Effects of angiotensin II on inotropy and intracellular Ca2+ handling in normal and hypertrophied rat myocardium

The direct inotropic effect of angiotensin II on the myocardium is still controversial and little information exists as to its potential modification by heart disorders. Therefore, this study performed simultaneous measurements of isometric force and intracellular Ca2+ concentrations ([Ca2+]i) in left ventricular papillary muscles from sham-operated and aortic-banded rats at 10 weeks post-surgery. Angiotensin II (10(-6) M) induced a reduction of peak systolic [Ca2+]i (0.56 +/- 0.03 to 0.48 +/- 0.04 microM; P<0.05) and a parallel but insignificant diminution of developed tension (10.5 +/- 1.3 to 9.6 +/- 0.8 mN/mm2) in normal papillary muscles from sham-operated animals. Hypertrophied papillary muscles from aortic-banded rats demonstrated a significant decline in both peak systolic [Ca2+]i (0.51 +/- 0.02 to 0.44 +/- 0.01 microM; P<0.05) and developed tension (8.4 +/- 1.1 to 6.8 +/- 1.7 mN/mm2; P<0.05) after addition of angiotensin II. The time courses of the mechanical contraction and the intracellular Ca2+ signal were prolonged by angiotension II in both groups. Isoproterenol dose-dependently increased developed tension and peak systolic [Ca2+]i in papillary muscles from sham-operated rats. In contrast, the positive inotropic response to isoproterenol was markedly reduced in hypertrophied muscles despite a seemingly unimpaired increase in peak systolic [Ca2+]i. Pretreatment with angiotensin II (10(-6) M) resulted in a significant attenuation of the systolic [Ca2+]i response to isoproterenol stimulation in both normal and hypertrophied papillary muscles. Neither the bradykinin B2 antagonist icatibent (10(-6) M) nor the nitric oxide (NO) inhibitor L-NMMA (10(-6) M) abolished the depressant effects of angiotension II. Thus, ANG II induces a parallel decline of the mechanical performance and Ca2+ availability in rat myocardium. These effects are more distinct in hypertrophied than in normal muscle and become accentuated during beta-adrenergic stimulation. The underlying mechanism is not associated with the NO pathway but might involve a negative functional coupling between the angiotensin and beta-adrenergic-receptor complex.     

Effects of ischemia on intracellular sodium and phosphates in the in vivo rat liver

Metabolic factors that influence the transition form reversible to irreversible ischemic injury were studied in the rat liver in vivo with 31P-nuclear magnetic resonance (NMR) spectroscopy. Hepatic ischemia for 15, 35, or 65 min was produced by occlusion of the hepatic artery and portal vein in rats. Ischemia caused a rapid decrease in the ATP concentration ([ATP])-to-P(i) concentration ratio and pH within 5 min, but there was little change in these variables detectable by 31P-NMR with longer periods of ischemia. After reperfusion, the [ATP] and P(i) concentration returned toward normal values in livers exposed to 15 or 35 min of ischemia, but 65 min of ischemia were associated with only modest recovery in [ATP], and the [ATP] later decreased. Because the 31P-NMR spectrum was similar after brief compared with prolonged ischemia, it appears that neither ATP depletion, P(i) accumulation, nor acidosis predicts metabolic recovery. Hepatic intracellular NA+ was also measured in separate groups of animals by 23Na-NMR in the presence of a shift agent, thulium (III) 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetrakis (methylene-phosphonate) (TmDOTP5-), and by atomic absorption spectroscopy. Under baseline conditions, the concentration of intracellular Na+ was 15.2 mM by atomic absorption spectroscopy and 16.5 mM by 23Na-NMR. Although the 31P-NMR spectrum responded very rapidly to the onset of ischemia, intracellular Na+ concentration measured by 23Na-NMR increased gradually but steadily at approximately 1.0 mM/min during early (up to 15 min) ischemia. These observations demonstrate that a rise in intracellular Na+ does occur early ischemia, that TmDOTP5- can be applied in vivo for analysis of intracellular Na+ in the ischemic liver, and that 31P-NMR spectroscopy is very sensitive to early ischemic injury.     

Effects of intracellular 4-aminopyridine and tetraethylammonium load on action potentials in the rabbit atrial myocardium

Investigated are rabbit atrial trabeculae (2-4 mm length, 150-800 micrometers diameter). When using a standard microelectrode technique, the action potentials after an intracellular 4-AP and TEA load are prolonged. Only the TEA load significantly diminishes the resting potential of the beating preparations. The typical configuration of the action potential following a period of rest (rapid initial repolarization, secondary depolarization and a late retarded repolarization) is not changed qualitatively. During a repetitive stimulation after a pacing pause the action potentials' restitution is accelerated at 4-AP. After 4-AP and TEA load the secondary depolarization of the first post rest action potential is more accentuated. By reconstructing the post rest action potentials a 4-AP sensitive current is determined. At constant drive this current shows a threshold potential at -40 and a reversal potential at -10 mV. The current is inward directed between -40 and -10 mV and is outward directed at more positive potentials than -10 mV. After a pacing pause the current-voltage relation is shifted to more negative potentials. The 4-AP sensitive current is modelled by consideration of a slow activated (during the action potential) and deactivated (during the pacing pause) conductivity. Processes of accumulation are discussed.     

Interactions between anemone toxin II and veratridine on single neuronal sodium channels

Restenosis is the single most important factor limiting a favorable long-term outcome following mechanical revascularization. The vascular endothelium, through the release of key regulatory compounds, may regulate vascular structure by exerting fundamental control over collagen synthesis following injury to the vessel wall. We tested the hypothesis that endothelin (ET-1), an endothelium-derived peptide previously shown to be increased in pathological states, differentially stimulates porcine coronary vascular smooth muscle cell collagen types I and III synthesis. Monocultures of porcine coronary vascular smooth muscle were exposed to varying concentrations of endothelin over a 24-96-h time period. The medium was assayed for soluble collagen types I and III using a sensitive and specific ELISA method. Experiments were also done with the ET-1 antagonists PD 145065 and BQ123. Cell counts and viability were serially monitored. Experiments were also conducted with angiotensin II (A-II). A-II and ET-1 stimulated cell proliferation. ET-1 maximally stimulated collagen type I synthesis at 48 h at an optimal concentration of 10(-8) M, with no significant stimulation of collagen type III synthesis. The ETA specific antagonist BQ123 significantly inhibited the stimulatory effects of ET-1. A-II also stimulated collagen type I synthesis above basal levels, but was less efficacious than endothelin (95 +/- 5%, A-II, v 189 +/- 14% ET-1). In contrast to ET-1, A-II stimulated collagen type III synthesis (31 +/- 6% above basal, compared to -4 +/- 5% for ET-1). Results are also reported using smooth muscle cells from porcine aorta. The data demonstrate that ET-1 and A-II stimulate collagen synthesis by coronary artery vascular smooth muscle, and that they exert a differential effect over the two types of collagen that are present in the intima following balloon injury. Thus, the over expression of key regulatory compounds by endothelium following balloon injury could enhance collagen deposition and, consequently, play an integral role in intimal hyperplasia and restenosis.     

Effects of cholera toxin on cellular and paracellular sodium fluxes in rabbit ileum

The diarrhea observed in patients with cholera is known to be related to secretion of water and electrolytes into the intestinal lumen. However, the exact mechanisms involved in these secretory processes have remained unclear. Although it is clear that purified toxin acts on epithelial cell metabolism, its activity on Na+ transport across intestinal mucosa is equivocal: reported either to prevent net Na+ absorption or to cause net secretion of Na+ from serosa to mucosa. Since total transmural Na+ fluxes across "leaky" epithelia involve very significant movement via a paracellular shunt pathway, we studied the effects of cholera toxin on the cellular and paracellular pathways of Na+ movement. Unidirectional Na+ fluxes were examined as functions of applied potential in control tissues and in tissues from the same animal treated with purified cholera toxin. Treatment of rabbit ileum in vitro with toxin simulated the cellular component of serosa-to-mucosa Na+ flux (from 2.41 +/- 0.49 muequiv./h per cm2 under control conditions to 4.71 +/- 0.43 muequiv./h per cm2 after treatment with toxin, P less than 0.01). The effect of cholera toxin on Na+ movement through the cells from mucosa to serosa appeared to be insignificant. Finally, a marked decrease in the Na+ permeability (P less than 0.01) and no detectable significant changes in transference number for Na+ of the paracellular shunt pathway were observed following treatment with cholera toxin. These results provide direct evidence for the hypothesis that purified cholera toxin stimulates active sodium secretion but has minimal effect on sodium absorption.     

The effects of Escherichia coli STa (heat stable) toxin on the contractility of isolated human myometrium in vitro

OBJECTIVE: The purpose of the study was to assess the effects of Escherichia coli STa (heat stable) toxin on isolated human myometrial response to oxytocin. METHODS: One hundred and sixteen muscle strips were obtained from the lower uterine segment of 42 women undergoing cesarean section at term. Amniotic membranes and decidua were excluded. Uterine contractility in response to cumulative doses of E. coli STa toxin was recorded, as well as uterine response to cumulative doses of oxytocin before and after incubation with STa toxin or vehicle. The 50th percentile effective oxytocin concentration (EC50) of muscle strips with and without spontaneous activity before and after the incubation with STa toxin or vehicle was calculated. A paired t test was used for comparison. RESULTS: Muscle strips with and without spontaneous activity responded to cumulative doses of oxytocin before and after the incubation with STa toxin or vehicle. No differences in contraction force, duration, or frequency were noted between the groups (P > 0.05). Furthermore, this toxin was not able to induce uterine contractility when tested alone. CONCLUSIONS: The inability of this toxin to affect myometrial response to oxytocin in this study may be due to the absence of amnion cells, chorion, or decidua. Other possible explanations for the lack of response are discussed.     

Excitation and contraction in atrial and ventricular myocardium of the guinea-pig

Unlike several other countries, the UK does not have a national occupational database describing jobs in terms of skill and other factors. Neither is there a nationally recognized method for assessing the functional skills which job seekers have to offer. If these two types of assessment were based on the same criteria, individuals could accurately match their profile to occupations or vacancies. Assistance with job placement is one of the most popular services offered by Royal National Institute for the Blind (RNIB) Employment Network to visually disabled people. Yet resources are stretched and the Network is considering computerizing its occupational information and job-matching activity to increase efficiency. By drawing upon a comparison of existing systems and recommendations in the literature this paper offers suggestions for the development of this system. Factors for consideration at the design stage are discussed, and the paper concludes with a programme for development, evaluation and implementation. The need to ensure quality standards through staff training and appropriate procedures is stressed.     

Effects of reserpine on tissue calcium and contractility of rat and rabbit aorta

Possible effects of reserpine on disposition and availability of tissue calcium, stores for excitation-contraction coupling in isolated rat and rabbit aortae were examined. Contral 40Ca uptake, 45Ca washout, and contraction in Ca2+-free medium (Ca2+-free PSS) indicate species differences in binding or disposition, apparent functional importance, and differential use of tissue calcium by adrenaline (Epi) and high K+. Rat aortae, normally refractory to Epi or high K+ after 7 min in Ca2+-free PSS, can gain labile calcium after brief exposure to Ca2+-rich PSS which supports short-lived responses to high K+ in Ca2+-free PSS. Rabbit aortae contain calcium stores which may sustain either Epi or high-K+ responses as well as more tightly held (or sequestered) stores released by Epi for contraction. After reserpine, decreased 45Ca uptake in a kinetically defined "fast" compartment likely to include membrane calcium could enhance availability of bound tissue as well as free Ca2+ in both species. Enhanced Epi response in Ca2+-free PSS is evidence of the former. Results suggest that increased availability of bound and possibly free calcium contribute to reserpine-induced supersensitivity, but supporting evidence will be required from tissue behavior after less rigorous treatment.     

Effects of oxytocin on in vitro ovarian contractility during the estrous cycle of the rat

Necrotizing skin lesions developed in a man with chronic ulcerative colitis. No evidence of intrinsic disease of medium or small-sized vessels was found. A circulating cryofibrinogen was thought to be responsible for in situ thrombosis leading to skin infarctions. Sodium warfarin in a daily dose of 2.5 to 5 mg appears to have thwarted progression of developing lesions and the occurrence of new ones.     

Effects of aging on the regulation of intracellular pH in the rat jejunum

Jejunal villus cells from young-adult (6 months) and senescent (24 months) male Wistar rats were studied to evaluate the effect of aging on intracellular pH (pHi) regulation. pHi was measured by quantitative fluorescence microscopy by using BCECF-AM [2',7'-bis(carboxyethyl)-5(6)-carboxy-fluorescein acetoxy methylester] under basal conditions and after inducing cytoplasmic acidification with pulsed NH4Cl. In the senescent rats, the recovery rate from the acidified levels was significantly lower than that in the young-adult rats (.208 +/- .005 vs .255 +/- .004 pH units/min). The relationship between pHi recovery and external Na+ concentration followed Michaelis-Menten type kinetics, the maximum velocity (Vmax) of alkalinization being significantly lower in the senescent rats than in the young-adult rats (.227 +/- .033 vs .297 +/- .024 pH units/min). These results indicate that the recovery of pHi from an acidic level was slower in the senescent rats, due to the reduced activity of Na+/H+ exchange as revealed by the decreased Vmax value.     

Effects of the nitric oxide donor sodium nitroprusside on intracellular pH and contraction in hypertrophied myocytes

BACKGROUND: We compared the effects of the nitric oxide donor sodium nitroprusside (SNP) on intracellular pH (pHi), intracellular calcium concentration ([Ca2+]i) transients, and cell contraction in hypertrophied adult ventricular myocytes from aortic-banded rats and age-matched controls. METHODS AND RESULTS: pHi was measured in individual myocytes with SNARF-1, and [Ca2+]i transients were measured with indo 1 simultaneously with cell motion. Experiments were performed at 37 degrees C in myocytes paced at 0.5 Hz in HEPES-buffered solution (extracellular pH = 7.40). At baseline, calibrated pHi, diastolic and systolic [Ca2+]i values, and the amplitude of cell contraction were similar in hypertrophied and control myocytes. Exposure of the control myocytes to 10(-6) mol/L SNP caused a decrease in the amplitude of cell contraction (72 +/- 7% of baseline, P < .05) that was associated with a decrease in pHi (-0.10 +/- 0.03 U, P < .05) with no change in peak systolic [Ca2+]i. In contrast, in the hypertrophied myocytes exposure to SNP did not decrease the amplitude of cell contraction or cause intracellular acidification (-0.01 +/- 0.01 U, NS). The cGMP analogue 8-bromo-cGMP depressed cell shortening and pHi in the control myocytes but failed to modify cell contraction or pHi in the hypertrophied cells. To examine the effects of SNP on Na(+)-H+ exchange during recovery from intracellular acidosis, cells were exposed to a pulse and washout of NH4Cl. SNP significantly depressed the rate of recovery from intracellular acidosis in the control cells compared with the rate in hypertrophied cells. CONCLUSIONS: SNP and 8-bromo-cGMP cause a negative inotropic effect and depress the rate of recovery from intracellular acidification that is mediated by Na(+)-H+ exchange in normal adult rat myocytes. In contrast, SNP and 8-bromo-cGMP do not modify cell contraction or pHi in hypertrophied myocytes.     

Effects of the Na+/H+-exchange inhibitor Hoe 642 on intracellular pH, calcium and sodium in isolated rat ventricular myocytes

The inhibitors of the Na+/H+-exchange (NHE1) system Hoe 694 and Hoe 642 possess cardioprotective effects in ischaemia/reperfusion. It is assumed that these effects are due to the prevention of intracellular sodium (Nai) and calcium (Cai) overload. The purpose of the present study was to investigate the effects of Hoe 642 on intracellular pH, Na+ and Ca2+ (pHi, Nai and Cai) in isolated rat ventricular myocytes under anoxic conditions or in cells in which oxidative phosphorylation had been inhibited by 1.5 mmol/l cyanide. In cells which were dually loaded with the fluorescent dyes 2, 7-biscarboxyethyl-5,6-carboxyfluorescein (BCECF) and Fura-2, anoxia caused acidification of the cells (from pHi 7.2 to pHi 6.8) and an increase in Cai from about 50 nmol/l to about 1 micromol/l. The decrease in pHi began before the cells underwent hypoxic (rigor) contracture, whereas Cai only began to rise after rigor shortening had taken place. After reoxygenation, pHi returned to its control value and Cai oscillated and then declined to resting levels. It was during this phase that the cells rounded up (hypercontracture). When 10 micromol/l Hoe 642 was present from the beginning of the experiment, pHi and Cai were not significantly different from control experiments. At reoxygenation, pHi did not recover, but Cai oscillated and returned to its resting level. To monitor Nai, the cells were loaded with the dye SBFI. After adding 1.5 mmol/l cyanide or 100 micromol/l ouabain, Nai increased from the initial 8 mmol/l to approximately 16 mmol/l. Hoe 642 or Hoe 694 (10 micromol/l) did not prevent the increase in Nai. In contrast, the blocker of the persistent Na+ current R56865 (10 micromol/l) attenuated the CN--induced rise in Nai. The substance ethylisopropylamiloride was not used because it augmented considerably the intensity of the 380 nm wavelength of the cell's autofluorescence. In conclusion, the specific NHE1 inhibitor Hoe 642 did not attenuate anoxia-induced Cai overload, nor CN--induced Nai and Cai overload. Hoe 642 prevented the recovery of pHi from anoxic acidification. This low pHi maintained after reoxygenation may be cardioprotective. Other possible mechanisms of NHE1 inhibitors, such as prevention of Ca2+ overload in mitochondria, cannot be ruled out. The increase in Nai during anoxia is possibly due to an influx of Na+ via persistent Na+ channels.     

Effects of hyperkalaemia on the depression of maximum rate of depolarization by class I antiarrhythmic agents in guinea-pig myocardium

1 Standard microelectrode methods were used to record intracellular action potentials from strips of guinea-pig right ventricular myocardium superfused with either standard physiological saline ([K+] = 5.6 mM) or the same solution modified to contain [K+] = 11.2 mM. 2 The effects on action potential parameters of three therapeutic concentrations of mexiletine, quinidine and disopyramide were studied under both conditions at four different drive rates (interstimulus intervals = 2400, 1200, 600 and 300 ms). 3 Hyperkalaemia in the absence of drugs produced reductions in resting potential (-86.7 +/- 2.5 mV to -71.8 +/- 3.7 mV; n = 30; P < 0.001), maximum rate of depolarization (300 +/- 46.5 V s-1 to 205.6 +/- 37.6 V s-1; P < 0.0001), and action potential duration (205 +/- 26 ms to 188 +/- 32 ms; P < 0.05). 4 All three drugs produced increased depression of maximum rate of depolarization in hyperkalaemia compared to control conditions, but at all three concentrations this enhancement of effect was greater for mexiletine than for quinidine, with disopyramide exhibiting intermediate behaviour. 5 Mexiletine behaved very similarly to therapeutic concentrations of lignocaine as described in previous reports from this laboratory. 6 Quinidine behaved very similarly to Class Ic agents. 7 It is concluded that mexiletine demonstrated significantly greater selectivity for depolarized myocardium than quinidine and that this may have implications in terms of proarrhythmic potential. 8 Disopyramide exhibited intermediate selectivity for depolarized myocardium between mexiletine and quinidine.     

Effect of dantrolene sodium on the contractility of rabbit jejunum in vitro

The effect of dantrolene sodium on the spontaneous contractions of rabbit jejunum was studied in vitro. Dantrolene sodium (4.5 x 10(6) to 4.5 10(4) M) reversibly decreased the amplitude of contractions in a dose-dependent manner. ED50 was found to be about 7.9 x 10(-5) M. Its effect was biphasic in that a period of potentiation preceded that of suppression of contractions. Lowering or increasing (2.5 fold in each direction) the calciumm concentration of bathing media did not affect the suppression of contraction caused by dantrolene sodium to any significant degree. Caffeine but not quinine was found to be able to restore the activity of the intestine to normal after a 50% inhibition caused by dantrolene sodium. Dantrolene sodium, verapamil and nifedipine were able to shift the dose-response curves of calcium in potassium-polarized rabbit jejunum to the right and pA2 values were found to be 4.18, 7.76 and 8.47 respectively. These data indicate that the effect of dantrolene on smooth muscle is mediated via inhibition of calciu movement across the membrane.     

Effects of simple indoles, noradrenaline, nicotine, and tyramine on action potential and contractility of the isolated guinea-pig papillary muscle

1. Simultaneous recordings of both the transmembrane action potential and the contractions were made in isolated electrically driven papillary muscles of the guinea pig in order to compare the effects of 6-methoxyindole (6-MOI), 3-methylindole (3-MI) and 5-methylindole (5-MI) with those of noradrenaline (1.2 - 10(-6) M), nicotine (2 - 10(-5) M), and tyramine (5.8 - 10(-6) M). 2. Noradrenaline, nicotine, tyramine and 6-MOI (5.4 - 10(-4) M) enhanced the contractility whilst 3-MI (3.8 and 7.8 - 10(-4) M) and 5-MI (1.9 and 3.8 - 10(-4) M) had only irregular effects. The active compounds shortened and time-to-peak tension and increased the rate of relaxation. 3. The duration of the action potential was prolonged by noradrenaline, nicotine, and tyramine, but shortened by 3-MI, 5-MI, and 6-MOI. 4. The results showed that the effect of drugs on the action potential are not necessarily linked to those on contractility.     

Effects of sodium bicarbonate on striated muscle metabolism and intracellular pH during endotoxic shock

The effects of HCO3Na load on acid-base balance and muscle intracellular bioenergetics have been investigated using 31P-magnetic resonance spectroscopy in an experimental model of endotoxinic shock. Anesthetized, mechanically ventilated, and paralyzed rats (n = 16) were given an intravenous bolus of Escherichia coli lipopolysaccharide (15 mg/kg). When shock was established they were randomly assigned to receive either HCO3Na intravenously (2 mmol/kg in 2 min) or an equimolar saline injection. Lipopolysaccharide induced a significant decrease in the levels of mean arterial pressure (58 +/- 6 vs. 120 +/- 8 mmHg), arterial pH (7.20 +/- .03 vs. 7.35 +/- .01), intracellular pH (6.86 +/- .04 vs. 7.08 +/- .01), a marked hyperlactatemia (7 +/- 3 vs. 1.2 +/- .2 mmol/L) and a drop in the phosphocreatine-inorganic phosphate ratio. In the bicarbonate-loaded rats, mean arterial pressure further decreased whereas it remained unchanged in the saline group. Bicarbonate increased arterial pH and PaCO2 transiently. In the saline group, arterial pH decreased and PaCO2 remained stable. In both groups, intracellular pH and high energy phosphates had a similar evolution. In this model of septic shock, partial correction of arterial pH using HCO3Na did not reduce the metabolic cellular injury in skeletal muscle. Based on these results, HCO3Na may be of limited therapeutic value in severe septic metabolic acidosis.     

The effects of some cholinesterase reactivators on contractility of the isolated guinea-pig heart atria

The effect of eight monoquaternary and bisquaternary pyridine aldoxime cholinesterase reactivators was tested on isolated guinea-pig heart atria. 2. Acetylcholine and methylfurthretonium in concentrations ranging from 10(-7) M to 10(-5) M have negative inotropic effects in the electrically stimulated atria and negative chronotropic effects in the spontaneously beating atria. 3. In the presence of higher concentration of cholinesterase reactivators alone, the parameters of heart muscle contractility are significantly altered. 4. Cumulative dose-response curves of methylfurthretonium in the presence of reactivators in the range of concentrations from 10(-5) M to 10(-3) M are shifted parallelly to higher concentrations of the agonist.     

Effects of sodium acetate on rat bone-nodule formation and mineralization in vitro

A new cell line, FR-car, has been established from a biopsy of a low-grade human cervical squamous intraepithelial lesion (SIL). We confirmed the epithelial origin of the cells by keratin staining using polykeratin, AE1/AE3 and CAM 5.2 antibodies. Sixty percent to 80% of the cultured cells stained positive for proliferative cell nuclear antigen (PCNA) and Ki-67. There was no overexpression of p53. Karyotyping revealed that the cell line was hypodiploid with clonal abnormalities on chromosome 6 and 16. Sections of a biopsy adjacent to the lesion from which the culture was initiated tested positive for human papillomavirus (HPV) 18 DNA by the polymerase chain reaction, but cultured cells tested at several passages were HPV-negative by either type-specific or consensus PCRs. This HPV-negative SIL line may be useful in studies into the cell biology of dysplastic epithelium.     

Influence of endotoxin on contractility in the rat gastric fundus

Cefoperazone amphotericin teicoplanin (CAT) agar was developed from cefoperazone deoxycholate (mCCD) agar by modification of the selective antibiotics in order to permit growth of strains of Campylobacter upsaliensis. In this study, 35 strains of Campylobacter and Arcobacter were tested for their ability to grow on CAT and mCCD media using the ecometric method. Six of these strains were also tested using the modified Miles-Misra method. Overall, nineteen strains out of the 35 tested grew better on CAT than on mCCD agar, although for eight strains, the difference was slight. These differences could not be attributed solely to poorer growth of C. upsaliensis on mCCD agar. No strain grew better on mCCD than CAT agar. Eight of the 35 strains tested did not grow on mCCD agar at all, however, only one strain failed to grow on CAT medium. The two methods of testing gave similar results, although the Miles-Misra method was found to be more sensitive and less prone to subjective interpretation. All four CNUPC (catalase negative, urease positive campylobacter-like) strains, one strain of C. sputorum biovar, fecalis, one of two Arcobacter cryaerophilus strains (incubated at 30 degrees C, aerobically) could be detected only using CAT agar. In addition, for some strains of A. butzleri, C. upsaliensis and C. hyointestinalis, CAT medium gave better growth scores than mCCD agar. The level of cefoperazone in mCCDA is inhibitory to some campylobacter strains, but suboptimal growth of Arcobacter strains is more probably due to synergistic interaction between deoxycholate and cefoperazone. CAT agar supports the growth of a wider variety of Campylobacter and Arcobacter species than mCCD agar.