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Biomedical subjects

I Novak

Publications and source records attributed to I Novak.

At least 37 records · Page 2Linked to original sources
PubMed1999

Enteral nutrition in intensive care patients: a practical approach.

Severe protein-calorie malnutrition is a major problem in many intensive care (ICU) patients, due to the increased catabolic state often associated with acute severe illness and the frequent presence of prior chronic wasting conditions. Nutritional support is thus an important part of these patient's management. Over the years, enteral nutrition (EN) has gained considerable popularity, due to its favorable effects on the digestive tract and its lower cost and rate of complications compared to parenteral nutrition. However, clinicians caring for ICU patients are often faced with contradictory data and difficult decision-making when having to determine the optimal timing and modalities of EN administration, estimation of patient requirements and choice of formulas. The purpose of this paper is to provide practical guidelines on these various aspects of enteral nutritional support, based on presently available evidence.

Contraindications↗
PubMed1998

Enteral nutrition in intensive care patients: a practical approach. Working Group on Nutrition and Metabolism, ESICM. European Society of Intensive Care Medicine.

Severe protein-calorie malnutrition is a major problem in many intensive care (ICU) patients, due to the increased catabolic state often associated with acute severe illness and the frequent presence of prior chronic wasting conditions. Nutritional support is thus an important part of the management of these patients. Over the years, enteral nutrition (EN) has gained considerable popularity, due to its favorable effects on the digestive tract and its lower cost and rate of complications compared to parenteral nutrition. However, clinicians caring for ICU patients are often faced with contradictory data and difficult decisions when having to determine the optimal timing and modalities of EN administration, estimation of patient requirements, and choice of formulas. The purpose of this paper is to provide practical guidelines on these various aspects of enteral nutritional support, based on presently available evidence.

Cost-Benefit Analysis↗
PubMed1998

Different purinergic receptors lead to intracellular calcium increases in pancreatic ducts.

Extracellular adenosine 5'-triphosphate (ATP) has been described to act as a regulator in many cells and tissues, including epithelia, and in the gastrointestinal tract ATP is one of the substances involved in non-cholinergic non-adrenergic control. However, very little is known about the effect of ATP on pancreatic ducts, which normally secrete bicarbonate-rich fluid in response to secretin. Hence, the aim of our present study was to test the effect of ATP and other nucleotides on intracellular Ca2+ activity ([Ca2+]i) of pancreatic ducts, and thereby get information about purinergic receptors that might play a role in the regulation of pancreatic bicarbonate transport. Native intralobular ducts were obtained from rat pancreas and [Ca2+]i in 10-20 cells was measured using the fura-2 method. ATP (10(-4) mol/l) evoked a characteristic biphasic Ca2+ transient in duct cells. Nucleotides, used to classify the P2 receptors, acted with the following potency on the peak Ca2+ in many ducts: uridine 5'-triphosphate (UTP) >/= ATP >inosine 5'-triphosphate >/= 2-methylthio-ATP > beta,gamma-methyl-ATP > adenosine. However, although the peak [Ca2+]i responses to ATP and UTP were similar, the plateau [Ca2+]i was nearly doubled with UTP. Moreover, in about one-third of the ducts studied, UTP had no effect on cell Ca2+, while the response to ATP was normal. In further experiments we found that removal of extracellular Mg2+ increased the peak [Ca2+]i evoked in response to ATP. 2'&3'-O-(4-benzoylbenzoyl) ATP (BzATP) evoked a monophasic and slower increase in [Ca2+]i, which was inhibited by removal of extracellular Ca2+, or by addition of 4,4'-diisothiocyanatostilbene-2, 2'-disulphonic acid (DIDS). Taken together, our data indicate that there are two types of purinergic receptors on pancreatic ducts through which ATP can act. These are pharmacologically known as P2U and P2Z receptors and may correspond to P2Y2 and P2X7 receptors.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1998

beta-Adrenergic regulation of ion transport in pancreatic ducts: patch-clamp study of isolated rat pancreatic ducts.

BACKGROUND & AIMS: In the intact pancreas, bicarbonate secretion is thought to be controlled by a number of regulators, including adrenergic agonists. The aim of this study was to investigate the effects of adrenergic agonists on pancreatic ducts, which are the site of bicarbonate secretion. METHODS: Small intralobular ducts were isolated from rat pancreas and studied in vitro by the whole-cell patch clamp technique. Cell membrane voltages and currents were indicators of cellular ion transport. In some ducts, intracellular Ca2+ activity was measured by fluorescence optical methods. RESULTS: Unstimulated duct cells had a membrane voltage (Vm) of about -50 mV. Isoproterenol had a concentration-dependent effect on Vm; at 10(-7) mol/L, it depolarized Vm by 20-25 mV and the cell conductance increased by 100 nanosiemens. These effects were a result of opening of luminal Cl- channels. Phenylephrine had much smaller effects. At comparable concentrations, it depolarized Vm by a few millivolts. Neither agonist had significant effects on intracellular Ca2+. CONCLUSIONS: This study provides the first direct evidence that adrenergic stimulation, namely, that of beta-adrenoceptors, controls ion transport in pancreatic ducts. Similar to secretin, isoproterenol stimulation leads to opening of luminal Cl- channels, and HCO3- enters the lumen in exchange for Cl-.

Adenosine Triphosphate↗
PubMed1997

Intracellular pH in rat pancreatic ducts.

In order to study the mechanism of H+ and HCO3- transport in a HCO3- secreting epithelium, pancreatic ducts, we have measured the intracellular pH (pHi) in this tissue using the pH sensitive probe BCECF. We found that exposures of ducts to solutions containing acetate/acetic acid or NH4+/NH3 buffers (20 mmol/l) led to pHi changes in accordance with entry of lipid-soluble forms of the buffers, followed by back-regulation of pHi by duct cells. In another type of experiment, changes in extracellular pH of solutions containing HEPES or HCO3-/CO2 buffers led to significant changes in pHi that did not seem to be back-regulated efficiently by duct cells. The sensitivity of pHi to the inhibitor HOE 694 and to changes in Na+ gradients, indicate that the Na+/H+ exchanger is present in this epithelium. Similarly, the sensitivity to Cl- and HCO3- gradients indicated the presence of the Cl-/HCO3- exchanger. Under some conditions, these exchangers can be invoked to regulate cell pH.

Animals↗
PubMed1996

Evidence for a Na+-Ca2+ exchanger in rat pancreatic ducts.

Only recently has it been recognized that intracellular Ca2+ is an important cellular mediator in pancreatic ducts. The aim of the present study was to characterize the Ca2+ efflux pathway in ducts freshly prepared from rat pancreas. Lowering of extracellular Na+ concentration resulted in a significant increase in intracellular Ca2+. This effect was fast, reversible, dependent on the extracellular Na+ concentration and did not correlate with intracellular pH changes. It was abolished in Ca2+-free solutions, indicating that the outwardly directed Na+ gradient was directly coupled to a flufenamate insensitive Ca2+ influx. Removal and reintroduction of extracellular Na+ induced transient hyperpolarization and depolarization of Vm, respectively. Taken together, our data indicate that pancreatic ducts possess an electrogenic Na+-Ca2+ exchanger, which under control conditions is responsible for transporting Ca2+ out of resting duct cells.

Acetates↗
PubMed1996

Calcium influx pathways in rat pancreatic ducts.

A number of agonists increase intracellular Ca2+ activity, [Ca2+]i, in pancreatic ducts, but the influx/efflux pathways and intracellular Ca2+ stores in this epithelium are unknown. The aim of the present study was to characterise the Ca2+ influx pathways, especially their pH sensitivity, in native pancreatic ducts stimulated by ATP and carbachol, CCH. Under control conditions both agonists led to similar changes in [Ca2+]i. However, these Ca2+ transients, consisting of peak and plateau phases, showed different sensitivities to various experimental manoeuvres. In extracellular Ca2+-free solutions, the ATP-induced [Ca2+]i peak decreased by 25%, but the CCH-induced peak was unaffected; both plateaus were inhibited by 90%. Flufenamate inhibited the ATP-induced peak by 35%, but not the CCH-evoked peak; the plateaus were inhibited by 75-80%. La3+ inhibited the ATP-induced plateau fully, but that induced by CCH by 55%. In resting ducts, an increase in extracellular pH, pHe, by means of HEPES and HCO3-/CO2 buffers, increased [Ca2+]i; a decrease in pHe had the opposite effect. In stimulated ducts the pH-evoked effects on Ca2+ influx were more pronounced and depended on the agonist used. At pHe 6.5 both ATP- and CCH-evoked plateaus were inhibited by about 50%. At pH 8.0 the ATP-stimulated plateau was inhibited by 27%, but that stimulated by CCH was increased by 72%. Taken together, we show that CCH stimulates Ca2+ release followed by Ca2+ influx that is moderately sensitive to flufenamate, La3+, depolarisation, it is inhibited by low pH, but stimulated by high pH. ATP stimulates Ca2+ release and probably an early Ca2+ influx, which is more markedly sensitive to flufenamate and La3+, and is both inhibited by low and high pH. Thus our study indicates that there are at least two separate Ca2+ influx pathways in pancreatic ducts cells.

Animals↗
PubMed1994

Effect of ATP, carbachol and other agonists on intracellular calcium activity and membrane voltage of pancreatic ducts.

The pancreatic duct has been regarded as a typical cAMP-regulated epithelium, and our knowledge about its Ca2+ homeostasis is limited. Hence, we studied the regulation of intracellular calcium, [Ca2+]i, in perfused rat pancreatic ducts using the Ca(2+)-sensitive probe fura-2. In some experiments we also measured the basolateral membrane voltage, Vbl, of individual cells. The resting basal [Ca2+]i was relatively high, corresponding to 263 +/- 28 nmol/l, and it decreased rapidly to 106 +/- 28 nmol/l after removal of Ca2+ from the bathing medium (n = 31). Carbachol increased [Ca2+]i in a concentration-dependent manner. At 10 mumol/l the fura-2 fluorescence ratio increased by 0.49 +/- 0.06 (n = 24), corresponding to an increase in [Ca2+]i by 111 +/- 15 nmol/l (n = 17). ATP, added to the basolateral side at 0.1 mmol/l and 1 mmol/l, increased the fluorescence ratio by 0.67 +/- 0.06 and 1.01 +/- 14 (n = 46; 12), corresponding to a [Ca2+]i increase of 136 +/- 22 nmol/l and 294 +/- 73 nmol/l respectively (n = 15; 10). Microelectrode measurements showed that ATP (0.1 mmol/l) hyperpolarized Vbl from -62 +/- 3 mV to -70 +/- 3 mV, an effect which was in some cases only transient (n = 7). This effect of ATP was different from that of carbachol, which depolarized Vbl. Applied together with secretin, ATP delayed the secretin-induced depolarization and prolonged the initial hyperpolarization of Vbl (n = 4). Several other putative agonists of pancreatic HCO3- secretion were also tested for their effects on [Ca2+]i.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1993

Effect of secretin and inhibitors of HCO3-/H+ transport on the membrane voltage of rat pancreatic duct cells.

The aim of the present study was to study the effect of secretin on the electrophysiological response of pancreatic ducts. Furthermore, we investigated the effects of lipid-soluble buffers and inhibitors of HCO3-/H+ transport. Ducts obtained from fresh rat pancreas were perfused in vitro. Secretin depolarized the basolateral membrane voltage, Vbl, by up to 35 mV (n = 37); a half-maximal response was obtained at 3 x 10(-11) mol/l. In unstimulated ducts a decrease in the luminal Cl- concentration (120 to 37 mmol/l) had a marginal effect on Vbl, but after maximal secretin stimulation it evoked a 14 +/- 2 mV depolarization (n = 6), showing that a luminal Cl- conductance (GCl-) was activated. The depolarizing effect of secretin on Vbl was often preceded by about a 6 mV hyperpolarization, most likely due to an increase in the basolateral GK+. Perfusion of ducts with DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid, 0.01 mmol/l) or addition of ethoxzolamide (0.1 mmol/l) to the bath medium diminished the effect of secretin. Acetate or pre-treatment of ducts with NH4+/NH3 (10 mmol/l in the bath) depolarized the resting Vbl of -65 +/- 2 mV by 16 +/- 4 mV (n = 7) and 19 +/- 3 mV (n = 10), respectively. The fractional resistance of the basolateral membrane (FRbl) doubled, and the depolarizing responses to changes in bath K+ concentrations (5 to 20 mmol/l) decreased from 22 +/- 1 to 11 +/- 2 mV.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1993

Effect of vasoactive intestinal peptide, carbachol and other agonists on the membrane voltage of pancreatic duct cells.

The regulation of pancreatic exocrine secretion involves hormonal, neural and neurohormonal components. Many agonists are known to be effective in pancreatic acinar cells, but less is known about the ducts. Therefore, we wanted to investigate the influence of various agonists on isolated perfused pancreatic ducts and, as a physiological response, we measured the basolateral membrane voltage of the duct cells (Vbl) with microelectrodes. Pancreatic ducts were dissected from pancreas of normal rats and bathed in a HCO(3-)(-containing solution. Under control conditions, the average Vbl was between -50 and -70 mV. Vasoactive intestinal peptide (VIP) and carbachol (CCH) reversibly depolarized Vbl when applied to the bath. VIP (9 x 10(-9) mol/l) depolarized Vbl from -72 +/- 3 mV to -53 +/- 3 mV (n = 20) and CCH (10(-5) mol/l) from -62 +/- 3 to -35 +/- 4 mV (n = 10). Furthermore, a decrease of the Cl- concentration in the lumen led to an increase of VIP-induced depolarization of Vbl, suggesting that a luminal Cl- conductance was increased. Cholecystokinin (CCK, 10(-10)-10(-7) mol/l) and bombesin (10(-8), 10(-5) mol/l), which stimulate pancreatic exocrine secretion in acini or whole glands, showed no significant effect on Vbl of the duct cells tested in our preparation (n = 7, 6). Neurotensin (10(-8) mol/l) had a marked depolarizing effect in two out of ten cases; Vbl depolarized from about -65 mV to -29 mV and the effect was reversible. Substance P (2 x 10(-7) mol/l), alone or in combination with secretin, had no effect on Vbl of the tested duct cells (n = 11).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Chloride and potassium conductances of cultured human sweat ducts.

The purpose of this study was to characterize the ion conductances, in particular those for Cl- and K+, of human sweat duct cells grown in primary culture. Sweat duct cells from healthy individuals were grown to confluence on a dialysis membrane, which was then mounted in a mini-Ussing chamber and transepithelial and intracellular potentials were measured under open-circuit conditions. Under control conditions the epithelia developed mucosa-negative transepithelial potentials, Vte, of about -10 mV. The apical membrane potential, Va, was -25 mV to -30 mV (n = 97) in most cells, but several cells had a higher potential of about -55 mV (n = 29). Mucosal amiloride (10 mumol/l) hyperpolarized Va from -31 +/- 1 mV to a new sustained level of -46 +/- 2 mV (n = 36). These changes were accompanied by increase in the fractional resistance of the apical membrane, fRa, and decreases of Vte and the equivalent short-circuit current, Isc. In amiloride-treated tissues an increase in mucosal K+ concentration (5 mmol/l to 25 mmol/l) depolarized Va by 5 +/- 1 mV (n = 8), while the same step on the serosal side depolarized Va by 20 +/- 2 mV (n = 8). A Cl- channel blocker 3',5-dichlorodiphenylamine-2-carboxylate DCl-DPC; 10 mumol/l) depolarized Va by 5 +/- 1 mV (n = 6), an effect that was lost after amiloride application. The blocker had no effect from the serosal side. Reduction of mucosal Cl- (from 120 to 30 or 10 mmol/l) depolarized Va by 9-11 mV (n = 35), an effect that was often followed by a secondary hyperpolarization of 10-30 mV (n = 27).(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1992

Noninvasive estimation of total body water in critically ill children after cardiac operations. Validation of a bioelectric impedance method.

The understanding of fluid fluxes in pediatric cardiac critical care is crucial to effective management. Knowledge of variations in total body water in this situation would aid this understanding, but most available methods are unsuitable for routine use. Recently, estimation of total body water by a tetrapolar bioelectric impedance has been validated in older children and adolescents. We undertook a study to validate the method in the taxing conditions of pediatric cardiac critical care. A prospective comparative study was done in 16 children whose ages ranged from 6 days to 10 years (mean 23 months) after a variety of cardiac operations. Total body water was estimated by a standard isotope dilution method (deuterium oxide) and by bioelectric impedance by means of a Holtain body composition analyzer. Individual estimations of total body water were made on two successive days on each patient at varying intervals after a cardiac operation, bioelectric impedance being measured hourly during 4 hourly urine collections for the deuterium oxide method. Thirty-two simultaneous values of total body water (by isotope and by impedance) were collected. Population-specific regression relationship was established by plotting total body water (isotope) against height2/bioelectric impedance. From this data plot r = 0.911, giving this equation: total body water = 0.158 +/- 0.662 x (height2/bioelectric impedance). Levels of agreement of -1.771 to +1.725 were observed, with a standard error of measurement of 16% across the range. The data suggest that bioelectric impedance is a satisfactory and reliable method of estimating total body water in children requiring cardiac critical care. The standard error of 16% suggests that the method may be more useful for measuring trends than absolute values, but the technique should be a valuable noninvasive tool both for continuous monitoring of total body water and in longitudinal research studies of rapid fluid flux and in the assessment of capillary leak.

Body Water↗
PubMed1991

Effect of bicarbonate on potassium conductance of isolated perfused rat pancreatic ducts.

The aim of this study was to investigate the role of the K+ conductance in unstimulated and stimulated pancreatic ducts and to see how it is affected by provision of exogenous HCO3-/CO2. For this purpose we have applied electrophysiological techniques to perfused pancreatic ducts, which were dissected from rat pancreas. The basolateral membrane potential PDbl of unstimulated duct cells was between -60 mV and -70 mV, and the cells had a relatively large K+ conductance in the basolateral membrane as demonstrated by (a) 20-22 mV depolarization of PDbl in response to increase in bath K+ concentration from 5 mmol/l to 20 mmol/l and (b) the effect of a K+ channel blocker, Ba2+ (5 mmol/l), which depolarized PDbl by 30-40 mV. These effects on unstimulated ducts were relatively independent of bath HCO3-/CO2. The luminal membrane seemed to have no significant K+ conductance. Upon stimulation with secretin or dibutyryl cyclic AMP, PDbl depolarized to about -35 mV in the presence of HCO3-/CO2. Notably, the K+ conductance in the stimulated ducts was now only apparent in the presence of exogenous HCO3-/CO2 in the bath solutions. Upon addition of Ba2+, PDbl depolarized by 13 +/- 1 mV (n = 7), the fractional resistance of the basolateral membrane, FRbl increased from 0.66 to 0.78 (n = 6), the specific transepithelial resistance, Rte, increased from 52 +/- 13 omega cm2 to 59 +/- 15 omega cm2 (n = 11), and the whole-cell input resistance, Rc, measured with double-barrelled electrodes, increased from 20 M omega to 26 M omega (n = 3).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Perioperative monitoring of total body water by bio-electrical impedance in children undergoing open heart surgery.

UNLABELLED: Knowledge of the changes in total body water (TBW) following cardiac surgery (OHS) in children would be of value in fluid therapy and in researching the causes and management of capillary leak. We have validated a bioelectrical impedance technique (BEI) for non-invasive estimation of TBW in children after OHS. We report the use of this method in a longitudinal study. Twenty patients (mean age 4.7 years +/- 3.5 (SD), mean weight (WT) 16.2 kg +/- 1 kg) undergoing a variety of complex OHS procedures were studied from 1 day preoperatively to 4 days postoperatively. Anaesthetic and basic bypass (CPB) techniques were uniform. Six patients underwent CPB at less than 20 degrees C, 10 at 20 degrees - 25 degrees C and 4 at 26 degrees - 33 degrees C. TBW (BEI), core (ctemp) and peripheral (ptemp) temperatures and fluid balance (TFB) were recorded at frequent intervals. TBW (by BEI) rose (P less than 0.001) following CPB in all patients from 62% +/- 9% (SD) body weight preoperatively to 73% +/- 13% in the ICU (an increase of 11% +/- 5%). TBW remained significantly elevated until the 3rd postoperative day. Multivariate analysis (MVA) confirmed that TBW was significantly related to TFB, but not to ctemp or ptemp. MVA also revealed smaller patient size (height and weight), younger age and longer CPB time as incremental risk factors for the rise in TBW. CONCLUSIONS: (1) BEI permits the non-invasive study of TBW in children after OHS, when TBW variation may be considerable. (2) The smaller the child and the longer the CPB, the greater the rise in TBW. (3) The technique should be a valuable tool in researching the major water fluxes associated with CPB in children.

Body Composition↗