascular-coupling mechanisms. These results collectively show that PIP2 sets the gain of capillary-initiated electrical signaling by modulating Kir2.1 channels. Endothelial PIP2 levels would therefore shape the extent of retrograde signaling and modulate cerebral blood flow.


2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S198-S198
Author(s):  
Joseph R Meno ◽  
Thien-son K Nguyen ◽  
Elise M Jensen ◽  
G Alexander West ◽  
Leonid Groysman ◽  
...  

1993 ◽  
Vol 21 (2) ◽  
pp. 173-180
Author(s):  
Gunnar Johanson

This presentation addresses some aspects of the methodology, advantages and problems associated with toxicokinetic modelling based on in vitro data. By using toxicokinetic models, particularly physiologically-based ones, it is possible, in principle, to describe whole body toxicokinetics, target doses and toxic effects from in vitro data. Modelling can be divided into three major steps: 1) to relate external exposure (applied dose) of xenobiotic to target dose; 2) to establish the relationship between target dose and effect (in vitro data, e.g. metabolism in microsomes, partitioning in tissue homogenates, and toxicity in cell cultures, are useful in both steps); and 3) to relate external exposure to toxic effect by combining the first two steps. Extrapolations from in vitro to in vivo, between animal and man, and between high and low doses, can easily be carried out by toxicokinetic simulations. In addition, several factors that may affect the toxic response by changing the target dose, such as route of exposure and physical activity, can be studied. New insights concerning the processes involved in toxicity often emerge during the design, refinement and validation of the model. The modelling approach is illustrated by two examples: 1) the carcinogenicity of 1,3-butadiene; and 2) the haematotoxicity of 2-butoxyethanol. Toxicokinetic modelling is an important tool in toxicological risk assessment based on in vitro data. Many factors, some of which can, and should be, studied in vitro, are involved in the expression of toxicity. Successful modelling depends on the identification and quantification of these factors.


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