Myocardial actions of prostaglandins in isolated cat cardiac tissue.

The inotropic responses to prostaglandins (PG) A₁, E₁, E₂ and F_2α were studied in isolated cat myocardial tissue. PGA₁ and F_2α exhibited no significant inotropic effects, whereas, PGE₂ and PGE₁ produced negative inotropic effects at concentrations of 2.8 × 10⁻⁷ and 2.8 × 10⁻⁶ M in isolated cat papillary muscles.In isolated perfused cat hearts, PGE₁ (2.8 × 10⁻⁶M) produced a negative inotropic effect along with a significant increase in coronary flow. As flow declined, the negative inotropic effect became more severe. PGE₁ at 2.8 × 10⁻⁹ M produced a sustained increase in coronary flow and oxygen consumption with no inotropic effect. PGE₂ and F_2α did not exert significant changes in coronary flow or contractile force.Thus prostaglandins do not appear to exert significant positive inotropic effects at physiologic or at generally accepted pharmacologic concentrations in isolated cat heart preparations. At extremely high concentrations, prostaglandins E₁ and E₂ exert a negative inotropic effect; however, this would not explain the protective effect of these prostaglandins in circulatory shock.     

Myocardial ischemia-reperfusion damage after pacing-induced tachycardia in patients with cardiac syndrome X

The presence of myocardial ischemia in syndrome X (chest pain, "ischemia-like" electrocardiogram changes, and normal coronary angiograms) is uncertain possibly because, when focally distributed, it may not cause contractile dysfunction or lactate production. We measured lipid hydroperoxides (ROOHs) and conjugated dienes (CDs), two sensitive, independent markers of ischemia-reperfusion oxidative stress, in paired aortic and great cardiac vein blood samples before and after pacing-induced tachycardia in nine patients with syndrome X. Diagnostic ischemic S-T segment changes during pacing were followed by a consistent increase in ROOH and CD levels in the great cardiac vein (from 4.83 +/- 1.18 micromol/l at baseline to 7.88 +/- 1.12 micromol/l and from 0.038 +/- 0.002 to 0.051 +/- 0.003 arbitrary units, respectively, P < 0.01). In controls, ROOH and CD levels did not change after pacing. The large postpacing cardiac release of lipid peroxidation products, consistently observed in all patients and similar to that previously observed after ischemia caused by percutaneous transluminal coronary angioplasty, is consistent with an ischemic origin of syndrome X.     

Maternal morbidity associated with in utero transfer.

OBJECTIVE--To determine the extent of maternal morbidity associated with in utero transfer. DESIGN--Retrospective study of 190 consecutive cases over two years. SETTING--Liverpool Maternity Hospital. PATIENTS--190 Pregnant women were transferred to the hospital under the in utero transfer arrangements from district general hospitals both within and outside the Mersey region. The women admitted were divided into two categories: those in threatened or established uncomplicated preterm labour and those who may or may not have been in threatened or established preterm labour but who had coexisting complicating factors affecting the mother or fetus, or both. INTERVENTIONS--Planned delivery of the fetus if indicated and arrangements for appropriate postpartum care of the mother. MAIN OUTCOME MEASURE--Assessment of the progress of labour and, if appropriate, resuscitation of the mother. RESULTS--Women who were transferred with no coexisting disease (124) had relatively uncomplicated deliveries whereas those transferred with coexisting diseases (66) exhibited considerable morbidity and 17 of these required prolonged intensive monitoring after delivery. CONCLUSIONS--In utero transfer in healthy mothers may have benefits for babies born very prematurely. If mothers have coexisting disease, however, the desirability of transfer should be reviewed urgently in the light of the considerable maternal morbidity associated with these problems. In these cases transfer may introduce an additional hazard.     

Perinatal mortality and morbidity associated with eclampsia.

Out of all the women who were delivered in Cardiff maternity units during 1965-74, 43 developed eclampsia, an incidence of 72/100 000 deliveries. The incidence in residents of Cardiff was 53/100 000 deliveries. None of the mothers with eclampsia died, but 10 of the 47 babies were lost, all but one having been born to women with antepartum eclampsia. The perinatal deaths were mainly associated with chronic placental insufficiency and preterm delivery. The extent to which the wide range of complex drug regimens used influenced perinatal outcome is not clear, although polypharmacy should be avoided. Because eclampsia is rare we advocate that its management should be planned and rehearsed and that a simple, standardised treatment regimen should be used. Failing placental function may be detected by monitoring fetal growth by ultrasound.     

Myocardial gene reprogramming associated with a cardiac cross-resistant state induced by LPS preconditioning

Lipopolysaccharide (LPS) preconditioning induces cardiacresistance to subsequent LPS or ischemia. This study tested thehypothesis that resistance to LPS and resistance to ischemiaare two manifestations of cardiac cross-resistance which may involvereprogramming of cardiac gene expression. Rats were preconditioned witha single dose of LPS (0.5 mg/kg ip). Cardiac resistance to LPS wasexamined with a subsequent LPS challenge. Cardiac resistance toischemia was determined by subjecting hearts toischemia-reperfusion. Total RNA was extracted from myocardiumfor Northern analysis of mRNAs encoding protooncoproteins, antioxidantenzymes, and contractile protein isoforms. Rats preconditioned with LPS1-7 days earlier acquired cardiac resistance to endotoxemicdepression. This resistance temporally correlated with resistance toischemia. Pretreatment with cycloheximide (0.5 mg/kg ip)abolished resistance to both LPS and ischemia. LPSpreconditioning induced the expression of c-jun andc-fos mRNAs. LPS also transientlyincreased mRNAs encoding catalase and Mn-containing superoxidedismutase. The expression of both - and -myosin heavy chain mRNAswas upregulated, whereas the expression of cardiac -actin mRNA wassuppressed. We conclude that 1)LPS induces sustained cardiac resistance to both LPS and ischemia, 2) resistance toischemia and resistance to LPS seem to be two mechanisticallyindistinct components of cardiac cross-resistance, and3) the cardiac cross-resistance isassociated with reprogramming of myocardial gene expression.

     

Mapping practice population and morbidity with a computer.

A method of dividing a map of the practice area into a grid based on postcode locations is described. The distribution of the practice population may thus be shown graphically and trends observed. The geographical incidence and prevalence of morbidity may also be charted and variations of statistical significance determined. This is a practical tool that will have greater potential as information technology in general practice develops.     

Myocardial lipid metabolism in cardiac hyper- and hypo-function. Studies on triiodothyronine-treated and transplanted rat hearts.

Lipid composition of the myocardium and in vitro lipid metabolism were studied in hearts from young rats after 30 days of treatment with triiodothyronine (100 microgram/kg per day) and in heterotopically isotransplanted hearts of inbred adult rats 6 days after surgery. The former served as an experimental model of cardiac hyperfunction, while the latter, empty beating hearts, served as a model of cardiac hypofunction. In hearts from hyperthyroid animals the concentration of phosphatidylcholine, phosphatidylethanolamine, cardiolipin, and the incorporation of 14C-labelled palmitic and erucic acid into these phospholipids were increased significantly as compared with controls. In contrast, the triglyceride concentration and the incorporation of palmitate into triglyceride was significantly decreased. In transplanted hearts, the phospholipid concentration and the incorporation of 14C-labelled fatty acids into phospholipids were significantly decreased as compared with the hearts of the inbred host rats of the same age. The results indicate that the mechanical performance of the heart affects the phospholipid composition, which may be a reflection of increased or decreased proliferation of subcellular membranes in sustained cardiac hyper- or hypo-function.     

Psychiatric morbidity among spouses of patients with stroke.

The medium term psychiatric morbidity of spouses of patients with stroke was evaluated one to three years after the event. Compared with a control group the spouses were more likely to be depressed (p less than 0.005) and had more physical symptoms (p less than 0.01). Depression increased with the severity of the stroke in the spouse (p less than 0.05) and with time during the three years. Regular contact with friends and neighbours protected spouses (p less than 0.005). Depressed spouses were more likely to be taking tranquillisers than non-depressed spouses (p less than 0.0001) but no more likely to be taking antidepressants. Social rehabilitation after stroke was less successful when the spouse was depressed. Proper attention paid to spouses of patients with stroke might improve the prospects of these patients.