Mothers' perceptions of primary health-care providers: thematic analysis of responses to open-ended survey questions.

General practitioners and maternal, child and family health nurses have a central role in postpartum primary health care for women and their infants. Positive client-provider relationships are particularly important for women experiencing mental health problems or unsettled infant behaviour. However, little is known about their experiences of postnatal primary health care. The study aimed to describe views of postnatal primary health care among women completing a residential early parenting programme and to identify potential strategies to enhance provider-patient interactions. Participants (n=138) were women admitted with their infants to a private or a public early parenting service in Melbourne, Australia. Women completed a detailed self-report survey, including open-ended questions about experiences of primary health-care services, and a structured psychiatric interview to diagnose anxiety and depression. Survey responses were analysed thematically. Womens' experiences of primary health care were influenced by their perceptions of provider competence and the quality of interactions. While similar positive characteristics of doctor and nurse care were valued, medical and nursing practices were judged in different ways. Women described GPs who listened, understood and were thorough as providing good care, and maternal, child and family health nurses were valued for providing support, advice and encouragement. Threats to therapeutic relationships with doctors included feeling rushed during consultations, believing that GPs were not mental health-care providers and the clinician not being 'good' with the infant; with nurses, problems included feeling judged or given advice that was inconsistent or lacked an evidence-base. Postpartum primary health care will be improved by unhurried consultations, empathic recognition, encouragement, evidence-informed guidance and absence of criticism.

Establishment and feasibility of community-based general-practitioner-led cardiology clinics.

BACKGROUND: Community-based general practitioner (GP) cardiology clinics (locality clinics) offer an alternative to hospital-based cardiology clinics. In the Greenwich area, four GPs were trained for 3 months in cardiology, followed by another 3 months in a hospital out-patient clinic. GPs then established cardiology clinics in their practices and continued to act as hospital clinical assistants on an alternate-week basis. AIM: To assess referral and investigation patterns for the locality clinics over their first 3 years. DESIGN: Pilot study, retrospective case-note audit. METHODS: We analysed 125 sets of notes selected at random from the locality and the hospital clinics, and compared them. RESULTS: There were no differences in demographics or the indication for referral between locality and hospital clinics, and despite the small sample size, no major differences in referral and investigation patterns. In both clinics, approximately 83% of patients had at least one cardiac investigation, and approximately 63% were discharged after initial consultation. Some 10% of locality patients were referred for follow-up in the hospital clinic. Beta-blockers were prescribed more by hospital doctors (14% vs. 3%), with no significant difference in other cardiac medications. Coronary risk factors were more often recorded in the notes of locality patients. DISCUSSION: Establishing community-based GP cardiology clinics seems feasible, and these clinics may be the way forward for enhancing cardiac care in the community.

New methods of making blocked coronary arteries patent again.

The use of percutaneous transluminal coronary angioplasty is limited by procedural complications and the serious drawback of restenosis, but some new techniques have been developed in an attempt to lower the complication rate for difficult lesions and reduce the rate of restenosis. These include devices to physically remove atheromatous plaque, such as the Simpson Coronary AtheroCath and the transluminal extraction catheter, as well as devices to ablate the plaque in situ, including the Rotablator and the excimer laser catheter. Although each device may have advantages in certain types of lesion, few data on their use have been reported in properly controlled randomised trials. The data available so far do not suggest that these devices will be safer than balloon angioplasty or that they will reduce restenosis. However, using metallic stents to support coronary arteries after balloon angioplasty seems to reduce acute complications and to lower the rate of restenosis, and the use of stents is likely to increase.

Analysis of P2-purinoceptor subtypes on the smooth muscle and endothelium of rabbit coronary artery.

We studied purinoceptor subtypes mediating constriction and dilatation in isolated rabbit coronary arteries with and without endothelium by comparing the effects of adenosine, ATP and the ATP analogues, alpha, beta-methylene ATP and 2-methylthio ATP. For contraction, the rank order of agonist potency was alpha, beta-methylene ATP > 2-methylthio ATP >> ATP; adenosine did not produce contraction. Removal of the endothelium did not affect these responses, but they were abolished by previous desensitisation with alpha, beta-methylene ATP. For relaxation, adenosine, ATP, and 2-methylthio ATP were equipotent, but alpha, beta-methylene ATP had no vasodilator effect and caused further contraction of the preparations. A transient contraction often preceded the relaxations to ATP at higher concentrations. The dilator responses to adenosine, ATP, and 2-methylthio ATP were significantly reduced but not abolished in preparations denuded of endothelium; previous desensitisation with alpha, beta-methylene ATP had no effect on the relaxant responses but abolished the initial transient contractions to ATP and 2-methylthio ATP. These results indicate the presence of vasodilator P1- and P2Y-purinoceptors on smooth muscle and, to a lesser extent, on endothelium and P2X-purinoceptors, mediating transient vasoconstriction on smooth muscle alone. The presence of smooth muscle P2Y-purinoceptors is unusual and has functional implications regarding the nature of the response of the coronary artery to ATP.

Microcoil embolization of large intercostal branches of internal mammary artery grafts.

Coronary artery steal via a large unligated intercoastal side-branch of the internal mammary artery graft has been previously described in two case reports. We report a series of 7 patients with post-operative angina in whom microcoil embolization of such branch was performed. In 5 patients in whom complete occlusion of the branch was achieved, anginal symptoms were relieved; in contrast the 2 patients with persistent flow through the intercostal branch remained symptomatic despite all their grafts being widely patent. We conclude that large unligated intercostal branches of the IMA graft may be related with post-operative angina and their embolization is a simple, safe, and effective procedure.

Effects of age and hyperlipidemia on rabbit coronary responses to neuropeptide Y and the interaction with norepinephrine.

In coronary arteries from New Zealand White (NZW) rabbits up to 12 months of age, both direct vasoconstriction to neuropeptide Y (NPY) and inhibition of relaxation to norepinephrine (NE) by NPY were age dependent (p < 0.02 and p < 0.05, respectively); maximal relaxation to NE was unaffected. NPY had no significant effect on arteries from NZW rabbits at 4 months of age, while vessels from Watanabe Hereditable Hyperlipidaemic (WHHL) rabbits showed enhanced direct (p < 0.001) and indirect effects of NPY (p < 0.02). We conclude that the postsynaptic vasoconstrictor effects of NPY on the epicardial coronary artery increase with age and the presence of hyperlipidemia.

Vasodilator response of coronary smooth muscle to the sympathetic co-transmitters noradrenaline and adenosine 5'-triphosphate.

1. Vasodilator and vasoconstrictor responses to noradrenaline (NA), adenosine and adenosine 5'-triphosphate (ATP) were examined in isolated ring segments of the left anterior descending coronary artery of the rabbit in the absence of endothelium. 2. NA caused dose-dependent relaxation of potassium-constricted vessels in the absence of beta-adrenoceptor blockade, with a pD2 of 5.96 +/- 0.21. This was inhibited by 1 microM propranolol. Constrictor responses of vessels at baseline tension were only seen at concentrations greater than 1 mM, and reached a maximum of 6% of the contraction to 30 mM KCl. 3. ATP caused relaxation of the potassium-constricted ring segments in a dose-dependent manner, although a transient constriction often preceded the relaxation. Adenosine was equipotent with ATP in producing relaxation; this was significantly inhibited by the P1-purinoceptor antagonist, 8-phenyltheophylline (8-PT). The responses to ATP were little affected by 8-PT, indicating that ATP was not acting through breakdown to adenosine. At basal tone, ATP produced transient vasoconstriction only at concentrations greater than 0.1 mM, reaching a maximum of 38% of the contraction of 30 mM KCl. 4. We conclude that in the rabbit coronary artery both NA and ATP produce vasodilatation by a direct action on the smooth muscle.

Responses of coronary arteries to neurotransmitters: changes with sexual maturity in the female rabbit.

Vasomotor responses of isolated coronary arteries to peptide and nonpeptide neurotransmitter agents changed with the development of sexual maturity in female New Zealand white rabbits aged 4-12 months. There was a significant reduction from 4- to 12-month-old animals in both the direct smooth muscle vasodilator responses to calcitonin gene-related peptide (p less than 0.01) and vasoactive intestinal polypeptide (p less than 0.001), and in the endothelium-mediated response to substance P (p less than 0.005). Vasodilator responses to concentrations of acetylcholine (ACh) greater than 0.1 microM were virtually absent in the 6- and 12-month-old animals. No change in maximal relaxation to noradrenaline was seen with maturation, although there was a small significant increase in potency. The contractile response of the smooth muscle to 30 mM KCl declined steadily as the animals matured, but the maximal contraction to ACh (p less than 0.05), neuropeptide Y (p less than 0.02), and serotonin (p less than 0.05) increased significantly between 4 and 12 months of age. These results indicate that following sexual maturation in the female rabbit, the epicardial coronary artery shows a significant increase in maximum responses to vasoconstrictor neurotransmitter agents and, at the same time, a marked decline in responses to some vasodilator agents, both those acting directly on the smooth muscle and those acting via the endothelium.

Magnesium inhibits the responses to neuropeptide Y in the rabbit coronary artery.

Neuropeptide Y (NPY) has been shown to cause direct vasoconstriction of coronary arteries in many species, including dogs, rabbits and man, which is selectively inhibited by calcium-channel blocking agents. Recently, NPY has also been reported to inhibit the relaxation to noradrenaline in isolated rabbit coronary arteries, but the composition of the Krebs solution described in this study indicated that it contained no magnesium. Since magnesium is known to be a physiological antagonist of calcium and to have a profound influence on the contraction of coronary vascular smooth muscle, we examined the importance of magnesium in modulating both the direct vasoconstrictor response to NPY and the NPY-induced inhibition of relaxation to noradrenaline, using ring preparations of rabbit circumflex coronary artery.

Responses of the rabbit epicardial coronary artery to acetylcholine and adrenoceptor agonists.

STUDY OBJECTIVE: The aim was to identify the role of the endothelium in mediating the responses to acetylcholine in the rabbit coronary artery, and to determine whether alpha or beta adrenergic stimulation may cause relaxation via endothelial receptors in the coronary arteries of this species. DESIGN: Responses to acetylcholine and adrenoceptor agonists were compared in isolated ring preparations with and without endothelium. The adrenoceptor agonists were examined in the presence of phentolamine or propranolol to block alpha and beta adrenoceptors, respectively. EXPERIMENTAL MATERIAL: 30 New Zealand white rabbits (2.3-3.4 kg) were killed by an overdose of barbiturate and exsanguination, and the left epicardial coronary artery was dissected free. Ring preparations were suspended in organ baths under isometric tension and, where required, the tone of the preparations was raised by KC1. MEASUREMENTS AND MAIN RESULTS: Concentrations of acetylcholine up to 10(-6) mol.litre-1 produced dose dependent relaxation of the preparations with endothelium intact, but no relaxation in preparations denuded of endothelium. At higher concentrations, a marked vasoconstrictor response was seen in all preparations regardless of the presence of endothelium. At basal tone, acetylcholine produced vasoconstriction which reached a maximum of 1.0 (SEM 0.14)g tension in preparations with endothelium and 1.74(0.27) g tension in those without endothelium (p less than 0.05). In coronary arteries pretreated with 50 mumol.litre-1 phenoxybenzamine to block alpha adrenoceptors, noradrenaline, isoprenaline, and salbutamol produced dose dependent relaxation of the preparations; this was unaffected by the absence of endothelium. In vessels not pretreated with phenoxybenzamine, propranolol inhibited the relaxation to noradrenaline and isoprenaline but again there was no difference between vessels with and without endothelium. CONCLUSIONS: In the rabbit isolated epicardial coronary artery, acetylcholine produces an endothelium dependent relaxant response over a limited concentration range; a vasoconstrictor response via smooth muscle dominates at higher concentrations. beta Adrenoceptors mediating relaxation are present on the smooth muscle, but there was no evidence for either alpha or beta adrenoceptor mediated responses via the endothelium. Important differences with coronary arteries from other species are discussed.

Neuropeptide Y in non-sympathetic nerves of the rat: changes during maturation but not after guanethidine sympathectomy.

Non-sympathetic neuropeptide Y-containing nerves were demonstrated by their persistence after destruction of sympathetic nerve terminals by acute 6-hydroxydopamine treatment for 48 h. In order to examine whether these neuropeptide Y-containing nerves reinnervate tissues following the loss of sympathetic nerves we administered guanethidine sulphate to one-week-old rat pups for three weeks to produce a complete and long-lasting sympathectomy and we monitored the innervation of the superior cervical ganglion, mesenteric vein, vas deferens and urinary bladder by noradrenaline- and neuropeptide Y-containing nerves two and 16 weeks later (assay and histochemical observations). By two weeks the reduction in neuropeptide Y content of tissues was similar to the reduction after acute sympathectomy with 6-hydroxydopamine treatment, indicating that there was no early reinnervation by non-sympathetic neuropeptide Y-containing nerve fibres at a time when sensory transmitters increase. Furthermore, there was no reinnervation by neuropeptide Y-containing nerve fibres by the time these sympathectomized animals had reached maturity, 16 weeks after cessation of treatment. Neuropeptide Y levels increased in the superior cervical ganglion with normal maturation but decreased in the prostatic end of the vas deferens. A non-sympathetic source of neuropeptide Y demonstrated in the immature rat vas deferens was no longer evident in the mature animal.

Sympathetic and nonsympathetic neuropeptide Y-containing nerves in the rat myocardium and coronary arteries.

We have examined the neuropeptide Y-containing intrinsic nerves of the heart in young (6-week-old) and adult (4-month-old) rats to determine whether they project to the coronary arteries or are capable of doing so if the neuropeptide Y-containing extrinsic nerves are removed. Chronic treatment of neonates with guanethidine was used to permanently destroy the sympathetic nerves. In the young treated animals, 33-54% of the neuropeptide Y remained in the heart despite a 90-99% reduction in norepinephrine; these proportions did not change in the animals that were allowed to develop to adulthood. The level of neuropeptide Y in the right atrium of young animals was unexpectedly high (252 +/- 28.7 pmol/g) compared with adults (75.4 +/- 18.8 pmol/g). The coronary arteries in the control rats received a moderately dense supply of neuropeptide Y-containing nerves; after guanethidine, all neuropeptide Y-containing nerves innervating the large coronary arteries disappeared, but some were still seen in association with small resistance vessels. No compensatory proliferation of the intrinsic neuropeptide Y-containing neurons occurred in the adult sympathectomized animals, and the intrinsic nerves did not reinnervate the large coronary arteries. These results are discussed in relation to the clinical syndrome of coronary artery spasm.