Evaluation of perioperative morbidity associated with single and multiple myomectomy.

The aim of the study was to evaluate the risk of intraoperative and postoperative complications associated with single and multiple myomectomy. The sample was a retrospective cohort study of 206 women undergoing abdominal myomectomy at a teaching hospital in the UK between 1999 and 2003. Means of continuous variables were compared using t-tests with Satterthwaite's correction for unequal variance. It was found that menorrhagia was the presenting symptom in 72% of the women. Estimated blood loss was significantly more in multiple myomectomy compared with single myomectomy. Preoperative use of GnRH analogue and intraoperative tourniquet was used in both groups at the surgeon's discretion. Major complications were rare and three patients needed hysterectomy. There was no significant difference in hospital stay: 5.73 vs 5.98 days. It was concluded that myomectomy is a relatively safe operation with low incidence of serious morbidity. Haemorrhage is the commonest complication and more likely during multiple myomectomy.

Case report: Postpartum pneumomediastinum and subcutaneous emphysema.

Postpartum pneumomediastinum is a rare complication of labour and delivery, where air leaks into the mediastinum following rupture of marginal alveoli. It follows prolonged and forceful Valsalva manoeuvres that increase intra-thoracic pressure. Subcutaneous emphysema may also develop. A chest radiograph can confirm the diagnosis, however a computed tomography thorax maybe required. Treatment is conservative as it is usually self-limiting. We present a case of postpartum pneumomediastinum following a delay in the second stage of labour and subsequent instrumental delivery. She developed chest pain and dyspnea 40 min post-delivery, and subcutaneous emphysema was palpable. Supplementary nasal flow oxygen was administered for 24 h prior to discharge. There is sparse evidence or guidance as to the management of postpartum pneumomediastinum, but consensus appears to be supplemental oxygen for 24 h. More data are needed on the type and duration of oxygen therapy, need for repeat imaging and management of subsequent pregnancies.

The eastern extent of seasonal iron limitation in the high latitude North Atlantic Ocean.

The availability of iron (Fe) can seasonally limit phytoplankton growth in the High Latitude North Atlantic (HLNA), greatly reducing the efficiency of the biological carbon pump. However, the spatial extent of seasonal iron limitation is not yet known. We present autumn nutrient and dissolved Fe measurements, combined with microphytoplankton distribution, of waters overlying the Hebridean (Scottish) shelf break. A distinct biogeochemical divide was observed, with Fe deficient surface waters present beyond the shelf break, much further eastwards than previously recognised. Due to along and on-shelf circulation, the Hebridean shelf represents a much-localised source of Fe, which does not fertilise the wider HLNA. Shelf sediments are generally thought to supply large quantities of Fe to overlying waters. However, for this Fe to influence upper-ocean biogeochemical cycling, efficient off-shelf transport mechanisms are required. This work challenges the view that the oceanic surface waters in close proximity to continental margins are iron replete with respect to marine primary production demands.

Receptor systems affecting force of contraction in the human heart and their alterations in chronic heart failure.

Catecholamines acting through beta 1- and beta 2-adrenergic receptors cause positive inotropic and chronotropic effects in the human heart. However, recent evidence suggests that in the human heart other receptor systems can also affect heart rate and contractility. Positive inotropic effects can be mediated by receptor systems acting through accumulation of intracellular cyclic adenosine monophosphate (cAMP; Gs-protein-coupled receptors such as 5-hydroxytryptamine(5-HT)4-like, histamine H2, and vasoactive intestinal peptide) or by receptor systems acting independently of cAMP, possibly through the phospholipase C/diacylglycerol/inositol-1,4,5-trisphophate pathway (such as alpha 1-adrenergic, angiotensin II, and endothelin). In the nonfailing human heart, activation of all these receptor systems induces only submaximal positive inotropic effects compared with those caused by beta-adrenergic receptor stimulation, indicating that in humans the cardiac beta-adrenergic receptor/Gs-protein/adenylate cyclase pathway is the most powerful mechanism to increase heart rate and contractility. However, the human heart contains only a few spare receptors for beta-adrenergic receptor-mediated positive inotropic effects and nearly all beta-adrenergic receptors are needed to cause maximal inotropic effects. Thus any decrease in the number of beta-adrenergic receptors will automatically lead to a reduction in functional responsiveness of beta-adrenergic receptors. In chronic heart failure the number and responsiveness of cardiac beta-adrenergic receptors are reduced, presumably because of the enhanced sympathetic drive to the heart and hence endogenous down-regulation by an elevated release of (cardiac-derived) norepinephrine, and this loss in cardiac beta-adrenergic receptor function is strongly related to the severity of the disease. However, beta 1- and beta 2-adrenergic receptors are differentially changed in different forms of heart failure. In dilated cardiomyopathy and possibly in aortic valve disease the number of cardiac beta 1-adrenergic receptors is selectively reduced without alteration in the number of beta 2-adrenergic receptors (although beta 2-adrenergic receptors become somewhat uncoupled). In ischemic cardiomyopathy, mitral valve disease, and possibly tetralogy of Fallot, the number of both beta 1- and beta 2-adrenergic receptors is concomitantly decreased. Because of the lack of a substantial receptor reserve, such a decrease in the number of beta-adrenergic receptors is accompanied by reduced inotropic and chronotropic responses to beta-adrenergic receptor stimulation in vitro and in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)

Comparison of the positive inotropic effects of serotonin, histamine, angiotensin II, endothelin and isoprenaline in the isolated human right atrium.

The receptor systems through which serotonin (5-HT), histamine, angiotensin II and endothelin increase the force of contraction were studied in isolated right atria from patients without apparent heart failure. All agonists increased the atrial force of contraction in a concentration-dependent manner; maximal effects, however, were significantly less than those evoked by isoprenaline or Ca2+. 5-HT and histamine, but not angiotensin II and endothelin, activated adenylate cyclase, whereas endothelin and angiotensin II stimulated inositol phosphate generation. Experiments with subtype-selective antagonists revealed that histamine effects were mediated by H2-receptors (sensitive to ranitidine), 5-HT-effects by 5-HT4-receptors (sensitive to SDZ 205-557) and angiotensin II effects by AT1-receptors (sensitive to losartan). We conclude that in human right atria the force of contraction can be increased by cyclic AMP-dependent (histamine, 5-HT) and -independent (angiotensin II, endothelin) pathways. Compared to beta-adrenoceptors, however, all other receptor systems increase the force of contraction only submaximally indicating that the beta-adrenoceptor pathway is the most important physiological mechanism to regulate force of contraction and/or heart rate in the human heart.

Receptor systems in the non-failing human heart.

Catecholamines acting through beta 1- and beta 2-adrenoceptors cause positive inotropic and chronotropic effects in the human heart. In recent years, however, evidence has accumulated that in the human heart also other receptor systems can affect heart rate and/or contractility. Positive inotropic effects can be mediated by receptor systems acting through accumulation of intracellular cAMP (Gs-protein coupled receptors such as 5-HT4-like, histamine H2, and vasoactive intestinal peptide) or by receptor systems acting independent of cAMP possibly through the phospholipase C/diacylglycerol/inositol-1,4,5-trisphosphate pathway (such as alpha 1-adrenergic, angiotensin II, and endothelin). In the non-failing human heart, however, activation of all these receptor systems induces only submaximal positive inotropic effects when compared with those caused by beta-adrenoceptor stimulation, indicating that in humans the cardiac beta-adrenoceptor-Gs-protein-adenylate cyclase pathway is the most powerful mechanism to increase heart rate and contractility. On the other hand, at least three receptor systems acting through inhibition of cAMP formation (Gi-protein coupled receptors) exist in the human heart: muscarinic M2-, adenosine A1-, and somatostatin-receptors. Activation of M2- and A1-receptors causes negative inotropic effects in the non-failing human heart: in atria activation of both receptors causes decreases in basal as well as in isoprenaline-stimulated force of contraction, but in ventricles only isoprenaline-stimulated force of contraction is depressed.

[A thirty-year old bodybuilder with septic shock and ARDS from abuse of anabolic steroids]. / 30-jähriger Bodybuilder mit septischem Schock und ARDS bei Abusus anabolandrogener Steroide.

We report the case of a 30-year-old body builder who developed a gluteal abscess at the site of injection of regularly self-administered anabolic steroids. After breaking the abscess under general anaesthesia, the patient developed septic shock and fulminant adult respiratory distress syndrome (ARDS). In addition to discussing the pathogenesis, differential diagnosis, and treatment, we focus on the immunomodulatory mechanisms of anabolic substances that may have contributed to the course of the disease in this particular patient.