Biomedical subjects

S B Gertner

Publications and source records attributed to S B Gertner.

30 records · Page 2Linked to original sources

PubMed1983

Lung lipoprotein lipase: inhibition by barbiturates.

The action of barbiturates on the enzymatic activity of lung lipoprotein lipase has been studied in vitro and in vivo. Mouse lung preparations can be separated into two fractions containing lipoprotein lipase activity and designated as soluble and membrane-bound. In vitro, both enzyme fractions were inhibited in a graded manner by the barbiturates when present in concentrations of 1-4 mg/ml. Experiments to determine the mechanism for the inhibition of lipoprotein lipase suggest that it may be related to non-specific binding of the drug to the enzyme since other drugs e.g., phenylbutazone and a coumarin derivative which bind non-specifically to serum albumin showed similar inhibitory activity. When rat lungs were perfused in situ with heparin, 49% of the total lipoprotein lipase activity was released into the perfusate. However, when pentobarbital was perfused prior to heparin, no lipoprotein lipase activity was observed in the perfusate. The possible clinical implications resulting from inhibition of pulmonary lipoprotein lipase by barbiturates are discussed in this paper.

Animals↗

PubMed1983

Soluble and membrane-bound forms of lipoprotein lipase in mouse lung tissue.

Homogenates of mouse lungs were separated by differential centrifugation into two fractions containing lipoprotein lipase, namely, a soluble and a membrane-bound fraction. Lipoprotein lipase was specifically identified by its inhibition by both protamine sulfate (3 mg/ml) and sodium chloride (0.9 mol/l). The enzymatic activity of each fraction was enhanced when serum was preincubated with the enzyme. Both enzyme fractions showed optimum activity at alkaline pH, but the membrane-bound enzyme showed a higher pH optimum. In addition, the apparent Km of the soluble enzyme was lower than that of the membrane-bound enzyme. It is concluded that there are two different forms of lipoprotein lipase in mouse lung tissue that differ in a number of aspects.

Animals↗

PubMed1982

Pulmonary vagal afferent stimulants in the conscious rat: opioids and phenyldiguanide.

Phenyldiguanide (PDG, 40 microgram/kg), D-ala2-met5-enkephalinamide (D-AME, 250 microgram/kg) and morphine sulfate (MS, 2 mg/kg) injected into the right atrium (RA) of conscious freely moving rats produced a profound bradycardia and hypotension 1-2 sec subsequent to administration. Concomitant with the cardiovascular effects apnea occurred and lasted approximately 5 sec. Atropine methyl nitrate (2 mg/kg, RA) significantly attenuated the bradycardia and hypotension produced by all three agents. Naloxone blocked only the opioid responses. Coordinated motor activity was impaired following the administration of PDG (40 microgram/kg, RA). Fifty percent of the animals receiving PDG failed to remain on a rotor rod for a 2 min period. Only 8 percent of the saline treated group fell off during this period. It was concluded that the cardiovascular, respiratory, and motor effects caused by PDG, in the conscious freely moving rat, were the result of stimulation of pulmonary vagal afferents (J-receptors). The cardiovascular effects of opioids are also believed to arise from the stimulation of J-receptors. However, unlike PDG, these effects are mediated by pulmonary opiate receptors.

Animals↗

PubMed1981

Evidence for a role of endogenous histamine in central cardiovascular regulation: inhibition of histamine-N-methyltransferase by SKF 91488.

Studies were undertaken to determine whether changes in endogenous brain histamine levels would occur concomitant with centrally mediated cardiovascular responses. All experiments were performed on conscious rats since previous findings by others have indicated anesthesia alters cardiovascular responses. Rats were injected intracerebroventricularly (i.c.v.) with SKF 91488 (10-100 micrograms), a potent inhibitor of histamine-N-methyltransferase, while blood pressure and heart rate were recorded. In all animals, there was a dose-related increase in mean arterial blood pressure and a fall in mean heart rate after this treatment. These responses were very similar to the cardiovascular effects observed after i.c.v. injections of exogenous histamine (0.1-5.0 micrograms). Within 5 min after i.c.v. injection of SKF 91488, there was a statistically significant increase in hypothalamic histamine levels; within 15 min, histamine levels were significantly elevated in the cerebral cortex, hypothalamus and the remainder of the brain. In other experiments, cardiovascular responses after i.c.v. injection of histamine were potentiated by prior treatment with SKF 91488. It is concluded that brain histamine is involved in central cardiovascular regulation and that the hypothalamus may be a site of action. These results also imply a neurotransmitter role for histamine in the mammalian brain.

Animals↗

PubMed1979