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Biomedical subjects

S A Rice

Publications and source records attributed to S A Rice.

At least 91 records · Page 5Linked to original sources
PubMed1982

Deuterated methoxyflurane anesthesia and renal function in Fischer 344 rats.

Inorganic fluoride (F-) production and renal function were assessed in six groups of Fischer 344 rats administered either methoxyflurane (MOF) or deuterated methoxyflurane (d4-MOF). One untreated and one phenobarbital (PB)-treated group were exposed for two hours to either air, 0.5 per cent (V/v) MOF, or 0.5 per cent (v/v) d4-MOF. Serum and urinary F- and serum urea nitrogen and creatinine were measured. Urine volume and urinary F- excretion were only slightly greater among MOF than among d4-MOF exposed animals. Pretreatment with PB, however, greatly enhanced F- production in MOF-exposed animals leading to marked renal impairment but only slightly enhanced F- production in d4-MOF animals leading to mild renal impairment. Thus, only in PB-pretreated animals could a biologically significant difference in nephrotoxicity be demonstrated for MOF and d4-MOF.

Anesthesia↗
PubMed1980

Hepatitis B virus, hepatitis A virus and persistently elevated aminotransferases in hemophiliacs.

To determine the exposure to hepatitis A and hepatitis B viruses (HAV, HBV) following intravenous replacement therapy in patients with classic hemophilia and to assess the role of these viruses in persistently elevated aminotransferases, sera were studied from 136 patients from 9 months to 67 years of age were transfused with either single-donor cryoprecipitate (CRYO) or Antihemophilic Factor Concentrate (AHF) for periods ranging from a few months to 15 years. Serologic evidence of past or present infection with HBV was detected in 90% of all 136 patients and in 85% of those 34 patients 10 years of age or younger. Sixty-four percent of those with serologic markers of hepatitis B had high titers of antibody to the hepatitis B surface antigen and low titers of antibody to the hepatitis B core antigen. These findings are consistent with the known high frequency of early exposure to HBV in hemophiliacs receiving replacement therapy and with recovery from these hepatitis B infections. Sixteen percent of these patients had persistently elevated aminotransferase levels; HBV could not be implicated as the cause of the enzyme elevations in most of these cases.

Adolescent↗
PubMed1980

Liver dysfunction in Pennsylvania's multitransfused hemophiliacs.

Transaminase values [alanine amino transferase (ALT) and aspartate amino transferase (AST)] and markers for hepatitis B were serially determined in 558 hemophiliacs exposed to blood products. Hepatitis B surface antigen (HBsAg) persistent for over 12 months was present in 6% of the patients. Antibody to hepatitis B surface antigen (anti-HBs) was noted in 90% of the 259 patients treated with factor VIII or IX concentrates but in only 49% of the 43 patients treated with fresh frozen plasma (FFP) or cryoprecipitate. Persistently abnormal transaminase values were noted in 31% of the patients treated with commercial concentrates but in only one (2%) of the patients exposed to cryoprecipitate or FFP. This difference continued even when the two groups of patients were matched for the amount of blood products, up to 50,000 units, which they had received in the study period. In the concentrate-treated patients, no correlation could be found between transaminase values and the number of units of factor VIII or IX they had received during the six years of the study (1973-1978).

Adolescent↗
PubMed1980

Hydrodynamic and diffusion considerations of rapid-mix experiments with red blood cells.

From studies of the oxygenation rate of red blood cells (RBC) using rapid-mix techniques, it has been suggested that RBC are surrounded by a stagnant layer of water that does not (or cannot) mix with the rest of the water. A consideration of the appropriate hydrodynamics and convective diffusion rates shows that a mixer can reduce the resolution time to approximately 1 ms (or possibly less) and give a diffusion layer around the TBC that is approximately 1 micron thick. In stopped flow equipment it expands to approximately 4 micron over approximately 10 ms, whereas in continuous flow work the diffusion layers expands slightly less rapidly and less far. Thus the rate of oxygenation of TBC should be slower when measured by stopped flow techniques than by continuous flow apparatus for which the rate will depend weakly on the Reynolds number of the flow in the interrogation tube.

Erythrocytes↗
PubMed1980

Comment on the rotational state dependence of indirect photodissociation of a polyatomic molecule.

The rotational state dependence of indirect photodissociation has been examined in the light of some recent developments in the theory of radiationless transitions in rotating molecules. A simple argument based on projection operators leads to the prediction of sequential kinetics from an initial singlet state through an intermediate triplet bound state and on to a final dissociative state. The results indicate that as long as the geometry of the molecule in the triplet state is not very different from that of the singlet state, only a very small rotational dependence will show up in the singlet state radiationless lifetime, in spite of the fact that the overall dissociation constitutes a large geometry change.

Journal Article↗
PubMed1980

Enflurane has no effect on haemopoiesis in mice.

Male and female Swiss/ICR mice were exposed to 0.3% enflurane in air, 4 h per day, 5 days per week for 52 weeks. A control group was exposed to air alone. After 52 weeks, all animals were sacrificed and peripheral blood and bone marrow samples were examined for alterations in haemopoiesis. In general, there was no difference between treated and control groups.

Animals↗
PubMed1980

Renal function in Fischer 344 rats with chronic renal impairment after administration of enflurane and gentamicin.

To assess the potential for producing nephrotoxicity in rats with abnormal renal function, the renal effects of enflurane or halothane anesthesia, 1 MAC for two hours, were examined in six groups of six Fischer 344 rats each with surgically induced chronic renal impairment. As an additional predisposing factor, gentamicin, 5 mg/kg/day, was administered for one week before and for one week after anesthesia to three of the groups, one anesthetized with enflurane, one anesthetized with halothane, and one unanesthetized. No significant change in renal function could be attributed to either anesthetic agent. Serum inorganic fluoride levels four hours and 24 hours after enflurane anesthesia were similar in the gentamicin-treated and the non-gentamicin-treated groups. Clinically small but statistically significant increases in serum creatinine concentration and urinary flow occurred in all three gentamicin-treated groups during the period of treatment. Anesthesia with either enflurane or halothane in rats with chronic renal impairment treated with gentamicin did not result in additional renal damage.

Acute Kidney Injury↗
PubMed1980

Metabolism by rat hepatic microsomes of fluorinated ether anesthetics following isoniazid administration.

The possibility that enflurane defluorination is increased following treatment with isoniazid was investigated in male Fischer 344 rats. The effects of various isoniazid dosage regimens on the hepatic microsomal defluorination rates of enflurane were compared with those of several other ether anesthetics, and the conditions for production of maximal enflurane defluorination rates were determined. Seven to ten days of treatment with 50 mg/kg/day isoniazid (Nydrazid) resulted in maximal rates of defluorination of methoxyflurane, enflurane, isoflurane, and sevoflurane with no overt sign of toxicity. Compared with saline treatment of control rats, isoniazid increased defluorination of enflurane 370 per cent, methoxyflurane 259 per cent, sevoflurane 283 per cent, and isoflurane 168 per cent. Previous studies have shown that while the enzyme inducer phenobarbital increased in vitro rates of methoxyflurane defluorination approximately 1000 per cent, the rate of enflurane defluorination remained unchanged or increased by 100 per cent at most. In this study, enhanced hepatic microsomal defluorination was not associated with an increase in cytochrome P-450 per mg protein. Anesthetic defluorination rates were not altered by treatment with chlorobutanol, the preservative contained in Nydrazid.

Animals↗
PubMed1980

Metabolic and toxicologic studies with enflurane in Swiss/ICR mice.

Swiss/ICR mice were tested to determine whether the volatile ether anesthetic, enflurane, causes induction of anesthetic defluorination and organ toxicity. Mice were exposed in utero and postnatally to 0.01, 0.1 and 1.0 volumes percent enflurane vapor. Body weight was measured at frequent intervals throughout the experiment. Animals were sacrificed at 73 days of age and liver microsomal cytochrome P-450 content and the rate of defluorination of enflurane, isoflurane, methoxyflurane ans sevoflurane were determined. In addition, the liver, kidney and testis were weighed and examined histologically for drug induced damage. The maximum tolerated dose of enflurane delivered over a twelve week period was determined to be 0.5 volumes percent for four hours a day, five days a week. Even at this high dose there was no evidence in either sex of liver, kidney or testicular damage. Following enflurane exposure, neither the liver microsomal cytochrome P-450 content nor the rate of anesthetic defluorination was increased. The rate of in vitro inorganic fluoride production per unit time was greatest for methoxyflurane, and approximately equal for enflurane, isoflurane and sevoflurane. Since there was no evidence of enzyme induction or specific organ toxicity, it was concluded that enflurane is a comparatively nontoxic volatile anesthetic under conditions of this study.

Animals↗
PubMed1979

Carcinogenicity of halothane in Swiss/ICR mice.

A simplified in-vivo bioassay system was used to test the carcinogenic potential of halothane in Swiss/ICR mice. Halothane was tested only at its maximum tolerated dose, and histologic examination was performed only on tumor masses and other grossly abnormal tissues found at necropsy. Two groups, each of 15 timed pregnant mice, were exposed to either halothane, 500 ppm (0.05 per cent), or compressed air for two hours on days 10--19 of pregnancy. Five days after birth the offspring were similarly exposed, three times weekly, for 78 weeks. After a ten-week, no-treatment, observation period, all remaining mice were examined by necropsy. Mice dying or killed in extremis before final sacrifice at 88 weeks of age also underwent complete gross necropsy unless extensive cannibalism or autolysis precluded examination. The incidences of malignant tumors, hepatomas or modular hyperplasias, and benign tumors in halothane-treated mice were 7, 6, and 20 per cent, respectively; there were similar incidences of these lesions in control animals. It is concluded that under the conditions of this experiment, lifetime administration of halothane at its maximum tolerated dose is not associated with an increased incidence of neoplasia in Swiss/ICR mice.

Adenoma↗
PubMed1979

Fetal morphology in mice exposed to halothane.

The teratogenic potential of subanesthetic and anesthetic exposure to halothane was studied in Swiss/ICR mice. Two treatment regimens were employed: daily exposure of males and females for nine weeks prior to conception and on days 1 through 17 of pregnancy; and exposure of females only on days 6 through 15 of pregnancy. Mice were exposed to subanesthetic concentrations of halothane for 0.025, 0.1, 0.4, and 1.2 MAC hours/day; anesthetic exposure was 4.0 MAC hours/day. Fetal morphologic development was normal at the two lowest exposures. Exposures of 0.4 MAC hours/day and more were associated with decreased fetal ossification. At the 1.2 MAC hour/day exposure, renal pelvic masturation was retarded and the incidence of skeletal variants was increased. The incidences of major malformations and minor anomalies were not increased following exposure to subanesthetic concentrations of halothane. Anesthetic exposure to 4.0 MAC hours/day was lethal to both dams and embryos, and resulted in major developmental malformations in surviving fetuses. These effects were probably due to altered maternal physiologic status. It is concluded that exposure of mice to subanesthetic concentrations of halothane does not result in important morphologic abnormalities in their offspring.

Abnormalities, Drug-Induced↗
PubMed1979

Effect of phenytoin (DPH) treatment on methoxyflurane metabolism in rats.

The toxicity and metabolism of the fluorinated anesthetic methoxyflurane were compared in Fischer 344 rats pretreated with phenytoin or phenobarbital. Treatment with either drug potentiated the polyuric effects of methoxyflurane by more than 100%. Also, serum inorganic fluoride (F-) levels and urinary F- excretions after methoxyflurane exposure were comparable in phenytoin- and phenobarbital-treated rats, a 26 to 49% increase as compared to rats treated with methoxyflurane alone. In vitro, 10-fold increases in the rate of hepatic microsomal methoxyflurane defluorination were observed after treatment of rats with either phenytoin or phenobarbital. Kinetic studies with microsomes demonstrated inhibition of methoxyflurane defluorination in the presence of phenytoin. Defluorination of three additional fluorinated ether anesthetics, enflurane, isoflurane and sevoflurane, also was examined in vitro. Phenytoin and phenobarbital treatment resulted in similar enhancement of defluorination of the latter two anesthetics, but not enflurane. Phenytoin and phenobarbital treatment increase defluorination of fluorinated ether anesthetics to approximately the same extent in vitro and in vivo in Fischer 344 rats.

Anesthetics↗
PubMed1979

Renal effects of enflurane anesthesia in Fischer 344 rats with pre-existing renal insufficiency.

Chronic renal insufficiency was produced surgically in Fischer 344 rats in order to evaluate the effects of enflurane anesthesia in animals with impaired renal function. Three groups of rats were anesthetized with enflurane: a control group without impairment of renal function (n = 7); a group with minimal impairment of renal function (n = 6); and a group with moderately severe renal impairment (n = 9). Another group of rats with moderately severe renal impairment (n = 8) was anesthetized with halothane. Two hours of anesthesia resulted only in mild transient depression of urea clearance in all groups. Six hours of anesthesia resulted in a 5 to 10 ml/day increase of urinary output in all groups and small increases in urea nitrogen levels in both groups with moderately severe renal impairment. Deterioration of the model was noted late in the experiment; at sacrifice, animals that had been anesthetized with enflurance and four with halothane had terminal renal failure. The morphological lesion in both groups was similar, resembling glomerulonephritis. Thus, there was no difference in the renal response to enflurane or halothane anesthesia among rats with chronic renal insufficiency.

Animals↗