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It is important to clear the bowel of its contents thoroughly before colonoscopy or radiological procedures such as barium enema. This article reviews laxatives for bowel clearing that can be taken by patients at home prior to the procedure. We concentrate on drug efficacy and patient acceptability.
Results of clinical islet transplantation remain disappointing despite the advances in islet technology. Availability of human organs and control of rejection by adequate immunosuppressive therapy remain the unsolved problems. Transplantation of xenogeneic tissue enclosed in immuno-separating membranes without immunosuppressive drugs may be a solution. In the present study porcine pancreatic islets were isolated by semiautomated method and purified utilizing discontinuous Euroficoll gradients on IBM 2991 cell separator. The porcine pancreatic islets were encapsulated with a new one-step method utilizing a home-made droplet generator. Each microcapsule contained one or two islets and microcapsule diameter was approximately that of the islets. This condition allows an optimal diffusion of insulin, glucose, nutrients and oxygen. Consequently, perifusion experiments with encapsulated porcine islets revealed a typical biphasic pattern of insulin release as it was seen in unencapsulated controls. Human erythrocytes were encapsulated and incubated with serum containing hemolysins and complement. These experiments showed that the encapsulated erythrocytes were protected against the hemolytic activity of Ig G and complement fractions. In conclusion, this encapsulation procedure allows the production of a very thin barium alginate membrane around the islets with very little increase of the total volume of transplanted tissue.
The effect of increased intrapelvic pressure on renal perfusion was examined by simple magnified angiography of freshly excised artificially perfused kidneys of adult Danish Landrace pigs. In all kidneys control angiography was performed at normal intrapelvic pressure (0-5 mmHg). Intrapelvic pressure was raised by retrograde ureteral perfusion of saline in 9 kidneys. Repeat angiography was performed at an intrapelvic pressure of 30-35 mmHg (4 kidneys), 50-55 mmHg (5 kidneys) or 0-5 mmHg (4 kidneys). Angiography demonstrated a delay in arterial filling in kidneys with increased intrapelvic pressure. Perfusate flow measurements showed a corresponding fall in perfusion flow. Retrograde ureteral perfusion was repeated at similar pressures using contrast medium. Intrarenal backflow (IRB) was demonstrated in all 9 kidneys with elevated intrapelvic pressure. IRB localized to 84 per cent of the compound papillae and to 40 per cent of the simple papillae, and was independent of the level of elevated intrapelvic pressure. One-third of the papillae with IRB had absent or markedly decreased arterial filling in the corresponding lobe at angiography. A third retrograde ureteral perfusion was done with a mixture of barium sulphate and gelatin in 4 kidneys. Light microscopy demonstrated that the primary pathway for IRB was canalicular. The contrast medium entered the interstice by three routes: (1) Tubular leakage in the papilla and the corticomedullary region, (2) tears originating in the papilla itself and (3) tears in the calyceal fornix with extension into the parenchyma.
A new family of salt-containing, mixed-metal silicates (CU-14), Ba6Mn4Si12O34Cl3 (1) and Ba6Fe5Si11O34Cl3 (2), was synthesized via the BaCl2 salt-inclusion reaction. These compounds crystallize in the noncentrosymmetric (NCS) space group Pmc2(1) (No. 26), adopting 1 of the 10 NCS polar, nonchiral crystal classes, mm2 (C2v). The cell dimensions are a = 6.821(1) A, b = 9.620(2) A, c = 13.172(3) A, and V = 864.4(3) A3 for 1 and a = 6.878(1) A, b = 9.664(2) A, c = 13.098(3) A, and V = 870.6(3) A3 for 2. The structures form a composite framework made of the (M(4+x)Si(12-x)O34)9- (M = Mn, x = 0; M = Fe, x = 1) covalent oxide and (Ba6Cl3)9+ ionic chloride sublattices. The covalent framework exhibits a pseudo-one-dimensional channel where the extended barium chloride lattice (Ba3Cl1.5)(infinity) resides, and it consists of fused eight-membered meta-silicate rings propagating along [100] via sharing two opposite [Si2O7]6- units to form an acentric lattice. Single-crystal structure studies also reveal the ClBa4 unit adopting an interesting seesaw configuration, in which the lone pair electrons of chlorine preferentially face the oxide anions of the transition metal silicate channel, thus forming the observed polar frameworks. Similar to the synthesis of organic-inorganic hybrid materials, the salt-inclusion method facilitates a promising approach for the directed synthesis of special framework solids, including NCS compounds, via composite lattices.
Acetylcholine (ACh), the major neurotransmitter released by efferent nerve fibers in the cochlea, has been shown to activate a Ca(2+)-dependent K+ conductance in outer hair cells (OHCs). Previously we reported that this ACh operated conductance is permeable to Cs+. The purpose of the present study was to characterize further this Cs(+)-permeable channel and its dependency on Ca2+ using isolated OHCs and the patch clamp technique in the whole cell configuration. The changes in the ACh response were examined when Cs+, Ba2+, Cd2+, N-methyl-D-glucamine (NMG+) and tetraethylammonium (TEA+) were placed in the external or internal solutions. Cs+ substituted for K+ in carrying the ACh-evoked Ca(2+)-dependent K+ current. When NMG+/TEA+ was substituted for internal K+ ACh-evoked an inward and an outward current, and Cs+ substituted for external K+ blocked the outward but not the inward current evoked by ACh suggesting it was carried by K+. In the NMG+/TEA+ condition, when the cell was held at different Vh values for an extended period of time, the ACh-induced K+ current rectified. In Ba2+ (3 mM) with zero Ca2+ ACh failed to induce any detectable current and the ACh response slowly recovered from the Ba2+ block, suggesting a block at an intracellular site. Cd2+ (1 mM) readily and reversibly blocked ACh-induced currents even when carried by Cs+. This data suggests that ACh opens a channel selective for K+, conductive to Cs+ and dependent on Ca2+.
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Mammalian astrocytes convert glutamate to glutamine and bee retinal glial cells convert pyruvate to alanine. To maintain such amination reactions these glial cells may take up NH4+/NH3. We have studied the entry of NH4+/NH3 into bundles of glial cells isolated from bee retina by using the fluorescent dye BCECF to measure pH. Ammonium caused intracellular pH to decrease by a saturable process: the rate of change of pH was maximal for an ammonium concentration of about 5 mM. This acidifying response to ammonium was abolished by the loop diuretic bumetanide (100 microM) and by removal of extracellular Cl-. These results strongly suggest that ammonium enters the cell by contransport of NH4+ with Cl-. Removal of extracellular Na+ did not abolish the NH(4+)-induced acidification. The NH(4+)-induced pH change was unaffected when nearly all K+ conductance was blocked with 5 mM Ba2+ showing that NH4+ did not enter through Ba(2+)-sensitive ion channels. Application of 2 mM NH4+ led to a large increase in total intracellular proton concentration estimated to exceed 13.5 mEq/L. As the cell membrane appeared to be permeable to NH3, we suggest that when NH4+ entered the cells, NH3 left, so that protons were shuttled into the cell. This shuttle, which was strongly dependent on internal and external pH, was quantitatively modelled. In retinal slices, 2 mM NH4+ alkalinized the extracellular space: this alkalinization was reduced in the absence of bath Cl-. We conclude that NH4+ enters the glial cells in bee retina on a cotransporter with functional similarities to the NH4+(K+)-Cl- cotransporter described in kidney cells.
1. Whole mount preparations from guinea-pig hearts were used to characterize the receptors and ionic mechanisms mediating the substance P (SP)-induced depolarization of parasympathetic postganglionic neurones of the cardiac ganglion. 2. Measurement of the amplitude of depolarization in response to superfusion of different tachykinin agonists (neurokinins A (NKA) and B (NKB), SP, and senktide) gave a rank-order potency of NKB = senktide > NKA > SP, indicating involvement of an NK3 receptor. The use of the selective tachykinin receptor antagonists SR 140333, SR 48986, and SR 142801 demonstrated that only the NK3 receptor antagonist SR 142801 inhibited the SP-induced depolarization. 3. The SP-induced depolarization was not inhibited by Ba2+, TEA, or niflumic acid, or altered by reduced Cl- solutions, but was attenuated in reduced Na+ solutions. Single electrode voltage clamp studies demonstrated that the SP-induced inward current increased in amplitude at more negative potentials, had a reversal potential of approximately 0 mV, and was reduced in amplitude in reduced Na+ solutions. 4. We conclude that the SP-induced depolarization in guinea-pig postganglionic parasympathetic neurones of the cardiac ganglion is due to NK3-mediated activation of a non-selective cation conductance.
1. Chronic dietary K+ loading stimulates an active K+ secretory process in rat distal colon, which involves an increase in the macroscopic apical K+ conductance of surface epithelial cells. In the present study, the abundance and characteristics of K+ channels constituting this enhanced apical K+ conductance were evaluated using patch clamp recording techniques. 2. In isolated non-polarized surface cells, K+ channels were seen in 9 of 90 (10%) cell-attached patches in cells from control animals, and in 247 of 437 (57%) cell-attached patches in cells from K(+)-loaded animals, with a significant (P < 0.001) shift in distribution density. Similarly, recordings from cell-attached patches of the apical membrane of surface cells surrounding the openings of distal colonic crypts revealed identical K+ channels in 1 of 11 (9%) patches in control animals, and in 9 of 13 (69%) patches in K(+)-loaded animals. 3. In isolated surface cells and surface cells in situ, K+ channels had mean slope conductances of 209 +/- 6 and 233 +/- 14 pS, respectively, when inside-out patches were bathed symmetrically in K2SO4 solution. The channels were sensitive to 'cytosolic' Ca2+ concentration, were voltage sensitive at 'cytosolic' Ca2+ concentrations encountered in colonic epithelial cells, and were inhibited by 1 mM quinidine, 20 mM TEA or 5 mM Ba2+ ions. 4. The data show that dietary K+ loading increases the abundance of Ca(2+)- and voltage-sensitive large-conductance K+ channels in the apical membrane of surface cells in rat distal colon. These channels constitute the enhanced macroscopic apical K+ conductance previously identified in these cells, and are likely to play a critical role in the active K+ secretory process that typifies this model of colonic K+ adaptation.
1. Post-ganglionic neurones of the rat superior cervical ganglion were studied in vitro (21-26 degrees C) using single intracellular micro-electrode methods. 2. Three Ca2+-dependent potentials were studied: the shoulder on the normal action potential, the hyperpolarizing afterpotential (h.a.p.), and th Ca2+ spike. 3. Bath-applied noradrenaline reversibly inhibited these Ca2+-dependent potentials. The EC50 for inhibition of peak h.a.p. amplitude was about 1 microM. The order of catetholamine potency was: L-adrenaline > L-noradrenaline > D-noradrenaline congruent to dopamine > DL-isoprenaline. Phentolamine (10 microM), an alpha-blocker, but not MJ-1999 (10 microM), a beta-blocker, antagonized the action of noradrenaline. 4. Noradrenaline (10 microM) hyperpolarized most neurones (1-6 mV) studied, with no detectable change in resting membrane conductance. 5. Superfusion with low external Ca2+ and high Mg2+ mimicked the effect of noradrenaline. Either procedure alone antagonized the h.a.p. conductance increase but did not alter the h.a.p. reversal potential. However, in the presence of low Ca2+, high Mg2+, the remaining action potential and h.a.p. were not further reduced by noradrenaline. 6. The Ca2+-dependent shoulder of the action potential did not appear dependent upon GK. Noradrenaline and low Ca2+ antagonized the shoulder when enhanced by TEA+ or Ba2+. 7. Both the rate of rise and amplitude of the Ca2+ spike were antagonized by noradrenaline. 8. We propose that activation of an alpha-adrenoceptor inhibits a voltage-sensitive Ca2+ conductance (GCa(V)), thereby reducing the inward Ca2+ current which may generate the noraml action potential shoulder and the rising phase of the Ca2+ spike. Reduction of Ca2+ current would also reduce the Ca2+-dependent portion of outward K+ current underlying the h.a.p.
1. Nerve terminals of the rat posterior pituitary were acutely dissociated and identified using a combination of morphological and immunohistochemical techniques. Terminal membrane currents were studied using the 'whole-cell' patch clamp technique and channels were studied using inside-out and outside-out patches. 2. In physiological solutions, but with 7 mM 4-aminopyridine (4-AP), depolarizing voltage clamp steps from different holding potentials (-90 or -50 mV) elicited a fast, inward current followed by a slow, sustained, outward current. This outward current did not appear to show any steady-state inactivation. 3. The threshold for activation of the outward current was -30 mV and the current-voltage relation was 'bell-shaped'. The amplitude increased with increasingly depolarized potential steps. The outward current reversal potential was measured using tail current analysis and was consistent with that of a potassium current. 4. The sustained potassium current was determined to be dependent on the concentration of intracellular calcium. Extracellular Cd2+ (80 microM), a calcium channel blocker, also reversibly abolished the outward current. 5. The current was delayed in onset and was sustained over the length of a 150 ms-duration depolarizing pulse. The outward current reached a peak plateau and then decayed slowly. The decay was fitted by a single exponential with a time constant of 9.0 +/- 2.2 s. The decay constants did not show a dependence on voltage but rather on intracellular Ca2+. The time course of recovery from this decay was complex with full recovery taking > 190 s. 6. 4-AP (7 mM), dendrotoxin (100 nM), apamin (40-80 nM), and charybdotoxin (10-100 nM) had no effect on the sustained outward current. In contrast Ba2+ (200 microM) and tetraethylammonium inhibited the current, the latter in a dose-dependent manner (apparent concentration giving 50% of maximal inhibition (IC50) = 0.51 mM). 7. The neurohypophysial terminal outward current recorded here corresponds most closely to a Ca(2+)-activated K+ current (IK(Ca)) and not to a delayed rectifier or IA-like current. It also has properties different from that of the Ca(2+)-dependent outward current described in the magnocellular neuronal cell bodies of the hypothalamus. 8. A large conductance channel is often observed in isolated rat neurohypophysial nerve terminals. The channel had a unit conductance of 231 pS in symmetrical 150 mM K+.(ABSTRACT TRUNCATED AT 400 WORDS)
Canine basilar artery rings precontracted with 5-hydroxytryptamine (0.1-0.5 microM) relaxed in the presence of acetylcholine (25-100 microM), sodium nitroprusside (0.1 microM), or stimulation of the electrogenic sodium pump by restoration of extracellular K+ (4.5 mM) after K(+)-deprivation. Acetylcholine-induced relaxation is believed to be caused by the release of endothelium-derived relaxing factor (EDRF) and is prevented by mechanical removal of the endothelium, while relaxations induced by sodium nitroprusside or restarting of the sodium pump are endothelium-independent. Acetylcholine-induced relaxation was selectively blocked by pretreatment of the tissue with the nonselective K+ conductance inhibitors, 4-aminopyridine (4-AP, 3 mM), Ba2+ (1 mM), and tetraethylammonium (20 mM), 4-AP also blocked ACh-mediated relaxation in muscles contracted with elevated external K+. Relaxation of 5-hydroxytryptamine-induced contraction by sodium nitroprusside, or by addition of K+ to K(+)-deprived muscle, was not affected by 4-AP. Relaxation of basilar artery with acidified sodium nitrite solution (containing nitric oxide) was reduced by 4-AP. These results suggest that 4-AP and possibly Ba2+ inhibit acetylcholine-induced endothelium-dependent relaxation by inhibition of the action of EDRF on the smooth muscle rather than through inhibition of release of EDRF. The increase in K+ conductance involved in acetylcholine-induced relaxation is not due to ATP-inhibited K+ channels, as it is not blocked by glyburide (10(-6) M). Endothelium-derived relaxant factor(s) may relax smooth muscle by mode(s) of action different from that of sodium nitroprusside or by hyperpolarization due to the electrogenic sodium pumping.(ABSTRACT TRUNCATED AT 250 WORDS)
PURPOSE: To compare fat-suppressed, gadolinium-enhanced, breath-hold magnetic resonance (MR) imaging after administration of dilute oral barium solution with unenhanced MR imaging and computed tomography (CT) in the detection of peritoneal tumors. MATERIALS AND METHODS: In 24 patients in whom peritoneal tumor was known or suspected, double-contrast MR imaging and CT were performed prospectively. MR imaging included T1-weighted, fast spin-echo T2-weighted, and immediate and delayed gadolinium-enhanced, breath-hold, fast multiplanar sequences with fat saturation. Helical and conventional dynamic CT were performed with intravenously and orally administered contrast media. MR images and CT scans were reviewed independently and prospectively by different pairs of radiologists for presence of peritoneal tumor in 17 anatomic sites. Imaging findings were compared with surgical and histopathologic results. RESULTS: Of the 24 patients, 18 had peritoneal tumor confirmed at surgery. Detection of tumor sites was superior with double-contrast MR images (mean sensitivity, specificity, and accuracy, 84%, 87%, and 86%, respectively) compared with CT scans (mean sensitivity, specificity, and accuracy, 54%, 91%, and 74%, respectively). Double-contrast MR imaging enabled better detection of carcinomatosis and tumors less than 1 cm in diameter (75%-80%) than CT (22%-33%; P < .0001). CONCLUSION: Double-contrast MR imaging demonstrated more peritoneal tumors than CT or unenhanced spin-echo MR imaging.
We explored the possibility that ATP-sensitive potassium (KATP) channels exist in urinary bladder smooth muscle, since synthetic openers (e.g., lemakalim) of KATP channels in other tissues relax bladder smooth muscle. Unitary currents through single potassium channels and whole cell potassium currents were measured in smooth muscle cells isolated from the detrusor muscle of the guinea pig bladder. Lemakalim (10 microM) increased whole cell K+ currents by 50 pA at -80 mV with 60 mM external K+ when the cells were dialyzed with 0.1 mM ATP and 140 mM K+. Glibenclamide (10 microM), a sulfonylurea blocker of KATP channels in other tissues, inhibited the entire lemakalim-stimulated current as well as 19 pA of the steady-state K+ current. Glibenclamide-sensitive K+ currents were not dependent on voltage. Increasing intracellular ATP from 0.1 to 3.0 mM reduced the glibenclamide-sensitive K+ current in both the presence and absence of lemakalim by about fourfold. External barium (100 microM) which blocks KATP channels in skeletal muscle reduced KATP channel currents in bladder smooth muscle by 50% at -80 mV. Lemakalim (10 microM) increased the open-state probability of single K+ channels in outside-out patches (with 0.1 mM internal ATP) by sixfold. The single-channel conductance was approximately 7 pS at 0 mV with a physiological K+ gradient. This single-channel conductance was in accord with estimates of conductance made from noise analysis of the lemakalim-induced whole cell current. Glibenclamide inhibited these channels. The number of channels per cell was estimated to be approximately 425. We conclude that urinary bladder smooth muscle has KATP channels and that these channels can be opened by the K+ channel opening drug, lemakalim, and blocked by external glibenclamide and barium. We propose that modulation of these channels may regulate bladder contractility.
The effects of low concentrations of Ba have been studied on dog Purkinje fibers and on guinea pig left ventricular epicardium. In both tissues, Ba induces diastolic depolarization at a membrane potential more negative than -80 mV. This effect becomes clearly detectable at concentrations as low as 10-20 microM in Purkinje fibers bathed in 5.4 mM K Tyrode solution and around 100 microM in ventricular epicardium. In both tissues the Ba-induced depolarization is blocked in a dose-dependent manner by low concentrations of Cs (0.5-5 mM) as is the normal pacemaker current (if) in Purkinje fibers. In ventricular muscle the Ba-induced depolarization develops at the same rate whether the tissue is at rest or depolarized by repetitive stimulation. The maximum (initial) slope of diastolic depolarization is insensitive to D 600, La, and 4-aminopyridine, increased by tetraethylammonium chloride, decreased by tetrodotoxin, and almost entirely suppressed by Na removal. Experimental data and reconstruction of electrical activity suggest that in ventricular muscle the Ba-induced diastolic depolarization results to a large extent from the unmasking of a small pacemaker inward current, mainly carried by Na ions and similar to the pacemaker current of Purkinje fibers. Unmasking of the depolarizing effect of the pacemaker current is very likely due to the decrease by Ba of the inward going rectification. Steady-state inward Na current flowing through the Na window can increase the diastolic depolarization. Residual Cs-insensitive, Ba-induced diastolic depolarization may result from a time-dependent blockade of the background K conductance like the one described in skeletal muscle.
We previously described a Ca2(+)-activated K+ channel (KCLIC) in airway epithelial cells [J. D. McCann, J. Matsuda, M. Garcia, G. Kaczorowski, and M. J. Welsh. Am. J. Physiol 258 (Lung Cell. Mol. Physiol. 2): L334-L342, 1990]. To determine whether the KCLIC channel is a basolateral membrane channel and to understand its role in Cl- secretion, we studied airway epithelial cells grown on permeable supports. When cells were stimulated with A23187, charybdotoxin (ChTX) inhibited Cl- secretion and 86Rb efflux at the same concentrations, indicating that the KCLIC channel is required for Ca2(+)-stimulated Cl- secretion. We also investigated the function of K+ channels in adenosine 3',5'-cyclic monophosphate-stimulated secretion. Addition of isoproterenol caused a biphasic increase in Cl- secretion; the time course of the transient component correlated with the time course of the isoproterenol-induced increase in Ca2+ concentration [( Ca2+]c). ChTX inhibited the transient component, but not the prolonged component of secretion; Ba2+ inhibited the sustained component. These results suggest that when cells are grown on permeable supports isoproterenol-induced secretion depends on activation of two types of K+ channel: the KCLIC channel that is stimulated initially and a ChTX-insensitive K+ channel that is stimulated during sustained secretion. This conclusion was supported by measurement of 86Rb efflux from cell monolayers.
Expression of "fast", TTX-sensitive sodium and high-threshold calcium channels in the membrane of Xenopus oocytes following mRNA injection from the rat brain has been detected using two microelectrode voltage clamp technique. Barium current through expressed calcium channels was blocked by 200 mumol/l Cd2+ and was insensitive to D-600 (20 mumol/l) and nitrendipine (50 mumol/l). Expressed barium current was inhibited within 20-40 min by omega-conotoxin, a peptide neurotoxin known to block high-threshold calcium channels of the neuronal membrane, in 1 mumol/l concentration. A steady-state inactivation curve for this current could be fitted by the Boltzmann relation with V1/2 = -50 mV and k = 14 mV. Voltage-dependent and pharmacological properties of calcium channels which appeared in the oocyte membrane following mRNA injection from the mammalian brain resembled most of all those of high-threshold inactivating (HTI- or N-type) calcium channels of neurons in spite they did not demonstrate prominent time-dependent inactivation. Evidences in favour of expressed calcium channels heterogeneity were not obtained.