Abortion attitudes and practices of family and general practice physicians.

BACKGROUND. Approximately 1.5 million abortions are performed each year in the United States. Little information has been published on the abortion attitudes and practices of family physicians. The object of this investigation was to assess the abortion attitudes and practices of family and general practice physicians in Kansas. METHODS. A 19-item self-administered survey questionnaire was designed and mailed to 856 family and general practice physicians in Kansas. RESULTS. A 63% survey response rate was obtained. Seventy-eight percent of the physicians reported that abortion should be legal, but only 56% of the respondents classified themselves as pro-choice. Conversely, only 8% reported that legal abortion should not be available, even though 33% classified themselves as pro-life. The majority of physicians reported that abortion is an appropriate option to save the life of the mother, in cases of rape or incest, and when a fetal anomaly is diagnosed. Only three respondents (0.5%) had performed abortions during the previous year. In general, female physicians and physicians over the age of 40 years (regardless of sex) were more likely to be pro-choice and to view a woman's personal decision as a circumstance in which abortion may be appropriate. CONCLUSIONS. Physician's views about abortion and their practice patterns are important components of health care for thousands of women each day.     

Effects of endothelin on regional hemodynamics in conscious rats

Endothelin is a potent vasoactive peptide in anesthetized rats and isolated vascular smooth muscle. This study was performed to describe the hemodynamic effects of endothelin in conscious, freely moving rats. Endothelin (0.067-2 nmol/kg i.v.) produced long-lasting, dose-dependent increases in arterial pressure, mesenteric and, to a lesser degree, hindquarters vascular resistances and decreases in heart rate. We suggest that endothelin may play an important role in regulation of arterial pressure by modulating peripheral vasomotor tone.     

Brain metabolic correlates of hypoxic-ischemic cerebral necrosis in mid-gestational sheep fetuses: significance of hypotension

Mid-gestational sheep fetuses exposed to marked hypoxia for 2 h remain brain intact if MABP is maintained above 30 mm Hg. On the other hand, similarly hypoxic fetuses, if they experience reductions in MABP below 30 mm Hg, develop foci of necrosis that predominantly affect hemispheric white matter and neostriatum. Cortex damage is more restricted and is usually associated with more massive underlying white matter damage. The present study examines the brain metabolic basis for the important role of hypotension in brain injury development in marked hypoxia. Sheep fetuses rendered hypoxic by respiring their ewes with 11% oxygen (fetal PaO2 = 8-12 mm Hg) in which MABP was maintained above 30 mm Hg showed increases in brain lactic acid concentrations to 7-13 mumol/g but unaltered energy charge. In contrast, fetuses that sustained MABP reductions below 30 mm Hg showed increases in lactic acid concentrations in vulnerable structures to 16-24 mumol/g accompanied by marked decreases in energy charge. The vulnerable structures also showed reductions in fructose concentrations but a variable behavior of other brain metabolites including phosphocreatine, glycogen, and glucose. Thus, the present findings suggest a relation between hypotension during marked hypoxia, low energy charge, lactic acid accumulation in brain at high concentrations, and fetal brain injury. The ewes of hypoxic hypotensive fetuses received pentobarbital at lower doses than did those of fetuses that maintained blood pressure. This suggests that pentobarbital plays an important role in protecting the fetal brain from asphyxia by extending the hypoxic fetus's ability to maintain blood pressure in addition to reducing its brain metabolism.     

Calcitonin gene-related peptide is the endogenous mediator of nonadrenergic-noncholinergic vasodilation in rat mesentery

In the isolated perfused rat mesenteric vascular bed pretreated with guanethidine and precontracted with methoxamine, periarterial nerve stimulation elicited a frequency-dependent and endothelium-independent vasodilation. The sustained vasodilation was slow-onset and reversible. It was resistant to propranolol or atropine but sensitive to tetrodotoxin and capsaicin suggesting that this is a nonadrenergic-noncholinergic vasodilation and is a neurogenic response. The vasodilation was abolished by anti-serum against calcitonin-gene related peptide (CGRP) in a concentration-dependent manner. These data suggest that the non-adrenergic-noncholinergic vasodilation is mediated by endogenous CGRP released from the primary sensory nerve terminals upon electrical stimulation. In addition to the vasodilator action, CGRP also inhibited nerve stimulation-induced and norepinephrine-induced vasoconstriction at extremely low concentrations. The inhibitory action of CGRP appeared to be mediated by postsynaptic mechanisms inasmuch as evoked norepinephrine release was not affected by CGRP when the vasoconstriction produced by norepinephrine or periarterial nerve stimulation was attenuated greatly by CGRP. These observations suggest that the vascular tone of the resistance vessels can be regulated by primary sensory nerve-derived CGRP.     

Modulation of serum cytokine levels by a novel superoxide dismutase mimetic,M40401, in an Escherichia coli model of septic shock: correlation with preserved circulating catecholamines

OBJECTIVES: We have shown previously that inactivation of catecholamines by superoxide anions contributes to the loss of vascular reactivity to norepinephrine and the subsequent hypotension that develops in Gram-negative endotoxic shock. In addition to their vasopressor actions, catecholamines, via beta-adrenoceptor activation, are important regulators of cytokine production. Here we examined if maintenance of serum catecholamine levels by the superoxide dismutase mimetic, M40401, modulates serum cytokine levels and arterial hypotension in an Escherichia coli-infected conscious rat model of septic shock. DESIGN: Controlled laboratory animal study. SETTING: University animal research laboratory. SUBJECTS: Pathogen-free male Sprague-Dawley rats (n = 51). INTERVENTIONS: Conscious, antibiotic-treated animals with chronic in-dwelling carotid arterial and jugular venous catheters were intravenously infected with 10(10) live E. coli bacteria (O55:B5, n = 51) over 30 mins, ending at time = 0 hrs. At 0.5 or 3 hrs, infected rats were administered an intravenous infusion of either M40401 (n = 33) or 0.9% saline (n = 18) for 6 hrs at a rate of 1 mL/h. In additional experiments, anesthetized animals with catheterized left femoral arteries and veins were administered a dose-range of norepinephrine (0.1-1 microg/kg) as bolus intravenous injections. Thereafter, E. coli lipopolysaccharide (4 mg/kg, n = 6) was administered as a 0.3-mL slow bolus intravenous injection. One hour later, the norepinephrine protocol was repeated, after which the rats were administered an intravenous infusion of either M40401 or 0.9% saline for 15 mins. At 2 hrs, the dose response to norepinephrine was repeated. MEASUREMENTS AND MAIN RESULTS: Rats infected with live E. coli exhibited a biphasic fall in mean arterial pressure, with mortality reaching 83% by 24 hrs. Rats treated with M40401 (0.25, 2.5, or 25 microg x kg-1 x hr-1 ) 3 hrs after bacteremic sepsis maintained a normal mean arterial pressure, and mortality was dose-dependently reduced to 44, 33, and 22%, respectively, at 24 hrs. Furthermore, serum catecholamine levels were diminished in E. coli-infected rats treated with saline compared with rats treated with M40401. In separate experiments, E. coli-infected rats were administered M40401 (25 microg x kg-1 x hr-1 ) 0.5 hr after bacterial challenge. Blood samples taken at 0, 1.5, 3.5, and 6 hrs were analyzed for tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, and IL-10 and for norepinephrine and epinephrine. Serum levels of tumor necrosis factor-alpha and IL-1 beta were significantly depressed in M40401-treated septic rats, whereas IL-10 was elevated. Moreover, serum catecholamine levels were greater in M40401-treated septic rats at the same time points. IL-6 levels were unaffected by M40401 treatment. Finally we examined whether treatment with M40401 could reverse the hyporeactivity to norepinephrine typifying early septic shock. Using the E. coli lipopolysaccharide (4 mg/kg) challenged anesthetized rat model of shock, we demonstrated that the vasoconstrictor ability of norepinephrine was indeed restored after M40401 treatment (25 microg/kg). CONCLUSION: Postinfection treatment with the superoxide dismutase mimetic M40401 protects against hypotension, vascular hyporeactivity to catecholamines, and mortality associated with septic shock. Such beneficial effects correlate with both reduced oxidative inactivation of serum catecholamines and a reduction in canonical cytokine mediators of inflammation.     

Diagnostic reasoning strategies of nurses and nursing students

This study described and compared the cognitive strategies of diagnostic reasoning used by junior nursing students (n = 15), senior nursing students (n = 13), and practicing nurses (n = 15). Verbal responses to three videotaped vignettes provided the data. Findings suggested that diagnostic reasoning processes of both nurses and nursing students can be described by a general model developed from studies of physicians. Subjects activated diagnostic hypotheses early in the encounter and used systematic information gathering to rule in and rule out hypotheses. With increased levels of knowledge and experience, there was a trend toward more systematic data acquisition and greater accuracy in diagnosis. The number of hypotheses activated, the earliness with which they were activated, and their diagnostic accuracy were task-specific components of the process, but selection of data-acquisition strategies appeared to be more generalizable across cases.     

Characterization of neuromedin U effects in canine smooth muscle

Two endogenous receptors for the potent smooth muscle-stimulating peptide neuromedin U (NmU) have recently been identified and cloned. Pharmacological, binding, and expression studies were conducted in an attempt to determine the receptor(s) involved in the smooth muscle-stimulating effects of NmU. The NmU peptides caused a concentration-dependent contraction of canine isolated urinary bladder. NmU did not have this same effect in the urinary bladder from rat, guinea pig, rabbit, mouse, or ferret. Although NmU had no effect on canine uterus it did cause contraction of canine stomach, ileum, and colon. As well as causing contraction of canine bladder in vitro, NmU administered systemically resulted in a significant increase in urinary bladder pressure in vivo. High-affinity binding sites for NmU were identified in canine bladder. The four NmU peptides porcine NmU-8, rat NmU-23, human NmU-25, and porcine NmU-25 displaced (125)I-NmU-25 binding with similar K(i) values (0.08-0.24 nM). A different binding profile was revealed in human embryonic kidney-293 cells transiently expressed with the canine NmU-2 receptor where porcine NmU-8 (K(i) = 147.06 nM) was much less potent than the other NmU peptides. Using TaqMan, expression of NmU-1 was detected in human urinary bladder, small intestine, colon, and uterus. Expression of NmU-2 was much lower or absent in these human tissues and undetectable in canine bladder and stomach. The results of this study reveal significant species differences in the activity of NmU. The contractile activity in human and canine smooth muscle seems to be mediated by the recently cloned NmU-1 receptor.     

Beta2-adrenoceptor-mediated prejunctional facilitation and postjunctional inhibition of sympathetic neuroeffector transmission in the guinea pig vas deferens.

This study examines the role of prejunctional and postjunctional beta-adrenoceptors in the modulation of sympathetic cotransmission in the guinea pig vas deferens. The prejunctional involvement of beta-adrenoceptors was evaluated by testing the effects of several agonists and antagonists on the nerve stimulation-evoked overflow of ATP and norepinephrine (NE) from the "in vitro" vas deferens. The nonsubtype-selective beta-adrenoceptor agonist isoproterenol and the beta2-subtype-selective agonist clenbuterol increased, to a similar degree, the overflow of ATP and NE, while the beta1-subtype-selective agonist xamoterol and the beta3-subtype-selective agonist BRL 37 344 had no effect. Pretreatment with ICI 118, 551, a beta2-subtype-selective antagonist, abolished the facilitation of cotransmitter release by isoproterenol and clenbuterol, while the beta1-subtype-selective antagonist atenolol had no effect. Activation of beta-adrenoceptors by either isoproterenol or clenbuterol, but not by xamoterol and BRL 37 344, reduced the amplitude of contractions evoked by exogenously applied ATP. Pretreatment with propranolol or ICI 118, 551, but not atenolol, prevented these inhibitory effects. Isoproterenol in lower concentrations produced dose-dependent reduction of the purinergic but not the adrenergic phase of nerve stimulation-induced contraction of the guinea pig vas deferens. When applied in concentrations greater than 1 microM, isoproterenol, but not clenbuterol, actually produced a concentration-dependent facilitation of contractions evoked by both nerve stimulation and exogenously applied ATP. Antagonists of alpha-adrenoceptors blocked these facilitatory effects. Together, these results demonstrate that beta2-adrenoceptors can influence sympathetic neuroeffector transmission both prejunctionally, where they facilitate equally well the release of sympathetic cotransmitters and postjunctionally, where they inhibit smooth muscle contractions evoked by ATP.     

RisedronatE and ALendronate Intervention over Three Years (REALITY): minimal differences in fracture risk reduction

Summary  The comparative effectiveness of alendronate and risedronate has received limited evaluation. Among 19,063 new users of bisphosphonates, risedronate users had a higher relative rate of hip fracture compared to alendronate users, but the difference in absolute fracture rate was small. We conclude that the agents have comparable efficacy. Introduction  Bisphosphonates differ in their in vitro potency, avidity for bone, and rapidity of onset in clinical trials. To address potential differences between bisphosphonates in comparative effectiveness, we compared new users of alendronate and risedronate to determine if there were differences in the risk of clinical fractures at 1 year and beyond. Methods  Using claims data from a U.S. health care organization, we identified new, adherent users of weekly alendronate or risedronate and assessed subsequent fractures. We calculated fracture incidence rate differences and ratios between the two agents. Results  There were no significant differences in fracture rates between alendronate users (n = 12,956) and risedronate users (n = 6,107) at 1 year. Using all available data, the rate of hip fracture was higher among risedronate users compared to alendronate users (absolute rate difference approximately five per 1,000 person-years). Risedronate users had a higher relative rate (RR) of hip fracture (RR = 1.77, 95% CI 1.15–2.74) and similar rates of clinical vertebral and nonvertebral fractures compared to alendronate users. Conclusions  The absolute rate of clinical fractures among alendronate and risedronate users was similar both at 1 year and beyond, suggesting comparable effectiveness between agents. Some of the investigators (JRC and KGS) receive salary support from the National Institutes of Health (AR053351, AR052361) and the Arthritis Foundation (JRC).