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PubMedDate not supplied

A chemically 'defined' diluent for cryopreservation of bovine spermatozoa.

A chemically 'defined' extender for the cryopreservation of bovine spermatozoa was developed using commercially available lecithin as an additive to protect cells against freeze damage. The effectiveness of different media in preventing cryoinjury was evaluated by assessing motion activity immediately post-thaw and after 2 h incubation at 37 degrees C by means of automatic computer image analysis. The extender best suited to maintains swimming activity consisted of the zwitter ion buffer system HEPES-Tris/Citrate (HTC) supplemented with 0.9% lecithin. The effectiveness of this diluent was compared with that of an extender containing egg yolk used routinely in breeding stations. While immediately post-thaw sperm samples frozen in HTC showed a lower motion activity than those preserved in egg yolk diluent, the opposite result was obtained after 2 h incubation at 37 degrees C.

Animals↗
PubMed1997

Effects of extracellular pH on receptor-mediated Ca2+ influx in A7r5 rat smooth muscle cells: involvement of two different types of channel.

1. The effects of extracellular pH (pHo) on receptor (vasopressin or endothelin-1)-mediated Ca2- entry and Ca(2+)-permeable channels were investigated in aortic smooth muscle cells (A7r5) from rat embryonic thoracic aorta. Intracellular Ca2+ ([Ca2+]i) was measured using fura-2 AM and whole-cell voltage clamp techniques were employed. 2. Vasopressin and endothelin-1 (100 nM) in the presence of nicardipine (10 microM) evoked a sustained rise in [Ca2+]i due to calcium entry. Extracellular acidosis decreased receptor (vasopressin or endothelin-1)-mediated Ca2+ entry, while extracellular alkalosis potentiated it. 3. Depletion of intracellular Ca2+ stores with thapsigargin (1 microM) also evoked Ca2+ entry activated by emptying of intracellular Ca2+ stores (capacitative Ca2+ entry). Extracellular acidosis decreased this capacitative Ca2+ entry, while extracellular alkalosis potentiated it. 4. Under voltage-clamp conditions with Ca+ internal solution, vasopressin and endothelin-1 activated non-selective cation currents (ICAT). Ba2+ or Ca2+ were also charge carriers of ICAT. Reducing the pHo inhibited ICAT, while increasing pHo potentiated it in a reversible manner. 5. Intracellular pH (pHi) changes did not cause the same marked effects as pHo changes, and a high concentration of Hepes (50 mM) in the patch pipette did not inhibit the effects of pHo on ICAT. 6. Similar results were obtained when ICAT was activated by GTP gamma S (1 mM) applied through the patch pipette, even in the absence of agonists, probably because of direct activation of GTP-binding proteins coupled to the receptors. 7. In cells treated with thapsigargin, addition of Ca2+ to the bath solution induced Ca(2+)-dependent K+ currents activated by capacitative Ca2+ entry. However, no measurable ionic currents activated by capacitative Ca2+ entry (ICRAC) were observed under conditions with Cs+ internal solution and EGTA (5 mM), although vasopressin still activated ICAT. 8. These results suggest that the contractile agonists vasopressin and endothelin-1 evoked Ca2+ entry through two different types of Ca(2+)-permeable channel (ICAT and ICRAC) and pHo affects these channels, which may modulate receptor-mediated Ca2+ influx in A7r5 cells. Thus, pH-induced changes of these channels may play a pathophysiological role in the control of receptor-mediated contractions.

Animals↗
PubMed1998

Evidence for an electrogenic Na+-HCO3- symport in rat cardiac myocytes.

1. The perforated whole-cell configuration of patch clamp and the pH fluorescent indicator SNARF were used to determine the electrogenicity of the Na+-HCO3- cotransport in isolated rat ventricular myocytes. 2. Switching from Hepes buffer to HCO3- buffer at constant extracellular pH (pHo) hyperpolarized the resting membrane potential (RMP) by 2.9 +/- 0.4 mV (n = 9, P < 0.05). In the presence of HCO3-, the anion blocker SITS depolarized RMP by 2.6 +/- 0.5 mV (n = 5, P < 0.05). No HCO3--induced hyperpolarization was observed in the absence of extracellular Na+. The duration of the action potential measured at 50 % of repolarization time (APD50) was 29.2 +/- 6.1 % shorter in the presence of HCO3- than in its absence (n = 6, P < 0.05). 3. Quasi-steady-state currents were evoked by voltage-clamped ramps ranging from -130 to +30 mV, during 8 s. The development of a novel component of Na+-dependent and Cl--independent steady-state outward current was observed in the presence of HCO3-. The reversal potential (Erev) of the Na+-HCO3- cotransport current (INa,Bic) was measured at four different levels of extracellular Na+. A HCO3-:Na+ ratio compatible with a stoichiometry of 2:1 was detected. INa,Bic was also studied in isolation in standard whole-cell experiments. Under these conditions, INa,Bic reversed at -96.4 +/- 1.9 mV (n = 5), being consistent with the influx of 2 HCO3- ions per Na+ ion through the Na+-HCO3- cotransporter. 4. In the presence of external HCO3-, after 10 min of depolarizing the membrane potential (Em) with 45 mM extracellular K+, a significant intracellular alkalinization was detected (0.09 +/- 0. 03 pH units; n = 5, P < 0.05). No changes in pHi were observed when the myocytes were pre-treated with the anion blocker DIDS (0.001 +/- 0.024 pH units; n = 5, n.s.), or when exposed to Na+-free solutions (0.003 +/- 0.037 pH units; n = 6, n.s.). 5. The above results allow us to conclude that the cardiac Na+-HCO3- cotransport is electrogenic and has an influence on RMP and APD of rat ventricular cells.

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

Out-of-equilibrium pH transients in the guinea-pig ventricular myocyte.

1. Following an intracellular alkali load (imposed by acetate prepulsing in CO2/HCO3- buffer), intracellular pH (pHi) of the guinea-pig ventricular myocyte (recorded from intracellular SNARF fluorescence) recovers to control levels. Recovery has two phases. An initial rapid phase (lasting up to 2 min) is followed by a later slow phase (several minutes). Inhibition of sarcolemmal acid-loading carriers (by removal of extracellular Cl-) inhibits the later, slow phase but the initial rapid recovery phase persists. It also persists in the absence of extracellular Na+ and in the presence of the HCO3- transport inhibitor DIDS (4,4-di-isothiocyanatostilbene-2, 2-disulphonic acid). 2. The rapid recovery phase is not evident if the alkali load has been induced by reducing PCO2 (from 10 to 5 %), and it is inhibited in the absence of CO2/HCO3- buffer (i.e. Hepes buffer). It is also slowed by the carbonic anhydrase (CA) inhibitor acetazolamide (ATZ). We conclude that it is caused by buffering of the alkali load through the hydration of intracellular CO2 (CO2-dependent buffering). 3. The time course of rapid recovery is consistent with an intracellular CO2 hydration rate constant (k1) of 0.36 s-1 in the presence of CA activity, and 0.14 s-1 in the absence of CA activity. This latter k1 value matches the literature value for uncatalysed CO2 hydration in free solution. Natural CO2 hydration is accelerated 2.6-fold in the ventricular myocyte by endogenous CA. 4. The rapid recovery phase represents a period when the intracellular CO2/HCO3- buffer is out of equilibrium (OOE). Modelling of the recovery phase using our k1 value, indicates that OOE conditions will normally extend for at least 2 min following a step rise in pHi (at constant PCO2). If CA is inactive, this period can be as long as 5 min. During normal pHi regulation, the recovery rate during these periods cannot be used as a measure of sarcolemmal acid loading since it is a mixture of slow CO2-dependent buffering and transmembrane acid loading. The implication of this finding for quantification of pHi regulation during alkalosis is discussed.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1991

Ionic basis for color changes in the iridescent cornea of the sand goby (Pomatoschistus minutus).

The iridescence from the cornea of the sand goby (Pomatoschistus minutus) occurs because of thin layer interference from the platelet-like cells in the stroma. It is suggested that ionic pumps across the epithelium control the water content in the stroma and thus the spectral reflection. A saline was perfused over goby eyes and simple ion manipulation was carried out to observe any changes in the iridescent characteristics. It was found that removal of Cl- and K+ ions reduced the peak reflected wavelength to the blue end of the spectrum, whereas Na+ had little effect. The removal of K+ also caused a dramatic change to the normal shift in reflected spectral intensity. The iridescence was also found to be sensitive to pH, and the buffer HEPES was detrimental to the cornea compared to controls. These results suggest similarities to amphibian and mammalian corneal hydration control.

Animals↗
PubMed2004

Volume regulation is defective in renal proximal tubule cells isolated from KCNE1 knockout mice.

The membrane protein KCNE1 has been implicated in cell volume regulation. Using a knockout mouse model, this study examined the role of KCNE1 in regulatory volume decrease (RVD) in freshly isolated renal proximal tubule cells. Cell diameter was measured using an optical technique in response to hypotonic shock and stimulation of Na(+)-alanine cotransport in cells isolated from wild-type and KCNE1 knockout mice. In HEPES buffered solutions 64% of wild-type and 56% of knockout cells demonstrated RVD. In HCO3- buffered solutions 100% of the wild-type cells showed RVD, while in the knockout cells the proportion of cells displaying RVD remained unchanged. RVD in the knockout cells was rescued by valinomycin, a K+ ionophore. In wild-type HCO3- dependent cells the K+ channel inhibitors barium and clofilium inhibited RVD. These data suggest that mouse renal proximal tubule is comprised of two cell populations. One cell population is capable of RVD in the absence of HCO3-, whereas RVD in the other cell population has an absolute requirement for HCO3-. The HCO3- dependent RVD requires the normal expression of KCNE1.

Animals↗
PubMed2003

Characterization of specific opioid binding sites in neural membranes from the myenteric plexus of porcine small intestine.

Delta- and kappa-opioid receptors (OPRs), but not micro-OPRs, are expressed in the myenteric plexus of the porcine distal small intestine. In a subpopulation of myenteric neurons, delta- and kappa-OPRs seem to be colocalized and may functionally interact. In this study, radioligand binding was used to characterize myenteric OPR populations in detail. The nonselective OPR antagonist [3H]diprenorphine bound to a single, high-affinity site in myenteric neural membrane homogenates. Naloxone displaced 65 and 59% of [3H]diprenorphine binding from this site in Na(+)-free Tris and Krebs-HEPES buffers, respectively. Naltrexone-derived delta- and kappa-OPR antagonists, including naltriben, 7-benzylidenenaltrexone, nor-binaltorphimine, and 5'-guanidinonaltrindole, displaced [3H]diprenorphine from two distinct binding sites to levels similar to that of naloxone. The selective delta-OPR ligands Tyr-1,2,3,4-tetrahydroisoquinoline-Phe-Phe-OH (TIPP), [D-Pen2,D-Pen5]enkephalin (DPDPE), [D-Ala2, Glu4]deltorphin II, and (+)-4-[(alphaR)-alpha((2S,5R)-4-allyl-2,5-dimethyl-1-piperazinyl-3-methoxybenzyl)-N,N-diethylbenzamide (SNC-80) and the kappa-OPR agonist (D-(5alpha,7alpha,8beta)-(-)-N-methyl-N-(7-(1-pyrrolidinyl)-1-oxoaspiro-(4,5)dec-8-yl) benzeneacetamide (U-69,593) displaced [3H]diprenorphine from three independent binding sites; these included high-affinity delta- and kappa-OPR sites, and a residual binding site. Residual [3H]diprenorphine binding was displaced by the selective kappa-OPR antagonist nor-binaltorphimine after saturation of delta and kappa sites, respectively, with DPDPE and U-69,593. The residual binding site displayed low affinity for delta- and kappa-OPR agonists and TIPP, as well as moderate affinity for naltrexone-derived ligands, properties reminiscent of delta-/kappa-OPR heterodimers.

Animals↗
PubMed1999

Transcriptional regulation of the esp genes of enterohemorrhagic Escherichia coli.

We have determined that the genes encoding the secreted proteins EspA, EspD, and EspB of enterohemorrhagic Escherichia coli (EHEC) are organized in a single operon. The esp operon is controlled by a promoter located 94 bp upstream from the ATG start codon of the espA gene. The promoter is activated in the early logarithmic growth phase, upon bacterial contact with eukaryotic cells and in response to Ca2+, Mn2+, and HEPES. Transcription of the esp operon seems to be switched off in tightly attached bacteria. The activation process is regulated by osmolarity (induction at high osmolarities), modulated by temperature, and influenced by the degree of DNA supercoiling. Transcription is sigmaS dependent, and the H-NS protein contributes to its fine tuning. Identification of the factors involved in activation of the esp operon and the signals responsible for modulation may facilitate understanding of the underlying molecular events leading to sequential expression of virulence factors during natural infections caused by EHEC.

Amino Acid Sequence↗
PubMed2002

Technical improvement to prevent DNA degradation of enteric pathogens in pulsed-field gel electrophoresis.

This study used a modified pulsed-field gel electrophoresis (PFGE) method with HEPES as a running buffer to prevent electrophoresis-related DNA degradation of nine Salmonella enterica subsp. enterica serovar Ohio, seven Salmonella serovar Newport, and two enterohemorrhagic Escherichia coli (non-O157) strains. All strains yielded identifiable bands with this method in contrast to a commonly applied PFGE method using Tris buffer.

Bacterial Typing Techniques↗
PubMed1990

Acetate absorption in the normal and secreting rat jejunum.

Acetate absorption was studied in rat jejunum using steady state perfusion in vivo. Absorption conformed to apparent saturation kinetics and was similar in magnitude to glucose absorption. When compared with normal saline, acetate perfusion was associated with luminal alkalinisation. There was no difference in total CO2 secretion when similar rates of acetate and glucose absorption were compared, suggesting that total CO2 secretion was the result of mucosal metabolism. Absorption of acetate and propionate were mutually inhibitory. Acetate absorption was also inhibited by Tris-Hepes pH 7.0. When the gut was pretreated with cholera toxin to induce a secretory state, acetate absorption was reduced by 41.9%. This effect could be reproduced if similar water secretion was osmotically induced by the addition of mannitol. These data suggest that acetate is absorbed, at least, partially by non-ionic diffusion in the rat jejunum and that its absorption is reduced in the secreting intestine by solvent drag.

Acetates↗
PubMed1987

Extracellular acidification at the surface of depolarized voltage-clamped snail neurones detected with eccentric combination pH microelectrodes.

A new design of double micropipette was used to measure intracellular pH, membrane potential, and surface pH of superfused snail neurones. A third double micropipette was used to control the membrane potential via a CsCl-filled barrel and inject HCl iontophoretically. In one series of experiments the surface pH fell by up to one-third of a pH unit when the membrane potential was clamped to 20 mV, pHi was initially 6.7, and extracellular pH was about 7.4 in a medium buffered either with 2 mM HEPES or 2.7% CO2 and 20 mM bicarbonate. In a second series in which surface pH was observed during brief depolarizations to different potentials with different pHi, the potential at which the surface began to acidify varied with pHi with a slope of 32 mV per pH unit. The results confirm that H+ ions leave depolarized snail neurones if the electrochemical gradient is favourable and show that CO2-bicarbonate buffered solutions have a low effective extracellular buffering power for rapid additions of acid.

Animals↗
PubMed1986

Chloride transport of frog gastric fundus: effects of omeprazole.

Omeprazole (10(-4) M) inhibited H+ secretion and increased potential difference (PD), resistance, and short-circuit current (Isc) in chambered bullfrog gastric mucosa, but the electrical changes developed only in tissues previously exposed to histamine. Net chloride transport (JnetCl) did not change after omeprazole under short-circuited conditions, and Isc increased to become equal to JnetCl. Under open-circuit conditions, JnetCl was reduced by 38%, the decrement attributable to the concomitant increase in PD, as evidenced by a linear relationship between JnetCl and PD in omeprazole-treated mucosae clamped to different PD (0-45 mV). The effect of omeprazole on PD and Isc could be blocked by metiamide and was absent in spontaneously resting tissues. HEPES nutrient solutions did not alter the electrical response or Cl- transport after omeprazole. In Na+-free solutions, omeprazole induced only a transient rise in PD and Isc. We conclude that omeprazole uncouples H+ and Cl- secretion. This Cl- secretion is electrogenic and dependent upon stimulation by histamine. Both Na+ and HCO3- seem to be involved in movement of Cl- across the basolateral membrane.

Animals↗
PubMed1989

Effect of PCO2 on intracellular pH in in vitro frog gastric mucosa.

Steady-state intracellular pH (pHi) in 0, 5, and 10% CO2-buffered Ringer solution in sheets of in vitro frog gastric antral or fundic mucosa has been measured using the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF). In tissues perfused with N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-100% O2 buffer [extracellular pH (pHo) = 7.14], steady-state pHi in antral surface cells was 7.08 +/- 0.06 (n = 8), in fundic oxynticopeptic cells 6.91 +/- 0.03 (n = 13), in the muscularis mucosa 7.58 +/- 0.06 (n = 4). In mucosae perfused with 17.8 mM HCO3- -95% O2-5% CO2 buffer (pHo = 7.14), steady-state pHi in antral surface cells was 6.97 +/- 0.02 (n = 22), in fundic oxynticopeptic cells 7.00 +/- 0.04 (n = 18), and in fundic muscularis mucosa 7.39 +/- 0.05 (n = 8). In fundic oxynticopeptic cells perfused with 35.6 mM HCO3- -90% O2-10% CO2 (pHo = 7.14) steady-state pHi was 6.77 +/- 0.07 (n = 4). In tissues equilibrated initially with 100% O2 and changed to 5% CO2, antral surface cells acidified by 0.21 pH units and fundic oxynticopeptic cells by 0.10 pH units, with restoration of pHi to resting levels within 30 and 10 min, respectively. Exposure of tissues initially equilibrated with 5% CO2 to 100% O2 alkalinized antral surface cells by 0.22 pH units and fundic oxynticopeptic cells by 0.23 pH units, with only partial recovery of pHi by 30 min. These data suggest that steady-state pHi is equivalent in surface and oxynticopeptic cells and is lower than in the muscularis mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Influence of Cl- on pH(i) in oxynticopeptic cells of in vitro frog gastric mucosa.

The effect of Cl- on intracellular pH (pH(i)) was studied using sheets of frog (Rana catesbeiana) fundic mucosa in which oxynticopeptic cells were selectively loaded with the acetomethoxy ester form of the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF/AM). Before the measurement of pH(i), tissues were exposed to either 10(-5) M forskolin in the serosal solution (stimulated tissues) or 3 x 10(-4) omeprazole in the serosal solution (inhibited tissues). In HCO3- and N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) buffers, pH(i) increased significantly after removal of Cl- from serosal and luminal solution, both in stimulated and inhibited tissues. The presence of Cl- in the luminal solution prevented this rise in pHi, an effect abolished by serosal 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS, 3 x 10(-4) M) but not by serosal amiloride (10(-3)M). In the presence of serosal Cl-, pH(i) increased after exposure to serosal DIDS, more prominently in the stimulated than in the inhibited tissues. These results confirm the presence of a Cl(-)-HCO3-exchanger in the basolateral membrane of oxynticopeptic cells in intact sheets of mucosa and suggest that luminal Cl- contributes to the regulation of pH(i) in oxynticopeptic cells.

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

Nonionic diffusion of short-chain fatty acids across rat colon.

Short-chain fatty acid (SCFA) transport across the colon may occur by nonionic diffusion and/or via apical membrane SCFA-/HCO3- exchange. To examine the relative importance of these processes, stripped segments of rat (Ratus ratus) proximal and distal colon were studied in Ussing chambers, and the unidirectional fluxes of radiolabeled SCFA butyrate, propionate, or weakly metabolized isobutyrate were measured. In N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) or 1 or 5 mM HCO3- Ringer, decreases in mucosal pH stimulated mucosal-to-serosal flux (Jm-->s) of all SCFA, decreases in serosal pH stimulated serosal-to-mucosal flux (Js-->m), and bilateral pH decreases stimulated both fluxes equally. These effects were observed whether the SCFA was present on one or both sides of the tissue, in both proximal and distal colon, in the absence of luminal Na+, and in the presence of either luminal or serosal ouabain. Changes in intracellular pH or intracellular [HCO3-] did not account for the effects of extracellular pH. Luminal Cl- removal, to evaluate the role of apical membrane Cl-/SCFA- exchange, had no effect on Jm-->s but decreased Js-->m 32% at pH 6.5 and 22% at 7.2. Increasing SCFA concentration from 1 to 100 mM, at pH 6.4 or 7.4, caused a linear increase in Jm-->s. We conclude that SCFA are mainly transported across the rat colon by nonionic diffusion.

Animals↗
PubMed2004

Disodium cromoglycate stabilizes mast cell degranulation while reducing the number of hemoglobin-induced microvascular leaks in rat mesentery.

Blood substitutes, such as diaspirin cross-linked Hb (DBBF-Hb), have been considered for use during blood transfusions. Unfortunately, bolus injection of modified Hb has been shown to rapidly increase the leakage of microvessels to plasma albumin. This effect may result from production of excess reactive oxygen species (ROS) and could be linked to the observed increase in degranulated mast cells (DMC). Disodium cromoglycate (cromolyn) stabilizes mast cells and therefore might minimize the venular permeability in the rat mesentery. In 10 anesthetized Sprague-Dawley rats, the mesenteric preparation was continuously suffused with cromolyn while the microvasculature was filled with DBBF-Hb solution (10 mg/ml) for 10 min. Six animals received cromolyn pretreatment [two intravascular injections over 30 min (experiment A)] and four animals received pretreatment with 2% HEPES-buffered saline (HBS)-BSA (experiment B). Two more animals were pretreated with HBS-BSA without DBBF-Hb infusion but with cromolyn suffusion (experiment C). Another set of experiments was performed on five animals without cromolyn suffusion or any pretreatment but with DBBF-Hb infusion (experiment D). All groups then received a 1-min perfusion of FITC-albumin, fixation for 60 min, and microscopic examination. Experiments A and B demonstrated a significant reduction in the number of venular leaks and DMC compared with experiment D, but not in the area of venular leaks. These results suggest mast cell degranulation is not a major contributor to microvascular leakage induced by DBBF-Hb.

Animals↗
PubMed2002

Manipulation of chloride flux affects histamine-induced contraction in rabbit basilar artery.

Cl(-) efflux induces depolarization and contraction of smooth muscle cells. This study was undertaken to explore the role of Cl(-) flux in histamine-induced contraction in the rabbit basilar artery. Male New Zealand White rabbits (n = 16) weighing 1.8-2.5 kg were euthanized by an overdose of pentobarbital sodium. The basilar arteries were removed for isometric tension recording. Histamine produced a concentration-dependent contraction that was attenuated by the H(1) receptor antagonist chlorpheniramine (10(-8) M) but not by the H(2) receptor antagonist cimetidine (3 x 10(-6) M) in normal Cl(-) Krebs-Henseleit bicarbonate solution (123 mM Cl(-)). The histamine-induced contraction was reduced by the following manipulations: 1) inhibition of Na(+)-K(+)-2Cl(-) cotransporter with bumetanide (3 x 10(-5) and 10(-4) M), 2) bicarbonate-free HEPES solution to disable Cl(-)/HCO exchanger, and 3) blockade of Cl(-) channels with the use of niflumic acid, 5-nitro-2-(3-phenylpropylamino) benzoic acid, and indoleacetic acid 94 R-(+)-methylindazone. In addition, substitution of extracellular Cl(-) (10 mM) with methanesulfonate acid (113 mM) transiently enhanced histamine-induced contraction. Manipulation of Cl(-) flux affects histamine-induced contraction in the rabbit basilar artery.

Animals↗
PubMed1975

Effects of synthetic buffers on reflexes in the isolated frog spinal cord.

Substitution of synthetic buffers (Tris, TES, HEPES, or 3,3-dimethylglutarate) for CO2-bicarbonate buffer in Ringer solution perfusing the isolated in vitro frog spinal cord preparation altered membrane properties and reflex activity. Perfusion with Ringer solution gassed with O2 and containing synthetic bu,fers consistently produced a depolarization of motoneurons and dorsal root fibers, decreased the amplitude (and usually the duration) of ventral and dorsal root potentials, and had variable effects on motoneuron and dorsal root reflex discharges. With Tris-Ringer these discharges decreased in amplitude; with Ringer containing one of the other synthetic buffers, these discharges were augmented. All changes were reversible when the cord was returned to bicarbonate-buffered Ringer aerated with 95% O2/5% CO2. The use of a combined buffer system-one containing a synthetic buffer and bicarbonate-induced smaller or minimal changes in bioelectric activity. At present the data are insufficient to allow firm conclusions concerning the mechanisms underlying these results; but it is evident 1) that changes in PCO2 and bicarbonate concentration and 2) that the pharmacological properties of synthetic buffers are important variables.

Animals↗