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Biomedical subjects

M A Horst

Publications and source records attributed to M A Horst.

12 recordsLinked to original sources
PubMed2000

Association of attending physician specialty with the cesarean delivery rate in the same patient population.

BACKGROUND AND OBJECTIVES: In the context of a dramatic increase in US cesarean delivery rates over the past 30 years and explicit national goals to decrease the cesarean rate, previous retrospective studies have shown that pregnant women cared for by family physicians may be less likely to undergo cesarean delivery, compared with patients cared for by obstetricians. METHODS: We conducted a retrospective chart review of 3,560 deliveries from the family practice service of a community-based family practice residency from 1986-1995, focusing primarily on cesarean delivery rates during two periods of time. During period 1 (n = 1,063), all attending were private practice obstetricians. After a transition period, all births were attended by family medicine faculty (period 2, n = 1,346). RESULTS: The total cesarean delivery rate declined from 16.7% in period 1 to 11.1% in period 2. Repeat cesareans declined from 8.5% to 2.9%. CONCLUSIONS: In this community-based residency, a change in the specialty of the attending physician was associated with a 34% decline in the cesarean delivery rate. The observed decline in the cesarean rate could not be accounted for by any change in patient demographics or secular trends in cesarean delivery rates.

Cesarean Section↗
PubMed1988

Maternal tobacco smoking and alterations in amino acid transport in human placenta: induction of transport systems.

The uptake of 14C-alpha-aminoisobutyric acid (AIB) by human placental villi from smokers and nonsmokers was measured. Washed placental villi of smokers exhibited higher uptake capacity for AIB than those of nonsmokers. The higher uptake capacity in smokers was due to increase in Vmax. Smoking increased Km and decreased affinity to AIB. This is possibly due to decreased fluidity of the plasma membrane of the villus during maternal smoking. These observations suggest that placenta utilizes its ability to increase the accumulation of amino acids during the adverse environmental conditions produced by maternal smoking.

Aminoisobutyric Acids↗
PubMed1987

Activities of 5-methylfurfuryltrimethylammonium iodide and related compounds at vascular endothelial muscarinic receptors of the rat aorta.

5-Methylfurfuryltrimethylammonium iodide (5-MFT) is a furan analog of muscarine and was studied for its cholinergic activity at vascular endothelial receptors of the rat aorta. Other related compounds have different substitutions at position 5 of the furan ring and include the following compounds: 5-hydroxymethyl- (5-HMFT), 5-chloromethyl- (5-CMFT), 5-bromomethyl- (5-BMFT), 5-iodomethyl- (5-IMFT), and 5-methoxy- (5-MOFT) furfuryltrimethylammonium salts. The furan analogs relaxed helical strips of rat aorta which contracted with norepinephrine (10(-6)M). These relaxations were endothelial cell-dependent. The ED50's for muscarinic activities increased in the following order: 5-MFT = ACh less than dl-muscarine less than 5-HMFT = 5-CMFT less than 5-MOFT less than 5-BMFT less than 5-IMFT. Among the furan analogs, 5-MFT was found to be a full agonist at the endothelial cells; other furan analogs were only partial agonists. The affinities and relative intrinsic efficacies of the most potent analogs decreased in the following order: ACh = 5-MFT greater than dl-muscarine greater than 5-HMFT greater than 5-CMFT. Atropine and scopolamine antagonized relaxations by furan analogs. KB values for atropine and scopolamine against ACh, 5-MFT or 5-HMFT as agonist were not different, indicating that these agonists and antagonists were acting at the same muscarinic receptors. The KB of atropine and of scopolamine increased when 5-CMFT was used as an agonist, indicating that 5-CMFT may cause relaxation by acting at other sites besides endothelial muscarinic receptors. The endothelial muscarinic receptor might be classified tentatively as of M2 or Ms type. These studies did not exclude the possible heterogeneity of the endothelial muscarinic receptors.

Animals↗
PubMed1986

Opioid receptors of human placental villi modulate acetylcholine release.

The human placental villous tissue contains components of the cholinergic system and opioid receptors of the kappa type. In vitro stimulation of the villous tissue releases acetylcholine in organ baths. A selective kappa agonist, ethylketocyclazocine, inhibits the release of acetylcholine. This inhibition is reversed by the antagonist Mr 2266. The antagonist alone stimulates the release of acetylcholine 18-fold over control. These results demonstrate an interaction between the placental opioid receptors and the cholinergic system in a non-neural tissue. The modulation of acetylcholine release by endogenous opioid peptides could be one of the in vivo functions of placental opioid receptors.

Acetylcholine↗
PubMed1985

Action of agonists and antagonists on adrenergic receptors in isolated porcine coronary arteries.

The adrenergic receptors of porcine coronary arteries were investigated in helically cut strips of small (less than or equal to 0.5 mm outer-diameter (od), medium (0.8-1.2 mm od), large (1.5-2.5 mm od), and very large (greater than 4 mm od) coronary arteries. Both the beta1 agonist dobutamine and the beta2 agonist terbutaline relaxed coronary arteries partially contracted by 25 mM of KCl. Dobutamine contracted small coronary arteries at 10(-5) M concentrations, then relaxed them at 10(-4) M. The beta1-adrenoceptor antagonist metoprolol contracted coronary arteries relaxed by either dobutamine or terbutaline, but the beta2 antagonist H35/25 did so only in high and probably nonselective concentrations. Alpha1-adrenoreceptor stimulating concentrations of phenylephrine did not contract any of the arteries. Metoprolol and high concentrations of H35/25 further contracted large coronary arteries partially contracted by 25 mM potassium. These contractions were blocked by verapamil and papaverine but not by atropine, phentolamine, yohimbine, mepyramine, or methysergide. This seems to indicate that beta-adrenergic receptors in porcine coronary arteries are beta1-receptors, or closely resemble beta1-receptors. They differ from many other beta1-receptors, however, in that they are stimulated by terbutaline. Alpha1 adrenoreceptors seem not to be present in these porcine coronary arteries to a significant extent. Metoprolol and high concentrations of H35/25 have a direct contractile effect in large porcine coronary artery that is not mediated by alpha-adrenergic, muscarinic, histaminergic, or serotonergic receptors but requires verapamil-sensitive calcium.

Adrenergic beta-Antagonists↗
PubMed1984

Lack of an effect of drugs acting at histamine receptors on norepinephrine-induced relaxation of porcine coronary arteries.

The effects of selective histamine receptor stimulation on relaxation to norepinephrine (NE) were determined in four sizes of spirally cut porcine coronary arteries. The four sizes of porcine coronary artery were designated very large (greater than 4.0 mm o.d.), large (1.5-2.5 mm o.d.), medium (0.8-1.2 mm o.d.), and small (less than or equal to 0.5 mm o.d.). Histamine, dimaprit, 2-pyridylethylamine, and histamine plus either mepyramine or metiamide did not alter the concentration-response curve to NE. Thus histamine receptor stimulation does not change relaxations of porcine coronary arteries to NE.

Animals↗
PubMed1983

Dibenamine enhancement of histamine-induced relaxation of the rabbit mesenteric artery.

Helically cut strips of rabbit mesenteric artery relax when exposed to histamine if their histamine H1 receptors are first blocked by 7 X 10(-6) M mepyramine. Relaxations are potentiated by 20 min pretreatment with 10(-6) M dibenamine. This dibenamine regimen also enhances relaxation of the strips to the selective H2 receptor agonist dimaprit, and to a lesser extent to papaverine which does not act on histamine receptors. This enhancement occurs both at 38 degrees and 22 degrees, and in mesenteric artery strips from rabbits reserpinized to deplete amine stores. Histamine has a greater relaxant effect on mesenteric artery strips at 22 degrees than at 38 degrees, normally. Dibenamine-treated strips do not relax more at the lower temperature, however. Thus, dibenamine nonselectively enhances relaxations of mesenteric artery and may enhance histamine-induced relaxations by an additional mechanism.

Animals↗
PubMed1982

Effects of dithiothreitol on the isolated rabbit mesenteric artery.

Rabbit mesenteric artery strips exposed to 10(-3) M dithiothreitol (DTT) were contracted with a series of concentrations of histamine and 2-pyridylethylamine (PEA). DTT exposure increased the sensitivity to histamine 100-fold but increased the sensitivity to PEA only 4-fold. DTT did not reduce dimaprit-induced relaxations, but reduced histamine-induced relaxations. Following a high concentration of histamine (10(-3) M), DTT itself produced a sustained, slowly developing contraction (29 +/- 6.8% of the maximal contraction) relaxed by 7 X 10(-6) M mepyramine but not by 10(-6) M phentolamine. Metiamide (3 x 10(-5) M) potentiated DTT-induced contractions (29 +/- 6.8 before, 57 +/- 7.5% after metiamide, as a percent of maximal contraction). Changing the bathing fluid and repeating DTT exposure slowly relaxed previously contracted strips. DTT did not prevent the increase in sensitivity of relaxant histamine receptors on exposure to cold. We conclude that DTT, in addition to potentiating histamine H1-receptor responses, releases histamine presumably from non-mast cell pools when they are loaded with a high concentration of exogenous histamine.

Animals↗
PubMed1982

Rabbit mesenteric artery receptors formed by cold exposure mediating increased histamine-induced relaxation.

On helically-cut strips of rabbit mesenteric artery contracted with phenylephrine, histamine in the presence of mepyramine caused a partial relaxation at 42 degrees C which was potentiated by reducing the temperature to 25 degrees C. However, under the same conditions, the selective H2 agonist, dimaprit, caused a smaller partial relaxation not enhanced by cooling the strips. Neither changing the temperature range (to 38 degrees and 22 degrees C), deleting the H1 blocker, nor substitution of another H1 blocker (pyribenzamine) resulted in an enhanced relation to dimaprit in the cold. Prior reserpinization of the rabbit did not abolish the cooling-enhanced relaxation to histamine, but did abolish the reversal of relaxation observed at high (10(-3) M) histamine concentrations. Metiamide (3 X 10(-4) M) blocked both histamine (H2)- and dimaprit-induced relaxations more effectively in cooled strips. Thus the H2 receptor activity observed in cooled strips differs in selectivity for the two agonists and antagonist from that observed at normal temperature.

Animals↗
PubMedDate not supplied

Maternal tobacco smoking and changes in amino acid uptake by human placental villi: induction of uptake systems, gammaglutamyltranspeptidase and membrane fluidity.

Maternal smoking depressed the active uptake of amino acids by human placentae and lowered their levels in the placenta and umbilical vein. During starvation of cells for amino acids, more amino acid carriers are induced and incorporated into the plasma membrane. A question arises whether there could be similar changes due to maternal smoking in the placental amino acid uptake carrier systems. Therefore, the characteristics of (a) the uptake of 2-amino[I-14C]-isobutyric acid (AIB) by isolated placental villi, (b) gammaglutamyltranspeptidase (GGTP), a critical enzyme of the gammaglutamyl cycle (GGC) for the uptake of amino acids in human placenta, and (c) lipid structural parameters (reciprocal of fluidity), by steady state fluorescence polarization of plasma membrane vesicles of microvilli (MV) and microsomal membranes (MM) of umbilical and chorionic plate arteries of placentae of smoking and non-smoking mothers were investigated. The above investigations gave the following results: (a) Washed placental villi of smokers exhibited higher capacity for AIB uptake than those of non-smokers. The higher uptake capacity was mainly due to increase in Vmax for AIB uptake in smokers. Km increased for placental AIB uptake in smokers. (b) Maternal smoking lowered GGTP activity of MV by decreasing its Vmax. Therefore, maternal smoking decreases the formation of gammaglutamyl-amino acid (GGAA) on the surface of trophoblast which are absorbed by the trophoblast. The degree of absorption of GGAA is considered as an inverse environmental signal for the cell to regulate amino acid transport systems. Maternal smoking seems to decrease the formation and absorption of GGAA and thereby induce the formation of new carriers for AIB uptake. (c) Maternal smoking increased the values for lipid structural order parameters and microviscosity of MV and induced tolerance against fluidization by ethyl alcohol in MM of umbilical and chorionic arteries. The alterations could increase Km for AIB uptake system and decrease the sensitivity of umbilical and chorionic arteries to vasoconstrictive substances like 5-hydroxytryptamine and catecholamine which are released by nicotine. All these changes tend to overcome the deficits produced in placental amino acid transport and satisfy the demands of the growing fetus for amino acids.

Amino Acids↗