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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cardiopulmonary effects of different levels of carbon dioxide insufflation (3, 5 and 2 mm Hg) under two-lung ventilation were studied in six sevoflurane (1.5 minimum alveolar concentration; MAC) anaesthetized dogs during left-sided thoracoscopy. An arterial catheter, Swan-Ganz catheter and multianaesthetic gas analyser were used to monitor the cardiopulmonary parameters during the experiment. Baseline data were obtained before intrathoracic pressure elevation and the measurements were repeated at intervals after left lung collapse induced by insufflation with carbon dioxide gas. The intrapleural pressure levels used were 3, 5 and 2 mm Hg. Arterial blood pressures, cardiac index, stroke index, left and right ventricular stroke work index, arterial haemoglobin saturation, arterial oxygen tension and systemic vascular resistance decreased significantly during hemithorax insufflation, whereas heart rate, right atrial pressure, mean, systolic and diastolic pulmonary arterial pressure, pulmonary capillary wedge pressure, pulmonary vascular resistance and arterial carbon dioxide tension significantly increased during intrapleural pressure elevation. Although carbon dioxide insufflation into the left hemithorax with an intrapleural pressure of 2-5 mm Hg compromises cardiac functioning in 1.5 MAC sevoflurane anaesthetized dogs, it can be an efficacious adjunct for thoracoscopic procedures. Intrathoracic view was satisfactory with an intrapleural pressure of 2 mm Hg. Therefore, the intrathoracic pressure rise during thoracoscopy with two-lung ventilation should be kept as low as possible. Additional insufflation periods should be avoided, since a more rapid and more severe cardiopulmonary depression can occur.
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PMID:The effects of intrathoracic pressure during continuous two-lung ventilation for thoracoscopy on the cardiorespiratory parameters in sevoflurane anaesthetized dogs. 1201 50

Obstructive sleep apnoea is a disease of increasing importance because of its neurocognitive and cardiovascular sequelae. Abnormalities in the anatomy of the pharynx, the physiology of the upper airway muscle dilator, and the stability of ventilatory control are important causes of repetitive pharyngeal collapse during sleep. Obstructive sleep apnoea can be diagnosed on the basis of characteristic history (snoring, daytime sleepiness) and physical examination (increased neck circumference), but overnight polysomnography is needed to confirm presence of the disorder. Repetitive pharyngeal collapse causes recurrent arousals from sleep, leading to sleepiness and increased risk of motor vehicle and occupational accidents. The surges in hypoxaemia, hypercapnia, and catecholamine associated with this disorder have now been implicated in development of hypertension, but the association between obstructive sleep apnoea and myocardial infarction, stroke, and congestive heart failure is not proven. Continuous positive airway pressure, the treatment of choice for obstructive sleep apnoea, reduces sleepiness and improves hypertension.
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PMID:Obstructive sleep apnoea. 1250 19

The Bible contains several interesting contributions to the history of neurology, as is the case of the High Priest Alkimos, who died suddenly in 159 BC. He was regarded as a stereotypical stroke victim for a long time. The reports on his death in the Septauginta and the later 'Jewish Antiquities' of Flavius Josephus present some typical symptoms of stroke (collapse, loss of speech and death within a short time), but they also describe severe pains, which are very unusual among patients with stroke. Similar symptoms can be found in the case of the Roman emperor Claudius, who was poisoned by his spouse Agrippina. It was thought that she used aconitine, an ingredient of the monkshood plant (Aconitum napellus L.), which imitates an apoplectic insult, but also causes vehement pains. It was therefore possible that something similar had happened to Alkimos, as aconitine was a common poison in ancient times and the surroundings of his death may confirm the suspicion. Reigning during a time of great upheaval, Alkimos was able to maintain his high office chiefly because of the help of the Seleucides. He has just begun construction work on the temple of Jerusalem, an order, which was regarded as a sacrilege by his foes. This impression was enhanced by his subsequent illness which could be considered as a divine punishment.
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PMID:Toxicology in the Old Testament. Did the High Priest Alcimus die of acute aconitine poisoning? 1229 23

For patients with acute respiratory distress syndrome (ARDS) the most important objective of mechanical ventilation is opening and keeping open the alveoli to achieve adequate oxygenation, without further damaging the lungs or negatively affecting the circulation. Alveolar recruitment is achieved by making use of positive end-expiratory pressure (PEEP). The best PEEP level is that with which the largest improvement in oxygen transport and lung compliance is achieved, without a decrease in the stroke volume of the left ventricle. In addition to the usual volume-controlled ventilation with PEEP, pressure-limited ventilation is also possible. In this a preselected pressure is never exceeded, whereas a maximum inspiratory airflow at the start of inspiration provides more opportunity for gaseous exchange. The oxygenation can possibly be further improved by increasing the inspiration-expiration ratio. As a result of the reduced expiratory period the alveoli which tend to collapse at the end of a normal expiration are kept open. Mechanical ventilation with a lower tidal volume decreases mortality. Ventilation in a prone position increases the end-expiratory lung volume and reduces the intrapulmonary shunt and the regional differences in the degree of ventilation. These factors possibly contribute to preventing ventilation-induced lung damage. Administration of natural surfactant during the ventilation of patients with ARDS seems to be a highly promising strategy; the clinical effectiveness still needs to be demonstrated.
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PMID:[Mechanical ventilation in acute respiratory distress syndrome (ARDS): lung protecting strategies for improved alveolar recruitment]. 1275 82

In an attempt to minimize late airway stenosis, a new tube with an oval cross-section has been developed. Two to three tracheal cartilage arches are usually incised anteriorly, partially excised or inadvertently broken to fit a tracheostomy tube. The risk of post-tracheostomy stenosis seems to be greater when several cartilages have been involved. If an oval tube with the shortest diameter in its symmetry plane is used, the tissue defect along the longitudinal axis of the trachea will be shorter than that caused by a round tube. When such a stoma is healing, the adjacent intact tracheal cartilages, which are located fairly close to each other, will support the bridging scar tissue, thereby preventing collapse of the tracheal wall. The tubes come in three lengths to fit most neck sizes. An oval trial tube with the same length as the shortest one has been used for cricothyroidostomy--the aim being to spread the cricoid and thyroid cartilages apart as little as possible. A series of 23 patients were treated with this tube. At follow-up, no stenosis was found at flexible fiberoptic laryngo-tracheoscopy. Fifteen patients reported no voice change, and five, who were singers, experienced lower pitch, but four of them were still singing. None of these five patients had speech problems. The other three patients had voice problems when speaking. One of these had chronic bronchitis and another had had a stroke. The third one had a rough voice. The voice problems were milder than those reported from previous series.
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PMID:New design of a tracheostomy-cricothyroidostomy tube. 1270 11

Poly(ADP-ribose) polymerase-1 (PARP-1) is an abundant nuclear enzyme that is activated primarily by DNA damage. Upon activation, the enzyme hydrolyzes NAD(+) to nicotinamide and transfers ADP ribose units to a variety of nuclear proteins, including histones and PARP-1 itself. This process is important in facilitating DNA repair. However, excessive activation of PARP-1 can lead to significant decrements in NAD(+), and ATP depletion, and cell death (suicide hypothesis). In response to cellular damage by oxygen radicals or excitotoxicity, a rapid and strong activation of PARP-1 occurs in neurons. Excessive PARP-1 activation is implicated in a variety of insults, including cerebral and cardiac ischemia, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinsonism, traumatic spinal cord injury, and streptozotocin-induced diabetes. The use of PARP inhibitors has, therefore, been proposed as a protective therapy in decreasing excitotoxic neuronal cell death, as well as ischemic and other tissue damage. Excitotoxic brain lesions initially result in the primary destruction of brain parenchyma and subsequently in secondary damage of neighboring neurons hours after the insult. This secondary damage of initially surviving neurons accounts for most of the volume of the infarcted area and the loss of brain function after a stroke. One major component of secondary neuronal damage is the migration of macrophages and microglial cells toward the sites of injury, where they produce large quantities of toxic cytokines and oxygen radicals. Recent evidence indicates that this microglial migration is strongly controlled in living brain tissue by expression of the integrin CD11a, which is regulated in turn by PARP-1, proposing that PARP-1 downregulation may, therefore, be a promising strategy in protecting neurons from this secondary damage, as well. Studies demonstrating an important role for PARP-1 in the regulation of gene transcription have further increased the intricacy of poly(ADP-ribosyl)ation in the control of cell homeostasis and challenge the notion that energy collapse is the sole mechanism by which poly(ADP-ribose) formation contributes to cell death. The hypothesis that PARPs might regulate cell fate as essential modulators of death and survival transcriptional programs is discussed with relation to nuclear factor kappaB and p53.
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PMID:Poly(ADP-Ribose) polymerase-1 in acute neuronal death and inflammation: a strategy for neuroprotection. 1285 16

Poly(ADP-ribose) polymerase 1 (PARP-1) protects the genome by functioning in the DNA damage surveillance network. In response to stresses that are toxic to the genome, PARP-1 activity increases substantially, an event that appears crucial for maintaining genomic integrity. Massive PARP-1 activation, however, can deplete the cell of NAD(+) and ATP, ultimately leading to energy failure and cell death. The discovery that cell death may be suppressed by PARP inhibitors or by deletion of the parp-1 gene has prompted a great deal of interest in the process of poly(ADP-ribosyl)ation. Suppression of PARP-1 is capable of protecting against cerebral and cardiac ischemia, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced parkinsonism, traumatic spinal cord injury, and streptozotocin-induced diabetes. The secondary damage of initially surviving neurons in brain stroke accounts for most of the volume of the infarcted area and the subsequent loss of brain function. Microglial migration is strongly controlled in living brain tissue by expression of the integrin CD11a, which is regulated in turn by PARP-1, proposing that PARP-1 downregulation may therefore be a promising strategy in protecting neurons from this secondary damage, as well. As PARP-1 is now recognised as playing a role also in the regulation of gene transcription, this further increases the intricacy of poly(ADP-ribosyl)ation in the control of cell homeostasis and challenges the notion that energy collapse is the sole mechanism by which poly(ADP-ribose) formation contributes to cell death. PARP(s) might regulate cell fate as essential modulators of death and survival transcriptional programs with relation to NF-kappaB and p53, proposing that inhibitors of poly(ADP-ribosyl)ation could therefore prevent the deleterious consequences of neuroinflammation by reducing NF-kappaB activity.
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PMID:Poly(ADP-ribosyl)ation enzyme-1 as a target for neuroprotection in acute central nervous system injury. 1452 60

Obstructive sleep apnea is an increasingly well-recognized disease characterized by periodic collapse of the upper airway during sleep. This leads to either complete or partial obstruction of the airway, resulting in apneas, hypopneas, or both. This disorder causes daytime somnolence, neurocognitive defects, and depression. It affects almost every system in the body, resulting in an increased incidence of hypertension, cardiovascular disease, stroke, pulmonary hypertension, cardiac arrhythmias, and altered immune function. It also increases the risk of having an accident, presumably as a result of associated somnolence. The gold standard for the diagnosis of sleep apnea is an overnight polysomnogram. Split-night studies are becoming increasingly common and allow for quicker implementation of therapy at a reduced cost. Treatment options for sleep apnea include weight loss, positional therapy, oral devices, continuous positive airway pressure (CPAP), and upper airway surgery. CPAP is the most efficacious and widely used therapy. Its complications include nasal congestion or dryness, mask discomfort, and claustrophobia. Heated humidifiers, newer types of masks, and nasal steroids have improved tolerance of this therapy. Bilevel positive-pressure therapy can be considered for patients who find it difficult to exhale against the consistently increased pressure of CPAP. The disease requires aggressive treatment to improve quality of life and prevent its complications.
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PMID:Obstructive sleep apnea. 1456 40

We previously showed that beta2-microglobulin knockout mice treated with anti-asialoGM1 (beta2M/alphaAsGM1 mice) exhibit less hypothermia, reduced production of proinflammatory cytokines, less metabolic acidosis, and improved survival after cecal ligation and puncture (CLP) compared with wild-type mice. The present study was designed to assess hemodynamics and left ventricular contractility at 18 h after CLP. Arterial pressure was measured by carotid artery cannulation, and left ventricular pressure-volume loops were obtained by insertion of a 1.4-F conductance catheter into the left ventricle. Heart rate, stroke volume, and cardiac output were not significantly different between wild-type and beta2M/alphaAsGM1 mice after CLP. However, beta2M/alphaAsGM1 mice exhibited improved mean arterial pressure and systemic vascular resistance compared with wild-type mice. Myocardial function was also better preserved in beta2M/alphaAsGM1 mice as indicated by improved left ventricular pressure development over time, time-varying maximum elastance, endsystolic pressure-volume relationship, and preload recruitable stroke work. Overall, this study shows that cardiovascular collapse characterized by hypotension, myocardial depression, and low systemic vascular resistance occurs after CLP in wild-type mice. However, beta2M/alphaAsGM1 mice exhibit improved hemodynamics and cardiac contractile function after CLP that may account, in part, for our previously observed survival benefit.
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PMID:Beta2-microglobulin knockout mice treated with anti-asialoGM1 exhibit improved hemodynamics and cardiac contractile function during acute intra-abdominal sepsis. 1463 Jun 24

This prospective cohort study evaluated the impact of the time-related elements of the "chain of survival" on the quality of life of patients, taking their characteristics into account. Between 1995 and 2002, consecutive, out-of-hospital cardiac arrest patients from Amsterdam and the surrounding areas were included in this study. A total of 227 patients (12%) survived to hospital discharge and 174 were definitive survivors who were available for assessment at 6 months. Quality of life was measured with the 136-item Sickness Impact Profile (SIP); cognitive functioning was assessed through the Mini Mental State Examination. SIP profiles were compared with profiles of an open Dutch population of the elderly and patients who experienced a stroke. Time intervals of the chain of survival were calculated from the estimated moment of collapse and related to outcome using regression analysis. The SIP profile of survivors was a little above the reference profile, indicating a slightly poorer quality of life, and below the profile of patients after stroke, indicating a better quality of life. Impaired cognitive function was associated with delay in the start of cardiopulmonary resuscitation (odds ratio 4.3, 95% confidence interval 1.0 to 19). Absence of the need for advanced cardiopulmonary life support was associated with better cognitive functioning (odds ratio 0.3, 95% confidence interval 0.1 to 0.9). Female gender and older age were associated with impaired physical functioning. Trends were found for better outcomes after early access, immediate resuscitation, early defibrillation, and early advanced care.
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PMID:Assessment of quality of life and cognitive function after out-of-hospital cardiac arrest with successful resuscitation. 1471 35


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