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Biomedical subjects

M E Gross

Publications and source records attributed to M E Gross.

8 recordsLinked to original sources
PubMed1992

Yohimbine/flumazenil antagonism of hemodynamic alterations induced by a combination of midazolam, xylazine, and butorphanol in dogs.

Reversal of hemodynamic alterations induced by midazolam maleate (1.0 mg/kg of body weight), xylazine hydrochloride (0.44 mg/kg), and butorphanol tartrate (0.1 mg/kg) with yohimbine (0.1 mg/kg) and flumazenil (0.25 mg/kg) was evaluated in 5 dogs. The dogs were anesthetized with isoflurane for instrumentation. With return to consciousness, baseline values were recorded, and the midazolam/xylazine/butorphanol mixture with glycopyrrolate was administered IV. Hemodynamic data were recorded for 60 minutes, and then a reversal mixture of yohimbine and flumazenil was administered IV. All variables were measured 1 minute from beginning of the reversal injection. Mean arterial pressure, pulmonary arterial pressure, systemic vascular resistance, and right ventricular stroke work index increased significantly (P < 0.05) above baseline at 60 minutes. Cardiac index and central venous pressure significantly decreased below baseline at 60 minutes. After reversal, mean arterial pressure and central venous pressure significantly decreased from baseline, whereas cardiac index, pulmonary arterial pressure, and right ventricular stroke work index increased significantly above baseline. Heart rate, cardiac index, and right ventricular stroke work index increased significantly above the 60-minute value after reversal. Mean arterial pressure and systemic vascular resistance decreased significantly (P < 0.05) below the 60-minute value after reversal. The hemodynamic alterations accompanying midazolam/xylazine/butorphanol sedation-anesthesia may be rapidly reversed with a combination of yohimbine and flumazenil.

Anesthesia↗
PubMed1991

Cellular growth response to epidermal growth factor in colon carcinoma cells with an amplified epidermal growth factor receptor derived from a familial adenomatous polyposis patient.

The receptor binding and cellular growth responses to exogenous epidermal growth factor (EGF) were studied using the DiFi cell line established from a familial adenomatous polyposis patient. The number of cell membrane EGF receptors on DiFi cells, as measured by competitive radioligand binding assays and Scatchard analysis of 125I-EGF binding isotherms, was calculated to be 4.8 x 10(6) receptors/cell. An acid prewash step performed prior to ligand binding assays did not reveal additional receptor numbers. A single, low-affinity receptor population was identified by Scatchard analysis, with an apparent Kd of 4.6 nM. This result was confirmed by radioligand binding studies performed in the presence and absence of the receptor-antagonist monoclonal antibody 528 IgG that binds predominantly to the low-affinity form of the EGF receptor. DiFi cells at 50-60% confluence, when exposed to 50 nM exogenous EGF, exhibited a rapid but partial (30%) reduction in their cell membrane-associated receptor, characteristic of sequestration. Exposure of DiFi cells to 50 nM EGF for longer periods of time (4 h) did not result in any further reduction in EGF-receptor number. The cellular growth response of DiFi cells to exogenous EGF was studied in monolayer cultures as well as in a soft agarose assay. Inhibition of soft agar colony formation was observed at exogenous EGF concentrations greater than 1.7 nM, and inhibition of monolayer growth occurred at EGF concentrations greater than 1 nM. In immune complex kinase assays, the DiFi receptor showed similar specific activity to that from the well-characterized A431 cell line. Additionally, phosphorylation of the receptor on tyrosine was qualitatively similar to that of A431 cells, further suggesting that the DiFi receptors identified by EGF-binding studies were biologically functional.

Adenomatous Polyposis Coli↗
PubMed1990

Pharmacokinetics of atenolol enantiomers in humans and rats.

Single dose pharmacokinetics of atenolol (AT) enantiomers was studied in human volunteers and in rats. After oral administration of 50 mg of racemic AT to humans, the areas under the plasma concentration-time curves (AUCs; mean +/- SD) were 1640 +/- 602 and 1860 +/- 652 (ng/mL)h for the S(-)- and R(+)-enantiomers, respectively (p less than 0.05). The small difference in the AUC was a reflection of a slight, but statistically significant (p less than 0.05) difference in the renal clearance (CLr, mL/min) of the enantiomers [129 +/- 32, S(-)-AT; 120 +/- 29, R(+)-AT]. However, the two enantiomers were not different from each other (p greater than 0.05) with respect to the volume of distribution (V lambda, L/kg) [0.879 +/- 0.342, S(-)-AT; 0.790 +/- 0.255, R(+)-AT] or the terminal elimination rate constant (lambda z, h-1) [0.113 +/- 0.038, S(-)-AT; 0.114 +/- 0.036, R(+)-AT]. After iv administration of 10 mg/kg of the racemic AT to rats, the R(+)-enantiomer achieved higher AUC values [(ng/mL)h] compared with its antipode (p less than 0.05) [3630 +/- 1040, S(-)-AT; 4020 +/- 1080, R(+)-AT]. Similar to the human results, this difference was due to a stereoselective renal clearance (mL/min/kg) in favor of S(-)-AT [14.9 +/- 5.78, S(-)-AT; 13.0 +/- 4.88, R(+)-AT; p less than 0.05].(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Introduction to endoscopy.

Endoscopy is an area of rapidly growing interest within veterinary medicine. This is understandable, because it is a relatively noninvasive procedure in which a tremendous amount of diagnostic data may be obtained. The purpose of this article is to introduce the novice to the equipment and potential uses of endoscopy.

Anesthesia↗
PubMed1988

Predator-induced trophic shift of a free-living ciliate: parasitism of mosquito larvae by their prey.

Larvae of the treehole mosquito, Aedes sierrensis, release a waterborne factor that induces morphogenesis of one of their prey, the tetrahymenid ciliate Lambornella clarki. Induced free-living trophonts of L. clarki undergo a synchronous response in which cells divide and transform into parasitic cells (theronts) that encyst on larval predators. Parasitic ciliates penetrate the cuticle, enter the hemocoel, and ultimately kill their predator-host. In nature, this trophic shift can lead to predator extinction and dramatic changes in microbial populations. Facultative parasitism by this polymorphic ciliate may have evolved as an antipredator strategy. The experimentally inducible parasitic response of L. clarki provides a novel model for studying cellular morphogenesis of ciliated protozoa.

Aedes↗
PubMedDate not supplied

Evaluation of three midazolam-xylazine mixtures. Preliminary trials in dogs.

The depressant effects of midazolam and xylazine on the central nervous system (CNS) were evaluated in 12 dogs. Xylazine was administered to six dogs (1.1 mg/kg intravenously [IV]) followed in 5 minutes by midazolam (1.0 mg/kg intramuscularly [IM]). In a second group of six dogs, xylazine (2.2 mg/kg IM) was followed in 5 minutes by midazolam (1.0 mg/kg IV). Both drug regimens induced rapid and profound sedation or anesthesia. Duration of action varied with the doses and routes of administration. Dogs given the high dose of xylazine IM had an arousal time of 95.4 +/- 8.9 minutes and a walking time of 155.4 +/- 8.8 minutes. These values exceeded the IV xylazine values threefold. Partial reversal of CNS depression was accomplished with either a benzodiazepine antagonist (flumazenil) or an alpha-2 antagonist (yohimbine). In a separate trial, a mixture of xylazine (0.55 mg/kg), midazolam (1.0 mg/kg), and butorphanol (0.1 mg/kg) with and without glycopyrrolate was evaluated in eight dogs. As with the xylazine-midazolam combinations, the CNS depressant effect of this mixture was clinically indistinguishable from anesthesia achieved with other rapid-acting injectable agents. Clinical signs of CNS depression were readily and completely antagonized by the simultaneous injection of flumazenil and yohimbine.

Anesthesia↗
PubMedDate not supplied

Hemodynamic effects of intravenous midazolam-xylazine-butorphanol in dogs.

The hemodynamic effects of a mixture of midazolam (1.0 mg/kg), xylazine (0.44 mg/kg), and butorphanol (0.1 mg/kg) were evaluated in six adult dogs. The dogs were anesthetized with isoflurane for instrumentation. As the dogs returned to consciousness, baseline values were recorded and the midazolam-xylazine-butorphanol mixture and glycopyrrolate (0.01 mg/kg) were administered intravenously (IV). Hemodynamic data were recorded 3, 10, 20, 30, 40, 50, and 60 minutes after injection. Mean arterial pressure (AP), mean pulmonary arterial pressure (PAP), heart rate (HR), rate-pressure product (RPP), mean pulmonary capillary wedge pressure (PCWP), systemic vascular resistance (SVR), and right ventricular stroke work index (RVSWI) were increased significantly above baseline values. Cardiac output (CO), stroke volume (SV), cardiac index (CI), stroke index (SI), mean central venous pressure (CVP), and left ventricular stroke work index (LVSWI) were decreased significantly below baseline values. When administered IV at the dosages used in this study, midazolam-xylazine-butorphanol-glycopyrrolate induced profound acute alterations in several critical hemodynamic variables.

Animals↗