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Biomedical subjects

B H Johnson

Publications and source records attributed to B H Johnson.

At least 91 records · Page 5Linked to original sources
PubMed1987

Does the duration of anesthetic administration affect the pharmacokinetics or metabolism of inhaled anesthetics in humans?

To define the effect of anesthetic duration on the pharmacokinetics of inhaled anesthetics, we determined the pharmacokinetics of isoflurane, enflurane, halothane, and methoxyflurane given simultaneously to seven healthy subjects for exactly 30 min and compared the results with data from a previous study in which these four anesthetics were administered for 120 min. End-tidal and mixed-expired anesthetic concentrations were measured during washin of anesthetic and for 3-9 days of washout. Multiexponential (multicompartment) models were fit by least squares to the alveolar washin and washout curves. We estimated the percentage of anesthetic that was metabolized from total uptake and recovery of anesthetic. Alveolar washout was more rapid after the shorter period of anesthetic administration. However, duration of administration did not affect the time constants determined, the number of compartments identified (i.e., five compartments were identified in both studies), or the percentages of anesthetic metabolized.

Adult↗
PubMed1986

The extent of metabolism of inhaled anesthetics in humans.

To determine the percentage of anesthetic metabolized and to assess the role of metabolism in the total elimination of inhaled anesthetics, the authors administered isoflurane, enflurane, halothane, and methoxyflurane simultaneously, for 2 h, to nine healthy patients. Total anesthetic uptake during the 2 h of washin and total recovery of unchanged anesthetic in exhaled gases during 5 to 9 days of washout were measured, and from these the per cent of anesthetic uptake that was recovered was calculated. Of the isoflurane taken up, 93 +/- 4% (mean +/- SE) was recovered. To compensate for factors other than metabolism that limit complete recovery of unchanged anesthetic, the percentage recovery of each anesthetic was normalized to the percentage recovery of isoflurane (which it was assumed undergoes no metabolism). Deficits in normalized recovery were assumed to be due to metabolism of the anesthetics. The resulting estimates of metabolism of anesthetic taken up were: enflurane 8.5 +/- 1.0%, halothane 46.1 +/- 0.9%, and methoxyflurane 75.3 +/- 1.6%. These results indicate that elimination is primarily via the lungs for isoflurane and enflurane, equally via the lungs and via metabolism for halothane, and primarily via metabolism for methoxyflurane.

Adult↗
PubMed1986

Effects of zeranol and trenbolone acetate on testis function, live weight gain and carcass traits of bulls.

The ability of zeranol and trenbolone acetate (trenbolone) to alter testis function, weight gain and carcass traits of young bulls was studied. In Exp. 1, the effects of age at initial zeranol implantation was determined. After a 235-d experimental period, sequential implantation (56-d intervals) beginning at 100 or 150 d of age had reduced testis growth (P less than .01), sperm production (P less than .01) and serum testosterone concentration in response to gonadotropin releasing hormone (GnRH; P less than .01). The 200-d age group was partially suppressed, while the 250-d age group was not affected. Body weights were similar to controls in all groups. In Exp. 2, bulls previously implanted with zeranol at 175 and 231 d of age received single implants of zeranol, trenbolone or trenbolone plus zeranol at approximately 300 d of age. At slaughter (135 d later), body weight and carcass characteristics in all treatments were similar to controls. However, trenbolone reduced sperm production (P less than .05), zeranol reduced sperm production and testes weight (P less than .05), but trenbolone plus zeranol was similar to controls. Mean testosterone response to GnRH was suppressed in all implant groups on d 65 (P less than .01), but only in trenbolone or trenbolone plus zeranol groups on d 112 (P less than .05). Results indicate that zeranol suppresses spermatogenesis and testosterone production if implanted before approximately 200 d of age. Reduction of endogenous testosterone without alteration of weight gain or carcass characteristics may be of benefit if behavioral or masculinity traits of bulls are altered. Also, it appears that no benefit is derived from implanting bulls with both trenbolone and zeranol.

Animals↗
PubMed1986

Pharmacokinetics of inhaled anesthetics in humans: measurements during and after the simultaneous administration of enflurane, halothane, isoflurane, methoxyflurane, and nitrous oxide.

To determine the relative washin and washout characteristics of isoflurane, enflurane, halothane, and methoxyflurane, we administered all four anesthetics simultaneously (total = 1.1 MAC) to nine healthy patients for 2 hr. Concentrations of anesthetics in end-tidal gases were measured during washin and for 5-9 days during washout. Multiexponential (multicompartment) models were fit to the washin and washout curves using least-squares analysis. Slowly equilibrating compartments could only be identified during washout. For 27 of the 36 data sets, five-compartment models fit the washout curves significantly better than four-compartment models. The time constant for our first compartment is consistent with that predicted for washout of the lungs. Time constants for the second, third, and fifth compartments were consistent with current data for blood flows and solubilities of vessel-rich, muscle, and fat tissue groups, respectively. The fourth compartment has a time constant that lies between the time constants predicted for muscle and fat.

Adult↗
PubMed1986

Is enflurane hepatotoxic?

We evaluated 88 cases of hepatic injury that followed, and were attributed to, enflurane anesthesia. In 30 of the cases, data were insufficient to assess the role of enflurane vs other variables as causal factors. In 43 ("unlikely") patients, factors known to produce hepatic injury were clearly present; in the remaining 15 ("possible"), such factors were not evident. No consistent pathologic change was found in liver specimens from either the unlikely or the possible group of cases. A syndrome suggested to be associated with enflurane-induced hepatic injury was present in both groups and did not differ between groups. We conclude that the data do not demonstrate a causal relationship between enflurane anesthesia and subsequent liver injury and that if severe injury is caused by enflurane anesthesia, it is an extremely rare event.

Adult↗
PubMed1985

Effects of zeranol upon bovine testicular function.

Effects of zeranol upon testicular function in bulls were studied. In Experiment I, young bulls (104+/-1.7 days of age) were either implanted with 36 mg zeranol or served as controls with reimplantation on days 56 and 112 after first implant. After a 168-day treatment period, half the bulls were orchidectomized with the remaining bulls assigned to a 168-day recovery period, after which they were also orchidectomized. Zeranol inhibited testicular development during the treatment period. Testosterone (T) concentrations were lower (P<0.01) in treated bulls. Spermatozoa were absent in testes of treated bulls while control bulls averaged 27x10(6) sperm per gram of testis. At the end of the 168-day recovery period, testes weights and sperm concentrations were similar (P>0.10) between bulls previously treated with zeranol and controls. Implantation of older bulls with either 36 mg (267+/-3.4 days of age: Experiment II) or 72 mg (16 months of age: Experiment III) of zeranol had no effect (P>0.10) upon spermatogenesis or T production over a 168-day treatment period. The results indicate that the inhibitory effects of zeranol upon bovine testicular function are age-dependent and suggest that there may be an increased sensitivity of the hypothalmic-pituitary-testicular axis to zeranol in the prepuberal bull.

Journal Article↗
PubMed1985

Nitrous oxide does not hinder the repair of halothane-induced hepatic injury in the rat.

Nitrous oxide administration may limit DNA synthesis by inactivating methionine synthetase, and may thus hamper the repair of an injured organ such as the liver. To test this possibility, we pretreated rats with phenobarbital and exposed them to 0.3 MAC halothane in 9% oxygen for 46 min, followed immediately and again 24 hr later by 70% nitrous oxide (0.25 MAC) at an FIO2 of 0.30 for 2 hr. The results from this group were compared with an anesthetic control group in which 0.35% isoflurane (0.25 MAC) was substituted for the nitrous oxide. Additional groups were given a third exposure to nitrous oxide or isoflurane 48 hr after the halothane exposure. All rats were killed 24 hr after their last anesthetic exposure. A second (nonanesthetic) control group of phenobarbital-pretreated rats received 0.3 MAC halothane in 9% oxygen for 46 min and no anesthetic thereafter. They were killed 24, 48, or 72 hr later. Histologic changes in the livers of rats did not differ among the groups given nitrous oxide, isoflurane, or no additional anesthetic after exposure to halothane alone. Thus neither nitrous oxide nor isoflurane appears to hinder the repair of hepatic injury produced by halothane in the hypoxic rat model.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1984

A search for mutagens in human aortal lipid extracts.

In view of hypotheses suggesting mutagenesis is implicated in atherosclerosis, a total of 18 lipid extracts of human aortal tissues was examined by the standard Ames mutagenicity bioassay using Salmonella typhimurium or by a liquid modification thereof. One lipid extract of intimal-medial tissue contained detectable mutagenic activity against test strain TA98 in the liquid medium bioassay and against TA1538 in the standard plate assay following metabolic activation. Six other samples appeared to have weak activity against strains TA98, TA1538, or TA100. The other aortal samples were nonmutagenic.

Aorta↗
PubMed1984

Variation in testosterone production among boards and its relationship to sexual interest and breeding performance.

Variation in ability to produce testosterone in response to both GnRH and ACTH administration and quatitative relationships between GnRH-stimulated testosterone levels, ACTH-stimulated testosterone levels, sexual interest and breeding performance were assessed in a group of 31 Duroc boars (115.4 +/- 2.5 kg body weight and 212.2 +/- 3.0 days of age). Mean area beneath the testosterone response curve increased (P<0.01) after GnRH and ACTH but the magnitude of response was variable among boars. Post-GnRH testosterone area varied from 7.44 to 50.86 ng/ml X h with a CV = 52.41% while post-ACTH testosterone area varied from 4.99 to 28.78 ng/ml X h with a CV = 45.46%. Mean sexual interest and mean breeding performance scores were correlated (r = 0.67, P<0.01); however, correlations of either variable with testosterone areas were low and nonsignificant. These results indicate that the testosterone-producing ability of boars of similar age and breeding is highly variable and suggest that peripheral testosterone concentrations may not be good indicators of either libido or breeding performance.

Journal Article↗
PubMed1984

Ability of cortisol and progesterone to mediate the stimulatory effect of adrenocorticotropic hormone upon testosterone production by the porcine testis.

The influence of corticosteroids and progesterone upon porcine testicular testosterone production was investigated by administration of exogenous adrenocorticotropic hormone (ACTH), cortisol and progesterone, and by applying a specific stressor. Synthetic ACTH (10 micrograms/kg BW) increased (P less than 0.01) peripheral concentrations of testosterone to peak levels of 5.58 +/- 0.74 ng/ml by 90 min but had no effect upon levels of luteinizing hormone (LH). Concentrations of corticosteroids and progesterone also increased (P less than 0.01) to peak levels of 162.26 +/- 25.61 and 8.49 +/- 1.00 ng/ml by 135 and 90 min, respectively. Exogenous cortisol (1.5 mg X three doses every 5 min) had no effect upon circulating levels of either testosterone or LH, although peripheral concentrations of corticosteroids were elevated (P less than 0.01) to peak levels of 263.57 +/- 35.03 ng/ml by 10 min after first injection. Exogenous progesterone (50 micrograms X three doses every 5 min) had no effect upon circulating levels of either testosterone or LH, although concentrations of progesterone were elevated (P less than 0.01) to peak levels of 17.17 +/- 1.5 ng/ml by 15 min after first injection. Application of an acute stressor for 5 min increased (P less than 0.05) concentrations of corticosteroids and progesterone to peak levels of 121.32 +/- 12.63 and 1.87 +/- 0.29 ng/ml by 10 and 15 min, respectively. However, concentrations of testosterone were not significantly affected (P greater than 0.10). These results indicate that the increase in testicular testosterone production which occurs in boars following ACTH administration is not mediated by either cortisol or progesterone.

Adrenocorticotropic Hormone↗
PubMed1984

Anesthesia does not increase opioid peptides in cerebrospinal fluid of humans.

One theory of narcosis postulates that inhaled anesthetics produce general anesthesia by causing the release of endogenous opioid peptides. In the present study, however, the concentration of immunoreactive beta-endorphin-like material (eight patients) or leu-enkephalin (four patients) did not increase in cerebrospinal fluid of patients 5 min after induction of anesthesia with thiopental, 2-5 mg/kg and N2O 70%; after an additional 10 min, during which halothane was added; at 5, 15, and 60 min after surgical incision; or after 30 min in the recovery room. Therefore, any contribution of the endorphin system to the production of general anesthesia does not appear to require the release of beta-endorphin.

Analgesia↗
PubMed1984

Genetic parameters for testes traits in swine.

Data were collected from 1,245 Duroc boars and 527 Yorkshire boars. This represents 128 Duroc and 57 Yorkshire sires. Body weights, testis length and combined testes width at 140 and 168 d were obtained. Of these boars, 432 were castrated at a later age to evaluate relationships between in situ measures and excised testis traits. Heritabilities for testis length, width and volume at 140 d ranged from .16 to .25 in both Duroc and Yorkshire data. Heritabilities for testis measurements at 168 d ranged from .16 to .36 in both data sets. Favorable negative genetic relationships were found between in situ testis measures and age to 104 kg and backfat adjusted to 104 kg. Correlations among in situ measurements were high and positive. All excised testicular traits were highly heritable except for right epididymis weight and excised testis width. Correlation estimates among excised testis traits were generally positive. Phenotypic and genetic correlation estimates between live (in situ testis and growth performance traits) measurements and excised testis traits were generally favorable. This study suggests that in situ testis measurements should be good predictors of sperm production. It also suggests that selection for testis size should not be antagonistic to selection for growth performance traits.

Animals↗
PubMed1984

Brief periods of hypoxia can produce hepatic injury in rats.

To determine whether brief periods of hypoxia could produce hepatic injury, we pretreated Sprague-Dawley rats with phenobarbital, deprived them of food for 24 hr, and then exposed them to various hypoxic mixtures of nitrogen and oxygen for various lengths of time. Rats exposed to 6% oxygen for 15 or more minutes had centrilobular injury, the severity of which was directly related to the length of exposure (r = 0.71). Extrapolation of these data indicated that no injury would occur if exposures were less than 5 min. Experiments using lower concentrations of oxygen did not reveal hepatic injury, probably because death of the animals occurred before the appearance of detectable injury of the liver. Feeding animals before imposition of hypoxia markedly decreased the risk of hepatic injury. Whether patients who are deprived of food preoperatively and whose liver enzymes are induced incur an increased risk of hepatic injury from brief periods of hypoxia remains to be determined.

Animals↗
PubMed1984

Isoflurane does not prevent hepatic injury produced by halothane in rats.

We speculated that the inhibitory effect of isoflurane on the metabolism of halothane might reduce hepatic injury produced by halothane. To test this hypothesis we pretreated male rats with phenobarbital and 24 hr later exposed them to one of three types of anesthesia. One group of rats was anesthetized with 0.6 MAC isoflurane in 21-25% oxygen for 20 min, followed by exposure to 0.3 MAC isoflurane and 0.3 MAC halothane either in 9% oxygen for 46 min (n = 5) or in 12% oxygen for 60 min (n = 11). A second group of rats received 0.3 MAC halothane in 9% oxygen for either 46 min (n = 12) or in 12% oxygen for 60 min (n = 10). The third group received 0.3 MAC isoflurane in 9% oxygen for either 46 min (n = 12) or for 120 min (n = 8). The rats were killed 24 hr after the exposures and liver slides prepared. Histologic examination revealed that rats treated with isoflurane plus halothane, or with halothane alone showed a significant hepatic injury (P less than 0.005) when compared with those treated with isoflurane. Thus isoflurane failed to protect the liver from halothane-induced injury.

Animals↗
PubMed1984

Nitrous oxide, too, is hepatotoxic in rats.

Anesthetic hepatotoxicity was tested under various conditions of hypoxia in rats pretreated with phenobarbital. Administration of 0.3 MAC halothane or fentanyl in 9% oxygen (fractional concentration of inspired oxygen = 0.09) for 46 min produced centrilobular hepatic injury in all rats (P less than 0.001 vs all other groups). Isoflurane, nitrous oxide, and thiopental at 0.3 MAC did not produce hepatic injury greater than that produced in control rats given 9% oxygen, nor was significant injury produced in control phenobarbital-pretreated rats who breathed 6 or 7.5% oxygen for 46 min. With an inspired oxygen concentration of 7.5%, hepatic injury occurred after exposure to 92.5% nitrous oxide (P less than 0.05), but not after enflurane, isoflurane, or thiopental. When hypoxia associated with 9% oxygen was extended to 2 hr, 91% nitrous oxide produced significant injury (P less than 0.001 compared with the controls), while enflurane, isoflurane, and thiopental did not. These and previous results suggest that all anesthetics can produce liver injury in the hypoxic rat model and that the ranking of hepatotoxicity (most to least) may be halothane, fentanyl, nitrous oxide, enflurane = isoflurane = thiopental.

Animals↗
PubMed1984

Celiac plexus block does not alter hepatic injury in rats.

We previously demonstrated that upper abdominal surgery on rats pretreated with phenobarbital and anesthetized with halothane caused centrilobular necrosis of the liver, which may be secondary to hepatic hypoxia induced by vasoconstriction. This study examined the possibility that celiac plexus blockade might decrease the degree of injury seen in the surgical model. Rats, pretreated with phenobarbital, were anesthetized with halothane, enflurane, isoflurane, or fentanyl with 100% oxygen. At the start of the hepatic artery dissection, the celiac plexus was blocked by injection of bupivacaine. Subsequently, the rat livers were evaluated for presence and degree of centrilobular necrosis. Animals anesthetized with halothane or fentanyl had a significantly greater incidence of centrilobular necrosis than controls (rats pretreated with phenobarbital who received no anesthesia or surgery). Hepatic injury in rats anesthetized with isoflurane or enflurane did not differ from that in controls. We conclude that celiac plexus blockade with bupivacaine provides no protection against hepatic necrosis in this model.

Anesthetics↗
PubMed1983

Phenotypic variation in testosterone and luteinizing hormone production among boars: differential response to gonadotropin releasing hormone and adrenocorticotropic hormone.

Variation in ability of boars to produce testosterone and luteinizing hormone (LH) in response to both gonadotropin releasing hormone (GnRH) and adrenocorticotropic hormone (ACTH) stimulation, as well as quantitative relationships between pretreatment and posttreatment responses, were assessed in a population of 38 boars of similar age and breeding. Peripheral testosterone concentrations following either GnRH or ACTH increased (P less than 0.01) to peak circulating levels of 7.16 +/- 0.62 and 8.42 +/- 0.81 ng/ml by 120 and 45 min, respectively. Post-GnRH testosterone area varied from 7.44 to 50.84 ng/ml X h (CV = 47.44%) and post-ACTH testosterone area ranged from 3.05 to 28.78 ng/ml X h (CV = 46.09%). GnRH-induced increases in testosterone were preceded by elevations (P less than 0.01) in peripheral LH concentrations but ACTH had no effect upon LH levels. Post-GnRH area varied from 7.07 to 125.45 ng/ml X h (CV = 76.61%). Significant (P less than 0.01) correlations were obtained between pre-GnRH and post-GnRH testosterone areas (r = 0.58) and between pre-ACTH and post-ACTH testosterone areas (r = 0.67). Nonsignificant (P greater than 0.10) correlations were obtained between post-GnRH and post-ACTH testosterone areas (r = 0.006) and between post-GnRH testosterone and LH areas (r = 0.09). The testosterone producing ability of boars was highly variable and their innate ability to produce testosterone influenced their response to GnRH and ACTH. Additionally, the mechanisms by which GnRH and ACTH influence testosterone production in boars appear to differ. Variation in the ability of boars to produce testosterone could not be explained on the basis of differences in circulating levels of LH.

Adrenocorticotropic Hormone↗