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Biomedical subjects

J R Wilson

Publications and source records attributed to J R Wilson.

At least 181 records · Page 10Linked to original sources
PubMed1986

Cardiopulmonary resuscitation. A current perspective.

Cardiopulmonary resuscitation is effective if established early and coupled with specific therapeutic interventions. Most cardiopulmonary arrest is due to ventricular fibrillation and early defibrillation offers the highest probability of success. External cardiac compression alone is inadequate to provide adequate perfusion to vital organs and, therefore, cannot sustain life unless coupled with advanced therapeutic interventions. Many new techniques for increasing flow have been developed, but have not been established clinically. The American Heart Association guidelines for CPR are still valid and are the basis for our current CPR. A practical perspective is presented whereby the therapeutic interventions are pursued systematically in an expeditious and coordinated fashion so that the key interventions are made within the first 10 to 15 minutes of the arrest.

Anti-Arrhythmia Agents↗
PubMed1986

Detection of skeletal muscle hypoperfusion during exercise using phosphorus-31 nuclear magnetic resonance spectroscopy.

Blood flow to working skeletal muscle is frequently reduced in patients with heart failure or peripheral vascular disease. To determine if phosphorus nuclear magnetic resonance (NMR) can noninvasively detect such muscle underperfusion, gated phosphorus-31 NMR spectroscopy was used to compare muscle inorganic phosphate, phosphocreatine and pH during mild wrist flexion exercise at 0.2, 0.4 and 0.6 W in eight normal men, before and after reduction of forearm blood flow. Forearm flow was reduced by cuff inflation to a pressure determined by Doppler ultrasound to bring flow to 40 to 60% of control. Attention was focused on the inorganic phosphate to phosphocreatine (Pi/PCr) ratio and pH, two variables potentially sensitive to muscle oxygen delivery. At rest with normal flow, Pi/PCr averaged 0.12 +/- 0.03 and pH averaged 7.02 +/- 0.04. Exercise produced a progressive increase in Pi/PCr (0.2 W = 0.43 +/- 0.12; 0.4 W = 0.75 +/- 0.31; 0.6 W = 1.04 +/- 0.47) and a modest decrease in pH (0.2 W = 6.94 +/- 0.04; 0.4 W = 6.86 +/- 0.18; 0.6 W = 6.85 +/- 0.06). Flow reduction had no effect on Pi/PCr or pH at rest. In contrast, flow reduction during exercise was associated with higher Pi/PCr at all three work loads (0.2 W = 0.60 +/- 0.27; 0.4 W = 0.99 +/- 0.50; 0.6 W = 2.00 +/- 1.26 [all p less than 0.05 versus normal flow]) and lower pH (0.2 W = 6.78 +/- 0.12; 0.4 W = 6.69 +/- 0.23; 0.6 W = 6.65 +/- 0.30 [p less than 0.01 versus normal flow at 0.2 and 0.4 W; p = 0.05 at 0.6 W]).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Use of regression residuals to quantify individual differences in acute sensitivity and tolerance to alcohol.

Due to the problem of correlation of errors inherent in the difference or ratio scores typically used to quantify individual differences in acute sensitivity and tolerance to alcohol, it is recommended that residual scores from regression analyses be used instead for such quantification. Conceptualizations of acute sensitivity and tolerance and problems with the reliability of change scores are also discussed.

Adoption↗
PubMed1986

Mechanism of skeletal muscle underperfusion in a dog model of low-output heart failure.

To investigate the mechanism responsible for underperfusion of working skeletal muscle in heart failure, we measured systemic and femoral bed hemodynamics during treadmill exercise and gracilis muscle resistance during contraction frequencies of 1-9 Hz in 8 dogs ventricularly paced at 260 beats/min for 3 wk to induce heart failure (HF) and in 9 control dogs. At peak treadmill exercise (4 mph, 10%), HF dogs had reduced cardiac outputs (control: 297 +/- 42 vs. HF: 212 +/- 16 ml X min-1 X kg-1) and femoral bed flows (control: 352 +/- 112 vs. HF: 229 +/- 95 ml/min) and elevated arterial lactates [control: 1.7 +/- 0.7 vs. HF: 4.1 +/- 0.7 mM (all P less than 0.04)], consistent with skeletal muscle underperfusion. This muscle underperfusion was associated with reduced mean arteriovenous pressure gradients [control: 119 +/- 12 vs. HF: 91 +/- 9 mmHg (P less than 0.001)] but with normal systemic vascular [control: 21 +/- 6 vs. HF: 23 +/- 5 U (P = NS)] and femoral bed resistances [control: 3.5 +/- 1.6 vs. HF: 4.4 +/- 2.3 X 10(2) U (P = NS)]. Both groups also had similar gracilis muscle minimal resistance during exercise (control: 2.0 +/- 1.1 vs. HF: 1.9 +/- 0.9 X 10(3) U/100 g) and following maximal vasodilation (control: 2.0 +/- 1.0 vs. HF: 2.1 +/- 1.0 X 10(3) U/100 g). These results suggest that 1) short-term rapid ventricular pacing in the dog produces a model of low output HF resembling HF in humans, and 2) skeletal muscle underperfusion in this model is due to a reduced muscle arteriovenous pressure gradient and not to impaired skeletal muscle arteriolar vasodilation.

Animals↗
PubMed1986

Abnormal skeletal muscle bioenergetics during exercise in patients with heart failure: role of reduced muscle blood flow.

Using phosphorous nuclear magnetic resonance, we have previously demonstrated that patients with heart failure often exhibit abnormal forearm muscle metabolism during forearm exercise. To determine if this altered metabolism is due to reduced muscle flow, we measured forearm blood flow with plethysmography and forearm muscle inorganic phosphate (Pi), phosphocreatine (PCr), and pH with 31P nuclear magnetic resonance spectroscopy at rest and during mild forearm exercise (0.2, 0.4, and 0.6 W) in 21 men with heart failure and in 12 age-matched normal male subjects. The Pi/PCr ratio was correlated with power output and the slope of this relationship was used as an index of forearm metabolism. At rest, both groups had similar Pi/PCr ratios (normal subjects 0.11 +/- 0.05; patients with heart failure 0.11 +/- 0.03; p = NS) and forearm blood flows (normal subjects 2.9 +/- 1.4 ml/min/100 ml; patients with heart failure 2.6 +/- 1.2 ml/min/100 ml; p = NS). In both groups, exercise resulted in a progressive increase in both Pi/PCr and forearm blood flow as power output increased. However, the patients exhibited a steeper slope of the Pi/PCr-to-power output relationship than did the normal subjects (normal subjects 1.4 +/- 0.6 Pi/PCr U/W; patients with heart failure 3.0 +/- 2.4 Pi/PCr U/W; p less than .03). In contrast, forearm blood flow was similar in both groups during exercise (at 0.2 W, 6.3 +/- 3.3 and 6.8 +/- 3.2 ml/min/100 ml in normal subjects and patients with heart failure, respectively; at 0.4 W, 8.7 +/- 6.5 and 8.3 +/- 3.3; at 0.6 W, 12.8 +/- 7.9 and 12.0 +/- 4.6; all p = NS). Nine of the 21 patients with heart failure had slopes of the Pi/PCr-to-power output relationship above the normal range. These nine patients also had forearm blood flows comparable to flows observed in the normal subjects. These data indicate that forearm muscle metabolism during forearm exercise is altered in a subpopulation of patients with heart failure. This metabolic alteration does not appear to be due to decreased muscle blood flow, suggesting that other mechanisms, such as alterations in mitochondrial population or substrate utilization, may be responsible.

Adult↗
PubMed1986

Vasodilatory behavior of skeletal muscle arterioles in patients with nonedematous chronic heart failure.

During maximal upright exercise, blood flow to working skeletal muscle is frequently reduced in patients with nonedematous chronic heart failure. It has been speculated that this reduced muscle flow may be caused in part by an intrinsic impairment of skeletal muscle vasodilatory capacity. To test this hypothesis, forearm blood flow and resistance were compared during forearm exercise and in response to transient forearm ischemia (10 min) in 22 patients with heart failure and in 11 normal subjects. During forearm exercise, both groups exhibited comparable forearm blood flows (ml/min/100 ml) (0.2 W: normal 5.9 +/- 3.1, heart failure 6.5 +/- 2.8; 0.4 W: normal 8.2 +/- 5.5, heart failure 8.2 +/- 3.6; 0.6 W: normal 11.5 +/- 6.8, heart failure 11.8 +/- 4.8 [all p = NS]) and forearm vascular resistance (mm Hg/ml/min/100 ml) (0.2 W: normal 23.1 +/- 12.4, heart failure 18.5 +/- 7.8; 0.4 W: normal 16.9 +/- 7.7, heart failure 14.7 +/- 6.4; 0.6 W: normal 13.1 +/- 7.7, heart failure 10.3 +/- 4.1 [all p = NS]). Ten minutes of forearm ischemia, an intervention that produces maximal forearm vasodilation, also resulted in comparable forearm vascular resistances in both groups (normal 4.1 +/- 2.4, heart failure 3.8 +/- 1.3 mm Hg/ml/min/100 ml/p = NS). These data suggest that skeletal muscle vasodilatory capacity is not intrinsically impaired in patients with nonedematous chronic heart failure.

Adult↗
PubMed1985

Effect of the renin-angiotensin system on limb circulation and metabolism during exercise in patients with heart failure.

The maximal aerobic exercise capacity of patients with chronic heart failure is frequently decreased because of inadequate blood flow to working skeletal muscle. To investigate whether this reduced flow is in part due to interference by angiotensin II with arteriolar dilation in working muscle, the effect of the angiotensin-converting enzyme inhibitor captopril on leg blood flow, leg vascular resistance, leg oxygen consumption (VO2) and leg lactate release during maximal upright bicycle exercise was examined in 12 patients with heart failure (maximal VO2 10.7 +/- 3.1 ml/min per kg). Captopril decreased leg resistance at rest (258 +/- 115 to 173 +/- 67 U, p less than 0.01) and maximal exercise (68 +/- 69 to 45 +/- 29 U, p less than 0.01) associated with proportionately similar decreases in systemic vascular resistance. However, maximal exercise duration and maximal VO2 were unchanged and, at identical peak exercise work times, there was no improvement in leg blood flow (2.0 +/- 0.9 to 2.0 +/- 1.1 liters/min, p = NS), leg VO2 (261 +/- 104 to 281 +/- 157 ml/min, p = NS) or leg lactate release (269 +/- 149 to 227 +/- 151 mg/min, p = NS). These data suggest that, during exercise in patients with heart failure, angiotensin II does not interfere with blood flow to working skeletal muscle.

Aged↗
PubMed1985

Body composition and its relation to systemic haemodynamics, fluid volume partitions and energy utilization in rats with bilateral ventromedial hypothalamic lesions.

Body composition and its relationship with intra-arterial pressure, fluid volume partitions and oxygen consumption were studied in male rats four months following ventromedial hypothalamic (VMH) destruction during the static phase of the development of obesity. Compared with sham-operated controls, rats with VMH lesions had a greater body weight which was related to an increased body lipid content and an elevated arterial pressure and total peripheral resistance. Fluid volume distribution was normal and total body oxygen consumption (per unit of body weight) was reduced. Bilateral destruction of the ventromedial hypothalamus was confirmed in each of the rats studied and no relationship could be demonstrated between the lesion size and the magnitude of haemodynamic changes. It is concluded that the increased arterial pressure observed in obese VMH lesioned rats was directly related to an elevated total body lipid content.

Animals↗
PubMed1985

Evaluation of energy metabolism in skeletal muscle of patients with heart failure with gated phosphorus-31 nuclear magnetic resonance.

Exertional fatigue is a major limiting symptom in patients with heart failure. To investigate the metabolic basis of this fatigue, we used gated nuclear magnetic resonance spectroscopy to compare inorganic phosphate (Pi), phosphocreatine (PCr) and pH levels, and fatigue (1 to 4+) during mild forearm exercise in eight normal men and nine men with heart failure. Wrist flexion every 5 sec for 7 min was performed at 1, 2, and 3 J (average power output = 0.2, 0.4, and 0.6 W). In both groups linear relationships were noted between power output and Pi/PCr; the slope of this relationship was used to compare PCr depletion patterns. At rest both groups had similar Pi/PCr ratios (normal subjects 0.12 +/- 0.06, those with heart failure 0.15 +/- 0.03) and pH (normal subjects 7.04 +/- 0.13, those with heart failure 7.10 +/- 0.11). In normal subjects exercise resulted in a progressive increase in Pi/PCr (slope = 1.17 +/- 0.20 Pi/PCr units/W), a reduction in pH only at 0.6 W (0.2 W: 7.03 +/- 0.10, 0.4 W: 7.01 +/- 0.10, 0.6 W: 6.88 +/- 16) and moderate fatigue (0.2 W: 0 +/- 0, 0.4 W: 1.3 +/- 0.5, 0.6 W: 1.9 +/- 0.6). In patients with heart failure exercise resulted in significantly greater fatigue at all workloads (0.2 W: 1.0 +/- 0.5, 0.4 W: 1.9 +/- 0.6, 0.6 W: 2.9 +/- 0.5).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1985

Effect of the sympathetic nervous system on limb circulation and metabolism during exercise in patients with heart failure.

During exercise in patients with heart failure, activation of sympathetic vasoconstrictor nerves may impair vasodilation in active skeletal muscle and thereby interfere with skeletal muscle blood flow. To investigate this hypothesis, we examined the effect of acute alpha-adrenergic blockade with systemic administration of prazosin (10 patients) or regional administration of phentolamine (eight patients) on blood flow, vascular resistance, oxygen consumption (VO2), and lactate release in the leg during maximal bicycle exercise in patients with heart failure. During control exercise, systemic VO2 increased to 12.6 +/- 4.3 ml/min/kg (normal greater than 20 to 25 ml/min/kg), leg blood flow to 2.8 +/- 1.8 liters/min, and leg lactate release to 362 +/- 256 mg/min. Prazosin decreased systemic vascular resistance (12.5 +/- 3.2 to 9.7 +/- 2.5 units; p less than .003) and mean arterial pressure (101 +/- 20 to 87 +/- 22 mm Hg; p less than .002) at maximal exercise, supporting the presence of substantial sympathetic vasoconstrictor nerve activity. Prazosin also decreased leg resistance during exercise. However, the magnitude of leg blood flow, leg oxygen extraction, and leg VO2 during exercise were unchanged, suggesting that vasodilation in the leg was produced by an autoregulatory response to the drop in blood pressure rather than by blockade of sympathetic vasoconstriction. Maximal systemic VO2 and leg lactate release were also not improved. Regional blockade with phentolamine did not substantially drop the arterial blood pressure and had no effect on vasodilation, blood flow, VO2, and lactate release in the leg during exercise. These data suggest that during exercise in patients with heart failure, the sympathetic nervous system helps to sustain arterial blood pressure and that this beneficial effect is not associated with adverse effects on blood flow to working skeletal muscle.

Aged↗
PubMed1985

A cross-ethnic comparison of reasons given for using alcohol, not using alcohol or ceasing to use alcohol.

In a study that included six different racial-ethnic groups in Hawaii, the reasons given by drinkers for drinking, abstainers for not drinking and former drinkers for ceasing to drink were assessed. Although there were group differences in frequencies of endorsement of given reasons for drinking, for not drinking or for ceasing to drink, the findings of similarity were most impressive. Drinkers, abstainers and former drinkers were similar across racial-ethnic groups in their proportions of endorsement of given reasons for drinking, abstaining or ceasing to use alcohol. Although reasons for drinking varied across racial-ethnic groups, they varied much more across groups that differed in alcohol consumption independent of ethnicity, with all reasons for drinking being more often endorsed as consumption increased. In addition, the citation of more pathological reasons for drinking was associated with a greater number of drinking problems.

Adult↗
PubMed1985

Extended-wear soft contact lenses for vision studies in monkeys.

The authors have designed and produced extended-wear contact lenses for rhesus monkeys. High-plus lenses to correct neonatal aphakia as well as lenses dyed black for use as occluders to treat amblyopia have been evaluated. Four infant monkeys fitted with soft lenses have successfully worn these extended-wear lenses almost continuously throughout their first year of life. These experiments demonstrate that rhesus monkeys tolerate extended-wear contact lenses well when these lenses are correctly designed, comfortably fitted, and their wear carefully monitored. Furthermore, the results demonstrate that usable levels of vision can be maintained in monocularly aphakic infant monkeys. Since similar methods are now used to treat children with monocular cataracts, our animal model using extended-wear contact lenses on young monkeys should facilitate new and clinically relevant amblyopia experiments.

Amblyopia↗
PubMed1984

Acute coronary vasoconstrictive effects of cigarette smoking in coronary heart disease.

To investigate the effect of cigarette smoking on the coronary vasculature, coronary sinus flow and myocardial oxygen delivery were measured at rest and during incremental atrial pacing in 10 patients with coronary artery disease. Measurements were then repeated while the patients smoked 2 unfiltered, high-nicotine cigarettes. Although smoking significantly increased the heart rate at rest and double product, coronary sinus flow did not change significantly (141 +/- 32 vs 146 +/- 28 ml/min). At the lowest equivalent pacing rate before and during smoking, the double products were comparable. However, coronary sinus flow was reduced by smoking (146 +/- 28 vs 159 +/- 28 ml/min, p less than 0.01) and coronary vascular resistance was increased (0.96 +/- 0.15 vs 0.83 +/- 0.13 mm Hg ml-1 min, p less than 0.02). The double products were also comparable at the peak pacing rate before and during smoking. Nonetheless, the coronary sinus flow was again lower (167 +/- 23 vs 227 +/- 41 ml/min, p = 0.02) and the coronary vascular resistance was higher (0.77 +/- 0.10 vs 0.63 +/- 0.09 mm Hg ml-1 min, p less than 0.01) during smoking. The transmyocardial arteriovenous oxygen difference was unchanged by smoking; therefore, myocardial oxygen delivery was reduced in proportion to the reductions in coronary sinus flow. Thus, cigarette smoking appears to acutely alter the ability of the coronary vasculature to regulate flow in accordance with the oxygen requirements of the myocardium.

Aged↗
PubMed1984

Fine structural morphology of identified X- and Y-cells in the cat's lateral geniculate nucleus.

Four physiologically identified neurons in the A laminae of the cat's dorsal lateral geniculate nucleus were filled with horseradish peroxidase and studied using the electron microscope. Two were X-cells and two were Y-cells. Each had electrophysiological properties appropriate for its X- Or Y-cell class, and each also had an axon that projected into the optic radiation, indicative of a geniculocortical relay cell. Representative samples from about 10% of each neuron's entire dendritic arbor (proximal and distal) were taken to obtain an estimate of the types and distributions of synapses contacting these arbors. One X-cell had a cytoplasmic laminar body, but there were no other significant cytological differences seen among the neurons. Common to each of the neurons were the following synaptic features: (i) retinal terminals (r.l.p.) were mostly or entirely restricted to proximal dendrites or dendritic appendages (less than 100 microns from the soma). These terminals constituted about 15-25% of the synapses on the proximal dendrites. (ii) Terminals with flattened or pleomorphic synaptic vesicles (f. terminals) were predominant on the proximal dendrites (30-55% of the total synapses for that region) and were mainly located near the retinal terminals. A smaller percentage (10-20%) were also distributed onto the distal dendrites. (iii) Small terminals with round synaptic vesicles (r.s.d.), many presumably having a cortical origin, predominated (60-80%) on distal dendrites (greater than 100 microns), but also formed a large proportion (40-70%) of the synapses on the intermediate (50-150 microns) dendrites. Total synaptic contacts for one X-cell and one Y-cell were estimated at about 4000 and 5000, respectively. The major fine structural differences observed between X- and Y-cells were almost entirely related to the retinal afferents. First, the retinal synapses for X-cells were mostly made on to dendritic appendages (spines, etc.), whereas Y-cells had most of their retinal synapses onto the shafts of primary and proximal secondary dendrites (that is, near branch points. Second, the retinal terminals that contacted X-cell dendrites nearly always formed triadic arrangements that included nearby f. terminals, but those on Y-cells rarely did so. Finally, the main type of f. terminals associated with X-cells were morphologically different from most of those associated with the Y-cells, and this also related directly to the triadic arrangements; that is, f. terminals in the triadic arrangements were morphologically distinguishable from f. terminals that did not participate in triadic arrangements.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Impaired skeletal muscle nutritive flow during exercise in patients with congestive heart failure: role of cardiac pump dysfunction as determined by the effect of dobutamine.

The maximal exercise capacity of patients with congestive heart failure (CHF) is frequently reduced, partly because of inadequate skeletal muscle nutritive flow. To investigate whether this altered muscle nutritive flow is a result of inability of the heart to increase cardiac output normally during exercise, the effect of dobutamine on systemic and leg blood flow and metabolism during maximal exercise was examined in 11 patients with CHF. At maximal exercise before dobutamine, all patients were limited by fatigue and had reduced maximal systemic oxygen uptake (11.9 +/- 1.1 ml/min/kg) (+/- standard error of the mean), markedly elevated leg oxygen extraction (85 +/- 2%) and elevated femoral venous lactate (53 +/- 5 mg/dl), consistent with impaired nutritive flow to working muscle. Dobutamine increased the peak cardiac output from (6.5 +/- 0.9 0.74 +/- 0.7 liters/min, p less than 0.01) and peak leg flow (from 1.7 +/- 0.3 to 2.1 +/- 0.3 liters/min, p less than 0.05) during exercise. In contrast, no change occurred in maximal exercise duration (5.5 +/- 0.8 vs 5.8 +/- 0.8 min), peak systemic VO2 (829 +/- 97 vs 869 +/- 77 ml/min), peak arterial lactate (34 +/- 2 vs 35 +/- 4 mg/dl) or peak leg lactate output (248 +/- 39 vs 275 +/- 53 mg/min), whereas peak leg oxygen extraction decreased (85 +/- 2 to 80 +/- 2%, p less than 0.01), suggesting no improvement in muscle nutritive flow. These data suggest that nutritive flow to working skeletal muscle is impaired in patients with CHF and that this impairment is not due simply to an inability of the heart to increase the cardiac output normally during exercise.

Blood Flow Velocity↗
PubMed1984

Intestinal epithelial cell differentiation-related changes in glycosyltransferase activities in rats.

Intestinal epithelial cells differentiate as they migrate from the crypt-to-villus tip. A ten-fraction crypt-to-villus gradient of epithelial cells from rat small intestine was prepared and homogenates assayed for three glycosyltransferases involved in elongation of asparagine-linked oligosaccharides. The N-acetylglucosaminyltransferases I and II (enzymes which attach N-acetylglucosamine to either the 3' or 6' core mannose, respectively) were assayed with structurally-defined glycopeptides as specific acceptors and galactosyltransferase was assayed with asialo, agalactosylfetuin (galactose is attached to exposed N-acetylglucosamine termini). Inhibitors of glycosidases and pyrophosphatases were included in the assays to minimize effects of breakdown of substrate or product. The results indicate the N-acetylglucosaminyltransferase I shows a gradient of activity increasing from a low at the villus tip to a peak in the lower crypt region. In contrast, N-acetylglucosaminyltransferase II showed two peaks of activity, one in the villus zone and another in the upper crypt region. Galactosyltransferase activity also defined a gradient quite similar to that observed for N-acetylglucosaminyltransferase I, its specific activity being highest in the crypt cells. The specific activity levels of the three enzymes correlated with the apparent order of their action: N-acetylglucosaminyltransferase I much less than N-acetylglucosaminyltransferase II much less than galactosyltransferase. These results suggest a developmental regulation of the glycosyltransferases involved in oligosaccharide chain elongation of glycoproteins during intestinal cell differentiation.

Animals↗
PubMed1984

Galactosyltransferase activity and cell growth: uridine diphosphate (UDP)galactose inhibition of murine leukemic L1210 cells.

UDPgalactose inhibits the growth of mouse leukemic L1210 cells. In calf serum supplemented Dulbecco's medium (CS-DMEM), 1.2 mM UDPgalactose (UDPgal) inhibited cell growth by 50% (IC50), and 5 mM UDPgalactose inhibited cell growth by 92%. Other nucleotide sugars as well as galactose, glucose, and galactose-1-phosphate had little or no effect on cell growth. Uridine nucleotides, which inhibit galactosyltransferase activity, protected L1210 cells from the growth inhibitory effect of UDPgalactose when both were added simultaneously to culture media. Unlike mouse 3T12 cells, in which no inhibition of cell growth was observed with heat-inactivated calf serum (HICS)-DMEM, 5 mM UDPgalactose inhibited L1210 cell growth in HICS-DMEM to the same degree as that observed in CS-DMEM. In contrast to 3T12 cells, L1210 cells secrete significant galactosyltransferase activity into the media. Complete inhibition of 3T12 cell growth by UDPgal was observed if HICS-DMEM medium was first conditioned by L1210 cells for 48 hours. No difference in cell growth or [3H]thymidine uptake was detected after 6 hours of exposure to UDPgalactose, but both were significantly decreased at 24 and 48 hours. Flow cytometric analysis of UDPgalactose effects on L1210 cells revealed no differences in the distribution of cells in G1, S, or G2-M of the cell cycle after 6 hours of incubation, but after 16 hours of UDPgalactose treatment, L1210 cells were arrested in early S phase. These cells were completely viable and morphologically similar to control L1210 cells. Normal growth was resumed when UDPgal was removed. The data suggest that UDPgalactose inhibition of cell growth requires extracellular galactosyltransferase activity and that the effect is mediated via the cell membrane.

Animals↗