Biomedical subjects

H Bouritius

Publications and source records attributed to H Bouritius.

8 recordsLinked to original sources

PubMed2005

Preoperative supplementation with a carbohydrate mixture decreases organ dysfunction-associated risk factors.

BACKGROUND & AIMS: Recently, both asymmetrical dimethylarginine and IL-6 have been suggested to be associated with the induction and severity of single and multiple organ dysfunction. The aims of the present study were to elucidate if these factors were increased in an ischemia reperfusion (IR) model and whether pre-operative carbohydrate supplementation can reduce the risk factors along with the IR injury. METHODS: One group of male Wistar rats was fasted for 16 h (water ad libitum) prior to clamping the superior mesenteric artery (IR fasted n=14). A second group had ad libitum access to a carbohydrate solution prior to clamping (IR fasted CHO group n=11). Sham-fasted animals, which only received laparotomy and no clamping, served as controls (n=4). RESULTS: Plasma urea and ALAT activity were both increased in the IR fasted animals when compared to the sham rats (P=0.007 and P<0.02, respectively). Furthermore, it was shown that IR fasted rats had increased ADMA and IL-6 concentration in plasma when compared to sham animals (P<0.02). Moreover, the GSH level in lung was significantly decreased in the IR fasted animals (P=0.014). IR CHO supplemented showed no significant increase of ALAT activity and decrease of lung GSH. Furthermore, significantly lower plasma urea, ADMA and IL-6 concentration was seen in the IR CHO supplemented group when compared to the IR fasted rats (P=0.028, P<0.01 and P<0.02, respectively). The liver glycogen concentration in IR fasted rats was 48% of that IR rats supplemented the carbohydrate mixture. CONCLUSION: The present rat intestinal ischemia reperfusion model not only induces organ injury indicated by the classical parameters such as plasma urea and ALAT activity, but also increased plasma IL-6 and ADMA and decreased lung GSH concentration in IR fasted rats. Pre-operative supplementation with the carbohydrate mixture significantly lowered the plasma urea, IL-6 and ADMA concentrations and maintained lung GSH concentration. This indicates that pre-operative carbohydrate supplementation reduces post-operative organ injury.

Alanine Transaminase↗

PubMed2001

Neuropeptide Y inhibits the protein kinase C-stimulated Cl(-) secretion in the human colonic cell line HT29cl.19A cell line via multiple sites.

Neuropeptide Y is known to exert inhibitory effects on ion secretion in the intestine by reducing the activity of adenylyl cyclase. In the human intestinal epithelial cell line HT29cl.19A, it has been previously shown that neuropeptide Y inhibits the electrophysiological phenomena related to Cl(-) secretion, when induced by elevation of cAMP via forskolin. Moreover, the secretion induced via elevation of intracellular calcium levels via muscarinic activation can be inhibited by neuropeptide Y. Part of these inhibitions appeared to be due to lowered calcium activity in the epithelial cells, thereby reducing the basolateral K(+) conductance. The phorbol ester 4-phorbol-12,13-dibutyrate (PDB) can induce secretion in this cell line via activation of protein kinase C as well; however, the effect of neuropeptide Y on this pathway has not yet been studied. In the present experiments, it is shown that neuropeptide Y inhibits the PDB-induced secretion at two sides: one located in the apical membrane and another in the basolateral membrane. It is shown that the latter effect can, at least partially, be explained via a direct effect of neuropeptide Y on the K(+) conductance. This was concluded from the observation that neuropeptide Y could also reduce basolateral K(+) conductance when intracellular calcium was dramatically increased by ionomycin. The observed inhibitory effects suggest that neuropeptide Y is a very powerful antisecretory peptide in human intestinal epithelial cells.

Calcium↗

PubMed1999

Microelectrode measurements of the effects of basolateral adenosine in polarized human intestinal epithelial cells in culture.

Activation of the basolateral receptor for adenosine in HT-29cl.19A cells, by 100 microM adenosine, increased the equivalent short-circuit current (DeltaIsc= 24+/-2 microA/cm2), depolarized the intracellular potential (DeltaVa= 26+/-2 mV) and decreased the fractional apical membrane resistance (DeltafRa=-0.48). The changes in all parameters reached their peak values simultaneously. This suggests that the primary action of the adenosine-activated pathway is on only one membrane. Bumetanide inhibited the transepithelial response and repolarized the cell potential. After preincubation with 100 microM forskolin, application of 300 microM adenosine caused a significant further change in Va, Isc, the transepithelial potential (Vt) and fRa. Together with the results from ion-replacement studies, the observations indicate that adenosine activates channels other than the cystic fibrosis transmembrane conductance regulator (CFTR). The rank order of potencies of adenosine and adenosine analogues implies that the receptor is of the A2 subtype. Preincubation with 4-bromophenacyl bromide (4-BPB) inhibited the effect of an adenosine analogue by 50%, indicating that activation of phospholipase A2 may be involved in the adenosine-induced response.

Acetophenones↗

PubMed1998

Neuropeptide Y inhibits ion secretion in intestinal epithelium by reducing chloride and potassium conductance.

Neuropeptide Y (NPY) is probably the most abundant neuropeptide, with a plethora of central as well as peripheral effects, including its proabsorptive action in the gastro-intestinal tract. The effects of NPY on electrical parameters related to three different pathways stimulating ion secretion were investigated using the human intestinal cell line HT29cl.19A. Transepithelial potential and resistance were measured with the preparation maintained in a horizontal Ussing chamber, allowing simultaneous measurement of the membrane potential and determination of the fractional resistance of the apical cell membrane. It was found that application of NPY, after the adenylyl-cyclase-activating drug forskolin, resulted in complete inhibition of forskolin-induced effects within approximately 20 min. The secretion stimulated by adenosine appeared to be insensitive to NPY. The acetylcholine analogue carbachol stimulates ion secretion by increasing intracellular free calcium concentrations ([Ca2+]i) which activates the basolateral potassium (K+) conductance. NPY caused 50% inhibition of the effect of carbachol. Measurements of [Ca2+]i showed that NPY inhibited the carbachol-induced rise in [Ca2+]i, which correlates with the reduced activation of basolateral K+ channels. From this study we conclude that NPY inhibits cAMP-stimulated as well as Ca2+-stimulated secretion via a reduction in the apical Cl- and basolateral K+ conductance. This double effect makes NPY an effective proabsorptive peptide.

Adenosine↗

PubMed1997

Apical adenosine activates an amiloride-sensitive conductance in human intestinal cell line HT29cl.19A.

We studied the effects of stimulation of the apical adenosine receptor on ion transport by HT29cl.19A cells with the conventional microelectrode technique. Adenosine (100 microM) caused an increase in the transepithelial potential (3.6 +/- 0.4 mV) and equivalent short-circuit current (I(sc), 21 +/- 3 microA/cm2), a transient depolarization of the apical membrane potential (14 +/- 2 mV), and a decrease in the apical membrane resistance. The increase in I(sc) was additive to the effect of forskolin or basolateral addition of a maximal concentration of adenosine. Bumetanide, applied after adenosine, caused a further depolarization (7 +/- 2 mV) concomitant with a decrease in I(sc) (-13 +/- 2 microA/cm2) and an increase in the basolateral membrane resistance. Substitution of Cl- with gluconate or Na+ with N-methylglucamine reduced the response to adenosine by >60%. The response was also reduced by a low concentration of amiloride. We conclude that stimulation of the apical adenosine receptor activated a cation conductance in the apical membrane.

Adenosine↗

PubMed1989

Adrenal and sympathetic catecholamines in exercising rats.

The effects of adrenodemedullation and/or adrenoceptor agonists and antagonists on plasma epinephrine (E) and norepinephrine (NE) concentrations during exercise were investigated in rats. Exercise consisted of strenuous swimming against a countercurrent for 15 min in a pool with water of 33 degrees C. Before, during, and after swimming, blood samples were taken through a permanent heart catheter. E was not detectable in plasma of adrenodemedullated (Adm) rats. A marked reduction in the normal exercise-induced increase in plasma NE concentrations occurred in both Adm rats as well as in intact rats injected with the beta 2-selective adrenoceptor antagonist ICI 118551. Intravenous infusion of either E or the beta 2-selective agonist fenoterol restored the increase in plasma NE in Adm rats. Injection of the alpha 2-selective antagonist yohimbine in combination with infusion of the beta 2-selective agonist fenoterol into Adm rats caused an enormous increase in plasma NE. It is concluded that all NE in plasma as released during exercise originates from the peripheral nerve endings of the sympathetic nervous system. Adrenal E influences the release of NE via activation of presynaptic beta 2-adrenoceptors.

Adrenal Medulla↗

PubMed1989

Sympathoadrenal influence on glucose, FFA, and insulin levels in exercising rats.

The effects of sympathoadrenal manipulations on the exercise-induced alterations in blood glucose, plasma free fatty acids (FFA), and insulin were investigated in intact and adrenodemedullated rats. Exercise consisted of strenuous swimming against a countercurrent for 15 min. Before, during, and after swimming, blood samples were taken through a permanent heart catheter. Adrenodemedullation (Adm) markedly reduced the exercise-induced increase in both glucose and FFA. This effect was counteracted by intravenous infusion of epinephrine (E, 20 ng/min). Intravenous infusion of 50 ng E/min into Adm rats caused an exaggerated increase in glucose. In two additional experiments 1) specific adrenoceptor agonists and antagonists were administered to exercising intact and Adm rats, and 2) E or norepinephrine (NE; 20 ng/min) was infused into intact resting rats. The results suggest that E from the adrenal medulla directly affects glucose and insulin but not FFA concentrations in the blood. NE released from peripheral sympathetic nerve endings probably acts in two different ways: as neurotransmitter on liver and pancreas and as a hormone on adipose tissue.

Adrenal Medulla↗

PubMedDate not supplied

Preoperative fasting: an outdated concept?

Recent studies have shown that fasting during the preoperative period for elective surgery induces a metabolic state that seems unfavorable for patients. Results from animal studies indicate that rapid depletion of liver glycogen before surgery leads to mobilization of muscle glycogen after surgery, in turn leading to reduced muscle strength. Depletion of liver glycogen also influences the function of the mononuclear phagocytic system (MPS), which is located predominantly in the liver. The MPS is essential in restricting endotoxin, which may translocate from the gut. In addition, surgery per se puts a substantial physical strain on the patient, and fasting may adversely affect the metabolic response to surgery. This paper presents experimental and clinical data that, when combined together, prove that fasting before surgery has adverse consequences for the patient.

Animals↗