Post-abortion care: a women's health initiative to combat unsafe abortion.

PIP: Improving postabortion care can reduce the negative impact of unsafe abortion. Of the 53 million estimated induced abortions occurring annually about two out of five involve unsafe procedures. About one abortion occurs for every three births annually. 96% of abortions in Africa and 85% of abortions in Latin America are unsafe. About 100,000 to 200,000 women die every year from unsafe abortion, or 1 out of 400 women. Family planning is unavailable to over 120 million women in developing countries who desire contraception. Past moral and political controversies divert attention away from death and injury. The international community can take the opportunity to change affairs by adopting a women's health initiative globally. Improvements are needed in quality of care and accessibility of emergency treatment services. Emergency treatment services are usually only available at the tertiary level of care in urban areas. Poor transportation systems limit access. Access is also impaired by women's attitudes toward treatment centers. Availability of services needs to increased through decentralized centers. Clear protocols and comprehensive, systematic training must be accomplished in tandem with improvements in quality. Provision of technology such as manual vacuum aspiration is cost effective and an easy way to improve quality in primary care or outpatient settings. Unsafe abortion is a byproduct of the failure to provide adequate family planning for prevention of unwanted pregnancy. The obstacles, that interfere with provision of family planning to abortion users, should be removed. These obstacles include providers' lack of understanding of women's needs and motivations, separation between abortion and family planning services, misinformation about contraception following abortion, lack of acknowledgement about unsafe abortion, and women's low status. National and international policies also interfere with provision of contraception. Complete reproductive health care is a necessity for improvement in maternal health and mortality.^ieng

Introduction of abortion technologies: a quality of care management approach.

PIP: Development of antiprogestins for use to induce early abortion clearly advances reproductive health to a higher level. A heated debate has arisen over the appropriateness of its being introduced in health care settings, however. Since the introduction of new contraceptive technologies into health care and family planning programs has produced serious shortcomings, some abortion care specialists propose a management approach to introducing RU-486/prostaglandin which stresses women's needs and preferences. This quality of care framework is based on 20 years of experience of introducing manual vacuum aspiration into developing countries. It takes into consideration that decisions about introducing RU-486/prostaglandin are country-specific and often program- or clinic-specific. Decision makers need to look at preparedness of local policy and service delivery infrastructure to take on the specific responsibilities of integrating it into ongoing programs and how this new technology will affect quality of care. The quality of care framework consists of those elements appropriate to women' access to care which include appropriate abortion care technology; technical competence of all members of the health care team at all levels of the health system; interactions between women and providers/staff (respect and support for women and nonjudgemental attitudes); comprehensive information and counseling; quality and accessible postabortion family planning and reproductive health care; and equipment, supplies, and medication. Decision makers need to consider whether RU-486/prostaglandin is acceptable to women and providers, manufactured to high standards, consistent with relevant regulatory requirements and appropriate to specific service delivery settings.^ieng

Heterogeneity of biochemical actions among vasodilators.

Thirty-four vasodilators were screened in several in vitro biochemical assays related to smooth muscle excitation-contraction coupling, binding to beta 1-,beta 2-, and alpha-adrenergic receptors, inhibition of phosphodiesterase activity, and antagonism of calcium accumulation. Isoproterenol and perhexiline only exhibited binding to beta-adrenergic sites. Ergocryptine, tolazoline, and amotriphene only bound to alpha-adrenergic receptors. Leniquinsin, papaverine, proquazone, dioxyline, hoquizil, quazodine, and theophylline were active only as phosphodiesterase inhibitors. Isoxsuprine, nylidrin, and bencyclane bound to alpha- and beta-receptors. Pentoxifylline bound to beta 1-sites and inhibited phosphodiesterase. Cyclandelate bound to beta 2-sites and blocked calcium accumulation. Cinnarizine and flunarizine antagonized calcium accumulation and bound to alpha-sites. Prazosin bound to alpha-sites and inhibited phosphodiesterase. Ethaverine and dipyridamole were inhibitors of phosphodiesterase and calcium accumulation. Nafronyl bound to beta 2- and alpha-sites and antagonized calcium accumulation. Mebeverine bound to beta 2- and alpha-receptors and inhibited phosphodiesterase activity and calcium accumulation. Verapamil bound to alpha-sites, and blocked phosphodiesterase and calcium accumulation. Quinazosin bound to beta 2- and alpha-receptors and antagonized both phosphodiesterase activity and calcium accumulation. Vasodilators that were inactive in all assays included niacin, nicotinyl alcohol, inositol nicotinate, amyl nitrite, sodium nitroprusside, diazoxide, hydralazine, and protoveratrine. Vasodilators should not be considered as a single drug class since they act on various mechanisms related to coupling of neuronal excitation to muscular contractility.

In vitro measurement of the beta-adrenergic blocking properties of ORF 12592, the 5-hydroxy analog of propranolol.

ORF 12592 caused concentration-dependent inhibition of isoproterenol stimulated adenylate cyclase activity in sarcolemma-enriched membrane preparations of guinea-pig myocardium. Its potency was slightly less than that of d,l-propranolol. ORF 12592 did not stimulate basal enzyme activity, suggesting it to be devoid of intrinsic sympathomimetic activity. It produced no marked inhibition of basal activity, nor did it inhibit sodium fluoride stimulated enzyme activity, indicating that the compound acts at the receptor rather than the catalytic site of the beta-adrenergic receptor-adenylate cyclase complex. ORF 12592 competed for binding of 3H-dihydroalprenolol to specific beta1 and beta2-adrenergic binding sites on turkey and leopard frog erythrocyte membranes respectively. Concentration-binding inhibition curves indicated that ORF 12592 is a non-selective beta-blocker with slightly less affinity for each beta-adrenergic receptor than propranolol.

Antihypertensive activity of a propranolol analog (ORF 12,592) in rodents.

Studies were carried out to determine the antihypertensive effects of the 5-hydroxy derivative (ORF 12,592) of propranolol. Acute administration of ORF 12,592 produced a reduction in mean systolic blood pressure in desoxycorticosterone acetate (DOCA) rats and in spontaneously hypertensive rats (SHR). Propranolol was not effective in DOCA rats and produced a significant blood pressure reduction in SHR 48 hr after acute administration. These results demonstrated antihypertensive activity of an analog of propranolol and support the concept that the antihypertensive effects of propranolol may be mediated through a metabolite.

Resistance of androgen-mediated aggressive behavior in mice to flutamide, an antiandrogen.

Flutamide (FTA), an anti-androgenic compound, inhibited the effects of methyltestosterone (MT) on the weight of the ventral prostate, seminal vesicles and levator ani in male castrate mice. Castration prevented the development of aggressive behavior in mice isolated for 3 weeks. While chronic administration of MT to castrate isolated mice returned the incidence of fighting behavior to control values, chronic administration of FTA + MTdid not significantly reduce the incidence of fighting as compared to castrate + MT values. These results suggest that the mechanism for androgen stimulation of secondary sex organ weight may differ from that involved in the development and maintenance of aggression resulting from isolation.