Do pulmonary artery catheters cause or increase tricuspid or pulmonic valvular regurgitation?

There are few quantitative data on the extent or mechanism of pulmonary artery catheter (PAC)-induced valvular dysfunction. We hypothesized that PACs cause or worsen tricuspid and pulmonic valvular regurgitation, and tested this hypothesis by using transesophageal echocardiography. In 54 anesthetized adult patients, we measured color Doppler jet areas of tricuspid regurgitation (TR) in two planes (midesophageal [ME] 4-chamber and right ventricular inflow-outflow views) and pulmonic insufficiency (PI) in one plane (ME aortic valve long-axis view), both before and after we advanced a PAC into the pulmonary artery. Regurgitant jet areas and hemodynamic measurements were compared by using paired t-test. There were no significant changes in blood pressure or heart rate after passage of the PAC. After PAC placement, the mean PI jet area was not significantly increased. The mean TR jet area increased significantly in the right ventricular inflow-outflow view (+0.37 +/- 0.11 cm(2)) (P = 0.0014), but did not increase at the ME 4-chamber view. Seventeen percent of patients had an increase in TR jet area > or =1 cm(2); 8% of patients had an increase in PI jet area >/=1 cm(2). IMPLICATIONS: In patients without pulmonic or tricuspid valvular pathology, placement of a pulmonary artery catheter (PAC) worsened tricuspid regurgitation, which is consistently visualized in the right ventricular inflow-outflow view, and often not seen in the midesophageal 4-chamber view. This is consistent with malcoaptation of the anterior and posterior leaflets. PAC-induced pulmonic insufficiency was rarely detected in the midesophageal aortic valve long-axis view. We conclude that a PAC is very unlikely to be the sole cause of severe tricuspid regurgitation or pulmonic insufficiency.     

Effects of protein kinase C activators on phorbol ester-sensitive and - resistant EL4 thymoma cells

Phorbol ester-sensitive EL4 murine thymoma cells respond to phorbol 12- myristate 13-acetate with activation of ERK mitogen-activated protein kinases, synthesis of interleukin-2, and death, whereas phorbol ester- resistant variants of this cell line do not exhibit these responses. Additional aspects of the resistant phenotype were examined, using a newly-established resistant cell line. Phorbol ester induced morphological changes, ERK activation, calcium-dependent activation of the c-Jun N-terminal kinase (JNK), interleukin-2 synthesis, and growth inhibition in sensitive but not resistant cells. A series of protein kinase C activators caused membrane translocation of protein kinase C's (PKCs) alpha, eta, and theta in both cell lines. While PKC eta was expressed at higher levels in sensitive than in resistant cells, overexpression of PKC eta did not restore phorbol ester-induced ERK activation to resistant cells. In sensitive cells, PKC activators had similar effects on cell viability and ERK activation, but differed in their abilities to induce JNK activation and interleukin-2 synthesis. PD 098059, an inhibitor of the mitogen activated protein (MAP)/ERK kinase kinase MEK, partially inhibited ERK activation and completely blocked phorbol ester-induced cell death in sensitive cells. Thus MEK and/or ERK activation, but not JNK activation or interleukin-2 synthesis, appears to be required for phorbol ester-induced toxicity. Alterations in phorbol ester response pathways, rather than altered expression of PKC isoforms, appear to confer phorbol ester resistance to EL4 cells.      

Perinatal stimulation and adaptation of the neonate

The present report describes psychobiological studies of behavior around the time of birth. An adaptive, ecological perspective is presented in which stimulation of the fetus and newborn is purported to instigate adaptive postpartum behavior. Studies describing the perinatal sensory environment are reviewed, with a consideration of emergent sensory function of the fetus. It is asserted that afferent input associated with parturition perturbs the fetus and neonate, producing a general arousal state that facilitates breathing, suckling, and early learning. The view developed herein is that perinatal sensory input induces and canalizes the newborn's behavior, thereby regulating adaptive postpartum function. Deviations in afferent input may alter ontogenetic trajectories and compromise developmental outcome by reducing availability of conditions necessary for adequate postpartum adaptation.     

In utero diagnosis of a vein of Galen aneurysm by ultrasound

Summary A large midline supratentorial cystic lesion with associated cardiomegaly was seen in utero by ultrasound during the 34th week of pregnancy. The provisional diagnosis of a vein of Galen aneurysm was confirmed with CT and angiography after birth.     

Differential onset of median nerve block: randomized, double-blind comparison of mepivacaine and bupivacaine in healthy volunteers

We have compared the delay in onset of 1% mepivacaine and 0.33% bupivacaine in different nerve fibre types in 10 volunteers undergoing median nerve blocks, in a randomized, double-blind, crossover study. Hot, cold, pinprick and light touch sensations, compound motor action potentials (CMAP), sensory nerve action potentials (SNAP) and skin temperature were recorded at 2-min intervals. Hot, cold, pinprick, light touch sensations, SNAP and CMAP were significantly inhibited, and skin temperature was significantly increased after administration of both agents. The first noticeable reduction in cold sensation was detected later after bupivacaine compared with mepivacaine, but after a delay similar to that of other nerve functions. Bupivacaine and mepivacaine inhibited SNAP and CMAP with a similar time delay to steady- state. Bupivacaine produced steady-state inhibition of hot and cold sensations significantly later than mepivacaine; nevertheless, the sequence that sensory modalities failed, with few exceptions, and the extent of anaesthesia at 40 min were similar for both agents. Our technique provides a novel, multi-modal method of comparing local anaesthetics and related agents over time.      

Establishing good practices in continuing care: a descriptive study of community nursing services for people with HIV infection

This paper presents findings from a 2-year study of community nursing services for people affected by HIV infection in six health authorities in England The research, commissioned by the Department of Health, England, aimed to identify the main bridges and barriers to effective home nursing care, focusing on discharge co-ordination, district nursing and multi-agency collaboration Using a triangulated, case study approach, the main methods of data collection included non-participant observation, case note analysis, semi-structured staff interviews, a postal questionnaire of district nurses and a series of focus groups with service users Study sites included three cities and surrounding districts in the north west, north and south east of England Findings suggest there is considerable room for improvement in discharge planning and that good practice is not the preserve of specialist units District nurses are shown to be willing providers of the majority of home nursing care to this client group, but there is a need for more focused training, greater use of care co-ordinators and more emotional and managerial support     

Amino acid changes in thiamine-deficient encephalopathy: some implications for the pathogenesis of Friedreich's ataxia.

Thiamine-deficient encephalopathy in the rat is characterized by ataxic gait, loss of righting reflex and curvature of the spine. Neurochemical changes include a diminished activity of cerebral pyruvate decarboxylase leading to abnormal pyruvate oxidation. The present study shows that this defective pyruvate oxidation produces a significant depletion of three important amino acid neurotransmitters, namely gamma aminobutyric acid (GABA), glutamic acid, and aspartic acid. Such changes could lead to severe neuronal dysfunction and the observed neurological symptoms of thiamine deficiency. Some implications for the pathogenesis of Friedreich's ataxia are discussed.