ABSTRACT
Alpha(2) agonist-induced pulmonary oedema in sheep might be related to alterations in pulmonary haemodynamics and/or activation of inflammatory processes. In seven sevoflurane-anaesthetized sheep pulmonary haemodynamics, arterial oxygen tensions, nitric oxide and prostaglandin E(2) concentrations were determined before and after intravenous dexmedetomidine (2microg kg(-1)). In a second trial, lung tissue was sampled for histopathology and quantitative real-time PCR for IL-1beta and iNOS mRNA in a control sheep and 2, 10 and 30min after dexmedetomidine. Computer tomography of the lung under sevoflurane anaesthesia before and after dexmedetomidine was performed. Two minutes after dexmedetomidine mean pulmonary artery pressure, pulmonary arterial occlusion pressure and estimated capillary pressurewere significantly increased to 34.5mmHg, 22.2mmHg and 27.1mmHg, respectively. On computer tomography, lung density increased immediately after dexmedetomidine, with maximal density occurring between 9 and 12min. Histopathology was consistent with vascular congestion followed by protein and erythrocyte extravasation into alveoli. Increased iNOS mRNA levels were detected in sevoflurane anaesthetized animals only. An IL-1beta signal occurred after morphological changes had occurred in lung tissue. These findings support hydrostatic stress as the underlying cause of alpha(2) agonist-induced pulmonary oedema in sheep.
Subject(s)
Adrenergic alpha-Agonists/adverse effects , Analgesics, Non-Narcotic/adverse effects , Dexmedetomidine/adverse effects , Pulmonary Edema/veterinary , Sheep Diseases/chemically induced , Animals , Blood Pressure/drug effects , Dinoprostone , Inflammation/chemically induced , Inflammation/veterinary , Lung/pathology , Nitric Oxide , Oxygen/blood , Polymerase Chain Reaction , Pulmonary Edema/chemically induced , Sheep , Vasoconstriction/drug effectsSubject(s)
Adrenergic alpha-Agonists/pharmacokinetics , Anesthesia, Inhalation , Anesthetics, Inhalation , Medetomidine/pharmacokinetics , Methyl Ethers , Adrenergic alpha-Agonists/metabolism , Animals , Area Under Curve , Biotransformation , Goats , Half-Life , Medetomidine/metabolism , Sevoflurane , Sheep , Stereoisomerism , Tissue DistributionABSTRACT
The human apolipoprotein E4 (ApoE4) isoform is associated with genetic risk for Alzheimer's disease. To assess the effects of different ApoE isoforms on amyloid plaque formation, human ApoE3 and ApoE4 were expressed in the brains of transgenic mice under the control of the human transferrin promoter. Mice were crossed with transgenic mice expressing human amyloid precursor protein containing the Swedish mutation (APPsw), which facilitates amyloid beta peptide (A beta) production. The following progeny were selected for characterization: APPsw+/- x ApoE3+/- and APPsw+/-, APPsw+/- x ApoE4+/- and APPsw+/- littermates. All mice analyzed were wild type for the endogenous mouse APP and ApoE genes. Mice expressing ApoE4 in combination with APPsw have accelerated A beta deposition in the brain as assessed by enzyme immunoassay for A beta40 and A beta42 extractable in 70% formic acid, by assessment of amyloid plaque formation using thioflavin-S staining, and by immunohistochemical staining with antibodies specific for A beta40 or A beta42 and the 4G8 monoclonal or 162 polyclonal antibody. No difference in the rate of A beta deposition in the brain was seen in mice expressing ApoE3 in combination with APPsw. Thus, our data are consistent with the observation in Alzheimer's disease that ApoE4 is associated with increased accumulation of A beta in the brain relative to ApoE3.
Subject(s)
Amyloid beta-Peptides/metabolism , Apolipoproteins E/genetics , Brain Chemistry/genetics , Peptide Fragments/metabolism , Age Factors , Amyloid beta-Peptides/analysis , Amyloid beta-Peptides/immunology , Amyloid beta-Protein Precursor/genetics , Amyloid beta-Protein Precursor/metabolism , Animals , Antibodies, Monoclonal , Apolipoprotein E4 , Brain/metabolism , Brain/pathology , Gene Expression , Humans , Immunoenzyme Techniques , Low Density Lipoprotein Receptor-Related Protein-1 , Mice , Mice, Inbred C57BL , Mice, Transgenic , Mutation , Peptide Fragments/analysis , Peptide Fragments/immunology , Plaque, Amyloid/chemistry , Plaque, Amyloid/metabolism , Plaque, Amyloid/pathology , Receptors, Immunologic/metabolismABSTRACT
Finding creative solutions to the critical shortage of available organs for transplantation continues to challenge those organizations and health care professionals who are intimately involved in donation procedures. This article describes Making the Critical Difference, an 8-hour continuing education program developed by the National Kidney Foundation and the American Association of Critical-Care Nurses. The program represents a model for identifying and addressing the barriers, attitudes, and needs of nurses as they participate in the donation process.
Subject(s)
Education, Nursing, Continuing/organization & administration , Nursing Staff/education , Tissue and Organ Procurement/methods , Health Knowledge, Attitudes, Practice , Humans , Models, Educational , Nursing Staff/psychology , Program EvaluationABSTRACT
The Making the Critical Difference continuing education program offers the critical care nurse a unique opportunity to assume the nurse moderator role. This article guides the nurse in the preparation for this role by providing detailed explanations and practical advice.
Subject(s)
Critical Care , Education, Nursing, Continuing/organization & administration , Nursing Staff , Role , Tissue and Organ Procurement/methods , Group Processes , Humans , Nursing Staff/education , Nursing Staff/psychologySubject(s)
Critical Care , Ethics, Medical , Ethics, Nursing , Humans , Societies, Medical , Societies, NursingSubject(s)
Intensive Care Units , Nursing Staff, Hospital/psychology , Adult , Attitude of Health Personnel , Female , HumansABSTRACT
The technique has exciting potential for elderly hemiplegic patients, even those who are confined to a nursing home. There are limiting factors, of course; the method is time-consuming and the initial outlay for equipment is high. But the rewards can be well worth the time, effort, and cost involved. The recovery potential of some geriatric patients after a cerebrovascular accident may seem bleak because of multiple disabilities, e.g., paralysis, delayed reflexes, aphasia. Fortunately, these disorders do not necessarily decree failure of biofeedback training. Neither does advanced age. The strongest component in success is motivation. A case in point is the 82 year old woman described here who had been hemiparetic for seven years. With biofeedback training, she gained--and maintained--muscle strength.
