Love and lifestyle: how 'relational healthism' structures couples' talk of engagement with lifestyle advice associated with a new diagnosis of coronary heart disease.

OBJECTIVES: Healthy lifestyle change improves outcomes in coronary heart disease (CHD), but is rarely sustained. To better understand barriers to lifestyle change, we examined couples' talk of engaging with lifestyle advice after one partner receives a diagnosis of CHD. DESIGN: A longitudinal qualitative design, in which a poststructuralist discourse analysis was performed on 35 interviews, conducted with 22 heterosexual British people in a long term relationship. The interviews occurred over three months after one partner was referred to a cardiac rehabilitation programme designed to support lifestyle change. RESULTS: Couples understood their health as a shared practice underpinned by an ideological framework of healthism, creating a form of 'relational healthism'. Practicing relational healthism was not straightforward because the practices of surveillance, control, and discipline related to healthism often contravened relationship norms of support, acceptance and respect for the other's autonomy. Couples struggled to resolve this tension, dynamically adopting, resisting, and occasionally transforming discourses of health and love in ways that worked for and against engagement in lifestyle change. CONCLUSION: In foregrounding the discursive and relational contexts of behavioural change engagement, we show the considerable complexity for couples, including costs related to engagement with lifestyle advice.

Right ventricular remodeling in response to volume overload in fetal sheep.

The fetal myocardium is known to be sensitive to hemodynamic load, responding to systolic overload with cellular hypertrophy, proliferation, and accelerated maturation. However, the fetal cardiac growth response to primary volume overload is unknown. We hypothesized that increased venous return would stimulate fetal cardiomyocyte proliferation and terminal differentiation, particularly in the right ventricle (RV). Vascular catheters and pulmonary artery flow probes were implanted in 16 late-gestation fetal sheep: a right carotid artery-jugular vein (AV) fistula was surgically created in nine fetuses, and sham operations were performed on seven fetuses. Instrumented fetuses were studied for 1 wk before hearts were dissected for component analysis or cardiomyocyte dispersion for cellular measurements. Within 1 day of AV fistula creation, RV output was 20% higher in experimental than sham fetuses ( P < 0.0001). Circulating atrial natriuretic peptide levels were elevated fivefold in fetuses with an AV fistula ( P < 0.002). On the terminal day, RV-to-body weight ratios were 35% higher in the AV fistula group ( P < 0.05). Both left ventricular and RV cardiomyocytes grew longer in fetuses with an AV fistula ( P < 0.02). Cell cycle activity was depressed by >50% [significant in left ventricle ( P < 0.02), but not RV ( P < 0.054)]. Rates of terminal differentiation were unchanged. Based on these studies, we speculate that atrial natriuretic peptide suppressed fetal cardiomyocyte cell cycle activity. Unlike systolic overload, fetal diastolic load appears to drive myocyte enlargement, but not cardiomyocyte proliferation or maturation. These changes could predispose to RV dysfunction later in life. NEW & NOTEWORTHY Adaptation of the fetal heart to changes in cardiac load allows the fetus to maintain adequate blood flow to its systemic and placental circulations, which is necessary for the well-being of the fetus. Addition of arterial-venous fistula flow to existing venous return increased right ventricular stroke volume and output. The fetal heart compensated by cardiomyocyte elongation without accelerated cellular maturation, while cardiomyocyte proliferation decreased. Even transient volume overload in utero alters myocardial structure and cardiomyocyte endowment.

NO and endogenous angiotensin II interact in the generation of renal sympathetic nerve activity in conscious rats.

Nitric oxide (NO) appears to inhibit sympathetic tone in anesthetized rats. However, whether NO tonically inhibits sympathetic outflow, or whether endogenous angiotensin II (ANG II) promotes NO-mediated sympathoinhibition in conscious rats is unknown. To address these questions, we determined the effects of NO synthase (NOS) inhibition on renal sympathetic nerve activity (RSNA) and heart rate (HR) in conscious, unrestrained rats on normal (NS), high-(HS), and low-sodium (LS) diets, in the presence and absence of an ANG II receptor antagonist (AIIRA). When arterial pressure was kept at baseline with intravenous hydralazine, NOS inhibition with l-NAME (10 mg/kg i.v.) resulted in a profound decline in RSNA, to 42 +/- 11% of control (P < 0.01), in NS animals. This effect was not sustained, and RSNA returned to control levels by 45 min postinfusion. l-NAME also caused bradycardia, from 432 +/- 23 to 372 +/- 11 beats/min postinfusion (P < 0.01), an effect, which, in contrast, was sustained 60 min postdrug. The effects of NOS inhibition on RSNA and HR did not differ between NS, HS, and LS rats. However, when LS and HS rats were pretreated with AIIRA, the initial decrease in RSNA after l-NAME infusion was absent in the LS rats, while the response in the HS group was unchanged by AIIRA. These findings indicate that, in contrast to our hypotheses, NOS activity provides a stimulatory input to RSNA in conscious rats, and that in LS animals, but not HS animals, this sympathoexcitatory effect of NO is dependent on the action of endogenous ANG II.

Is osmolality a long-term regulator of renal sympathetic nerve activity in conscious water-deprived rats?

Acute increases in osmolality suppress renal sympathetic nerve activity (RSNA). However, it is not known whether prolonged physiological increases in plasma osmolality chronically inhibit RSNA. To address this hypothesis, mean arterial blood pressure (MAP), heart rate (HR), and RSNA were measured during acute normalization of plasma osmolality in conscious rats made hyperosmotic by 48 h of water deprivation. Water deprivation significantly elevated MAP (120 +/- 1 vs. 114 +/- 3 mmHg, P < 0.05) and plasma osmolality (306 +/- 1 vs. 293 +/- 1 mosmol/kgH2O, P < 0.01). When plasma osmolality was subsequently lowered to normal (-17 +/- 1 mosmol/kgH2O) with a 2-h (0.12 ml/min) infusion of 5% dextrose in water (5DW), MAP decreased (-11 +/- 1 mmHg), and RSNA increased (25 +/- 10% baseline). To assess the role of circulating vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist before infusion of 5DW. The antagonist lowered MAP (-4 +/- 1 mmHg) and raised RSNA (31 +/- 3% baseline) and HR (25 +/- 5 beats/min) in water-deprived rats (all changes P < 0.05). However, V1-vasopressin receptor blockade did not increase RSNA or HR independently of baroreflex responses to decreases in arterial pressure. After V1 blockade, infusion of 5DW lowered blood pressure (-8 +/- 1 mmHg) but did not further affect HR or RSNA. An isotonic saline infusion that produced the same volume expansion as 5DW lowered MAP (-5 +/- 2 mmHg) and HR (-68 +/- 2 beats/min) but had no effect on osmolality or RSNA in water-deprived rats. Finally, 5DW infusion had negligible effects in water-replete animals. In conclusion, these results fail to support the hypothesis that sustained increases in plasma osmolality, either directly or via increased vasopressin, tonically suppress RSNA.