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Biomedical subjects

A L Riley

Publications and source records attributed to A L Riley.

67 records · Page 4Linked to original sources
PubMed1975

The effect of ischemia on renal blood flow in the dog.

Renal blood flow (RBF) and the distribution of cortical blood flow (microspheres) were measured in the dog after 90 min of total unilateral renal ischemia. RBF was 21% greater than control 2 min after release of the renal artery occlusion, and returned toward control 60 min later. At 2 min after release there was a small but significant increment in deep cortical blood flow which reverted to control by 60 min. When renal artery occlusion was maintained for 180 min, return of blood flow was blunted at 2 min after release of the occlusion, but was not significantly different from control within 10 min after release. Clearance rates of inulin and para-aminohippurate (Cin and Cpah) were 81 and 82% below control after release of occlusion. These data demonstrate that in the dog there is prompt and complete return of blood flow to or above control levels after complete renal artery occlusion. There was no evidence for the "no-reflow" phenomenon.

Aminohippuric Acids↗
PubMed1975

Effect of hemodilution on the distribution of renal blood flow.

We evaluated the effects of hemodilution, expansion of intravascular volume, and expansion of interstitial volume on the distribution of cortical renal blood flow, utilizing the microsphere technique. Hemodilution without volume expansion (saline exchange) produced an increase in fractional blood flow in zone 1 (outermost zone) of the cortex from 34 plus or minus 1% to 43 plus or minus 2% and a decrease in fractional blood flow in zone 4 (innermost zone) from 16 plus or minus 2% to 13 plus or minus 2%. Hemodilution without volume expansion or a decrease in plasma protein concentration (isoncotic exchange) produced a similar redistribution in blood flow in zone 1 from 34 plus or minus 2% to 41 plus or minus 2% and in zone 4 from 14 plus or minus 2% to 10 plus or minus 1%. Hemodilution with intravascular volume expansion (hyperoncotic albumin infusion) also produced a superficial shift; blood flow in zone 1 increased from 27 plus or minus 1% to 30 plus or minus 1% and that in zone 4 decreased from 19 plus or minus 2% to 15 plus or minus 1%. Previous studies have demonstrated a redistribution to the juxtamedullary area after saline expansion. Our data demonstrate that hemodilution causes flow to redistribute to the superficial rather than the deep cortex. This superficial shift appears to be secondary to decrease hematocrit rather than to dilution of plasma proteins or expansions of intravascular volume. The deep shift in cortical blood flow which occurs during saline loading is presumably a consequence of expansion of interstitial volume.

Animals↗
PubMed1974

Superficial and juxtamedullary nephron function during saline loading in the dog.

A modification of the microdissection technique of Hanssen was utilized in dogs to measure superficial (SNGFR) and juxtamedullary nephron filtration rate (JMGFR) in control and saline-expanded dogs. During control studies SNGFR was 60+/-4 and JMGFR was 72+/-5 nl/min. During saline loading SNGFR was 74+/-8 and JMGFR was 65+/-6 nl/min. The ratio SNGFR: JMGFR significantly increased from 0.84+/-0.03 to 1.15+/-0.08. Glomerular perfusion rate (GPR) was measured with the microsphere method during control and saline loading. Superficial GPR did not change significantly but juxtamedullary GPR increased from 225+/-42 to 323+/-39 nl/min. Calculated superficial nephron filtration fraction was unchanged after saline expansion but juxtamedullary filtration fraction decreased from 0.34+/-0.07 to 0.24+/-0.07. The data demonstrate a tendency for filtration to shift toward the superficial part and plasma flow toward the deep part of the kidney cortex. GFR in juxtamedullary nephrons appears to be less plasma flow-dependent than in superficial nephrons. The fall in filtration fraction in the deep cortex may affect sodium excretion by juxtamedullary nephrons.

Animals↗
PubMedDate not supplied

Effect of prenatal cocaine on the acquisition of cocaine-induced taste aversions.

Pregnant Long-Evans rats were injected SC twice daily with 20 mg/kg cocaine from gestational days (GD) 7-19. Vehicle controls were administered distilled water on these days. Pair-fed controls were similarly treated but allowed the same amount of food as consumed by the cocaine-exposed mothers. On postnatal day 1 (PND 1), pups of the mothers exposed to cocaine were surrogate-fostered. On PND 41, all subjects were grouped according to their history (cocaine, vehicle, and pair-fed) and were tested for their behavioral sensitivity to the aversive effects of cocaine by assessing their ability to acquire a cocaine-induced taste aversion. Rats from all three conditions were given saccharin to drink and then injected SC with either 0, 18, 32, or 50 mg/kg cocaine. Prenatal exposure to cocaine had no effect on the acquisition of aversions. Specifically, the prenatally exposed animals acquired the taste aversion in a dose-dependent manner similar to that of the controls. These data indicate that changes in sensitivity to cocaine are not necessary consequences of prenatal cocaine exposure.

Animals↗
PubMedDate not supplied

The inability of CCK to block (or CCK antagonists to substitute for) the stimulus effects of chlordiazepoxide.

To further examine the relationship between cholecystokinin (CCK) and GABA, the present study assessed the ability of the CCK-A antagonist devazepide and the CCK-B antagonist L-365,260 to substitute for the stimulus effects of chlordiazepoxide (CDP), as well as the ability of CCK-8s to block these effects, in female Long-Evans rats within the conditioned taste aversion baseline of drug discrimination learning. Both devazepide and L-365,260 failed to substitute for the discriminative stimulus properties of CDP, and CCK-8s failed to block its stimulus effects. The benzodiazepine diazepam did substitute for, and the benzodiazepine antagonist flumazenil did block, the stimulus effects of CDP. This suggests that the lack of substitution for, or antagonism of, CDP by the CCK antagonists and CCK-8s, respectively, was not due to the inability of the present design to assess such effects. Possible bases for the current findings, e.g., necessity of an anxiogenic baseline, drug and receptor specificity, as well as the dose-response nature of the interaction, were discussed. Given that a relationship between CCK and GABA has been reported in other designs, the present results suggest that such a relationship may be preparation specific.

Animals↗
PubMedDate not supplied

Effects of mu- and delta-opioid-receptor antagonists on the stimulus properties of cholecystokinin.

Melton and Riley recently reported that the relatively selective mu-opioid-antagonist naloxone potentiated the stimulus properties of the gut peptide cholecystokinin (CCK). To assess whether such opioid potentiation is limited to activity at the mu-receptor subtype, in the present experiment the effects of the highly selective delta-antagonist naltrindole on CCK's stimulus properties were examined. Because in the initial report of naloxone's potentiation of CCK a relatively high, nonphysiologic dose of CCK (i.e., 13 micrograms/kg) was used as the training drug, in the current analysis subjects were trained to discriminate 5.6 micrograms/kg CCK from its vehicle and the assessments and comparisons of the effects of naloxone and naltrindole were based on this dose. Specifically, rats were administered 5.6 micrograms/kg CCK before saccharin-LiCl pairings and the CCK vehicle before saccharin alone. With such training, they rapidly acquired the drug discrimination, avoiding saccharin consumption when it was preceded by CCK and consuming the same saccharin solution when it was preceded by its vehicle. In subsequent generalization tests, doses of CCK that were ineffective in suppressing saccharin consumption (i.e., did not substitute for the training dose of CCK) did result in the suppression of saccharin consumption when combined with doses of the mu antagonist naloxone that alone had no effect on saccharin intake. On the other hand, the highly selective delta-opioid-receptor antagonist naltrindole was ineffective in potentiating the effects of CCK. Specifically, when naltrindole was combined with ineffective doses of CCK, subjects drank at control levels. The ability of naloxone to potentiate CCK's stimulus effects is consistent with a range of other demonstrations of the role of the mu-opioid-receptor subtype in CCK-opioid interactions, although the specific basis for the interaction remains unknown. Given recent findings on the effects of delta agonists and antagonists on CCK-induced activity, the failure of naltrindole to potentiate CCK's stimulus effects may be due to the absence of delta activity within this preparation, rather than the absence of delta mediation of CCK-opioid interactions in general.

Animals↗
PubMedDate not supplied

Assessment of cocaethylene lethality in Long-Evans female and male rats.

Cocaethylene, the metabolite of cocaine produced only in the presence of alcohol, produces a number of pharmacological, physiological, and behavioral effects. It also has a range of toxicological consequences, the most severe being lethality. Given that the assessments of cocaethylene lethality have been limited to mice, the present study assessed the lethality of cocaethylene in rats. Further, because of within-species sex differences with its parent compound, cocaine, cocaethylene lethality was also examined in both females and males. Specifically, female and male rats were injected IP with 75, 87, 100, 115, and 133 mg/kg cocaethylene and observed over a 24-h period. Deaths were dose dependent and occurred within 30 min for both females and males. For females, the LD50 was 96 mg/kg; for males, the LD50 was 70 mg/kg. The percentage of rats displaying severe effects (i.e., seizure and death) increased with dose across all postinjection times. Further, these effects occurred earlier as dose increased. Differences in the LD50 for rats and mice, as well as the greater sensitivity to cocaethylene in male rats, are discussed.

Animals↗
PubMedDate not supplied

Effects of trimethyltin chloride on the LiCl dose-response function for conditioned taste aversions in rats.

Twenty-one days following intragastric administration of 6.0 mg/kg of TMT (TMT chloride base/kg) or equivolume distilled water, groups of rats were injected with various doses of LiCl (0, 0.15, 0.60 or 1.8 mEq/kg) following the consumption of a novel saccharin solution. Both groups subsequently avoided the consumption of saccharin, with the degree of the aversion directly related to the dose of LiCl. Further, there was no difference between the TMT- and non-TMT-treated rats in the degree of aversion at any dose. These data suggest that the previously-reported effect of TMT on long-delay taste aversion learning was not likely due to changes in sensory responsiveness.

Animals↗
PubMedDate not supplied

Sex differences in taste aversion learning: an analysis of the minimal effective dose.

Male and female rats injected with various doses of LiCl following the consumption of a novel saccharin solution subsequently avoided consumption of saccharin, with the degree of the aversion directly related to the dose of LiCl. Although this dose-response relationship was evident for both males and females, the minimal effective dose for inducing an aversion was lower for males, an effect consistent with previous work examining sex differences in taste aversion learning. The necessity of considering sex as a variable when comparing the relative sensitivity of behavioral measures of toxicity was discussed.

Animals↗
PubMedDate not supplied

Effects of trimethyltin chloride on differential-reinforcement-of-low-rate responding.

The effects of a range of doses of trimethyltin chloride (1.8-7.0 mg/kg, TMT) on responding maintained under a differential-reinforcement-of-low-rate 15-sec schedule of water presentation were examined in rats. TMT produced a large decrease in the percent of reinforced responses and consequently a decrease in the rate of reinforcement. These effects were due primarily to prolonged bursts of nonreinforced responses. In contrast to the gradual dose-related decrease in body weight produced by TMT, responding was disrupted only at the highest dose tested, i.e., 7.0 mg/kg. The results were discussed in terms of the neurotoxic effects of TMT on the limbic system.

Animals↗
PubMedDate not supplied

Conditioned flavor aversions: a toxicity test of the anticholinesterase agent, physostigmine.

The viability of the conditioned flavor aversion test as a behavioral index of the toxicity of physostigmine, an anticholinesterase agent, was evaluated in a series of three experiments. Experiments 1 and 2 used the flavor aversion paradigm and Experiment 3 used a more traditional behavioral testing paradigm in which the effect of physostigmine on a specified set of behaviors was measured. In the flavor aversion paradigm, the rats were allowed to consume 0.5% saccharin solution before being injected with one of various doses of physostigmine (0.025--0.50 mg/kg) or saline. They were subsequently tested for a learned flavor aversion by means of a one-bottle test in Experiment 1 and a two-bottle test in Experiment 2. In the behavioral testing paradigm used in Experiment 3, each rat was injected with one of various doses of physostigmine within the range of those used in the prior experiments, and thirty minutes later was placed in a chamber for observation for 15 minutes. The procedures of Experiment 3 were much more time consuming than those of Experiments 1 and 2. By the two-bottle aversion test of Experiment 2, a dose as low as 0.05 mg/kg of physostigmine produced a reliable flavor aversion which persisted for three extinction test trials. On the other hand, robust and reliable behavioral differences of decreased rearing and consumption of water in Experiment 3 were only evident in rats given 0.25 mg/kg of physostigmine. We conclude that the flavor aversion test is a simple and sensitive behavioral measure of toxicity.

Animals↗