In this study, two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular changes before and
after IV atropine in 31 infants and small children during halothane (n = 15) or isoflurane (n = 16) anaesthesia. Prior to
induction of anaesthesia heart rate (HR), mean blood pressure (MBP), and two0dimensional echocardiographic dimensions of the
left ventricle and pulmonary artery bloodflow velocity were measured by pulsed Doppler echocardiography. Cardiovascular measurements
were repeated while anaesthesia was maintained at 1.5 MAC halothane (n = 15) or isoflurane (n = 16). Atropine 0.02 mg·kg−1 IV was then administered and two minutes later, a third set of cardiovascular data was obtained. Heart rate decreased during
halothane anaesthesia but did not change significantly during isoflurane anaesthesia. Mean blood pressure, cardiac output
(CO) and stroke volume (SV) decreased similarly during 1.5 MAC halothane or isoflurane anaesthesia. Ejection fraction (EF)
decreased and left ventricular end-diastolic volume (LVEDV) increased significantly in bothgroups, but decreases in EF (32
± 5 percentvs18 ± 5 per cent) and increases in LVEDV (18 ± 7 per cent vs7 ± 5 per cent) were significantly greater during
halothane than during isoflurane anaesthesia. Following atropine, HR increased more in the patients maintained with halothane
(31 ± 6 per cent), than during isoflurane anaesthesia (18 ± 5 per cent). Atropine increased CO in both groups of patients,
but SV and EF remained unchanged. When compared with awake values, HR increased similarly and significantly (18 ± 4 per cent)
following atropine in both groups, and CO returned to control levels. Halothane decreased EF and increased LVEDV more than
isoflurane at 1.5 MAC end— expired anaesthetic levels. Atropine did not diminish the myocardial depression produced by halothane
or isoflurane. The increase in CO following atropine during halothane and isoflurane anaesthesia in infants and small children
is the result of increases in HR alone.
Nous avons utilisé un appareil à échocardiographie bi-dimensionnelle couplé à un Doppler pulsé chez des bébés et de jeunes
enfants pour évaluer l’impact hémodynamique de l’halothane (n = 15) et de l’isoflurane (n = 16) et la modification possible
de ces effets par l’atropine. Nous avons mesure la frequence cardiaque (FC), la pression artérielle moyenne (PAM), la dimension
de la cavité ventriculaire gauche (par écho bi-dimensionnelle) et la vélocité du flot sanguin pulmonaire (par Doppler) et
ce, en trois occasions soit avant l’induction, après l’instauration de 1.5 MAC d’halothane ou d’isoflurane et finalement,
deux minutes après l’injection IV de 0.02 mg·kg−1 d’atropine. On ne nota une baisse de la frequence cardiaque qu’avec l’halothane tandis que la PAM, le débit cardiaque (DC)
et le volume d’éjection (VE) diminuaient autant avec l’un ou l’autre anesthésique. La diminution de la fraction d’éjection
(FE) et l’augmentation du volume télédiastolique du ventricule gauche (VTDVG) significatives pour les deux groupes, étaienl
plus marqué avec l’halothane qu’avec l’isoflurane: FE 32 ± 5 pour cent vs18 ±5 pour cent; VTDVG 18 ± 7 pour cent vs 7 ± 5
pour cent. Avec l’atropine, la FC monta plus dans le groupe halothane (31 ± 6 pour cent) que dans le groupe isoflurane (18
± 5 pour cent), le DC augmentant dans les deux groupes, alors que le VE et la FE demeuraient inchangés. Comparée aux mesures
pré-induction, l’atropine amenait une hausse significative de la FC, semblable dans les deux groupes (18 ± 4 pour cent) et
restaurait le DC. Donc, chez les bebes et les jeunes enfants, a 1.5 MAC, l’halothane diminue la FE et augmente le VTDVG plus
que ne le fait l’isoflurane. L’atropine ne modifie pas la depression myocardique et elle ne restaure le DC que par une hausse
de la FC.
Supported by PHS Grant No. 8507300 from the College of Medicine, University of Iowa Hospital, Iowa City, IA. 相似文献
Trypsin treatment of chronic lymphocytic leukaemia (CLL) cells which have the capacity to rosette with mouse erythrocytes (M), the BM+ subtype, inhibits their capacity to rosette and releases a substance into the supernatant which agglutinates mouse and rat erythrocytes but not erythrocytes of five other species tested. This substance has been named immature B-cell lectin (IBL). The specificity of IBL was further demonstrated by fluorescence labelling, absorption and latex rosetting. IBL does not bind to pronase-treated M (pro M), indicating that it has the specificity of R1 as distinct from R2 which binds to a pronase-resistant ligand on M. Other evidence that IBL is associated with B-cell membrane receptors for mouse erythrocytes is as follows: (1) The amount of IBL released into the supernatant correlated with the trypsin sensitivity of M rosetting with different clones of BM+ CLL cells. (2) Only small amounts of IBL were released from non-rosetting cells (T cells and mature B cells). (3) Binding properties of IBL were inhibited by extract of M but not extract from ox erythrocytes. (4) High-titre solutions of IBL conferred the capacity to form M rosettes on certain types of non-rosetting B cells. IBL has a dual binding specificity. Its binding to M is inhibited by fetuin and mannan, while its binding to B cells is not inhibited by these substances. The relationship of IBL to other membrane lectins including fibronectin is discussed. Preliminary characterization indicates a high-molecular-weight (at least 300,000 daltons) glycoprotein which has a pronounced tendency to aggregate in solution. The relationship of IBL to stages of human B-cell maturation is discussed. 相似文献
Serum IgE levels were high in a Papua New Guinean population infested with hookworm. Serum IgE and blood eosinophil levels fell after treatment with anthelmintics. 相似文献
Smith-Lemli-Opitz syndrome (RSH/SLOS) is an autosomal recessive, malformation syndrome caused by mutations in the 3beta-hydroxysterol delta7-reductase gene (DHCR7). DHCR7 catalyzes the reduction of 7-dehydrocholesterol (7DHC) to cholesterol. We report the mutation analysis and determination of residual cholesterol synthesis in 47 SLOS patients, and the effects of treatment of SLOS skin fibroblasts with simvastatin. Using deuterium labeling we have quantified the amount of synthesized cholesterol and 7DHC in homozygote, heterozygote, and control fibroblast cell lines. In SLOS fibroblasts, the fraction of synthesized cholesterol to total sterol synthesis ranged from undetectable to over 50%. This establishes that different mutant alleles encode enzymes with varying degrees of residual activity. There was a correlation between increased phenotypic severity and decreased residual cholesterol synthesis (r(2)=0.45, p<0.0001). Simvastatin treatment of SLOS fibroblasts with residual DHCR7 enzymatic activity decreased 7DHC levels and increased cholesterol synthesis. This increase in cholesterol synthesis is due to increased expression of a mutant allele with residual function. Determination of residual enzymatic activity for specific DHCR7 mutant alleles will help in understanding the processes underlying the broad phenotypic spectrum found in this disorder and will be useful in identifying patients who may benefit from simvastatin therapy. 相似文献
Total ascertainment revealed 28 families with haemophilia B in the west of Scotland (prevalence 1/26 870 males). In 12 of these families more than one person was affected and 26 living obligate carriers were identified and tested. Of these, 42% were heterozygous for a DNA polymorphism recognised by a factor IX genomic probe. No recombination was observed in 11 phase known and four phase unknown informative meioses. Definitive genetic counselling was possible for 14 of 42 females at risk, 11 could not be traced, in 10 the probe was not informative, and in seven paternal absence prevented interpretation. Linkage disequilibrium was apparent for this restriction fragment length polymorphism and haemophilia B in the west of Scotland. 相似文献
The occurrence of mitotic and chromosomal aberrations was examined in cultured lymphocytes from 25 African children suffering from acute measles at an early stage (0-5 days after onset of rash).
In eight cases the mitotic response to phytohaemagglutinin was impaired. In two cases extensive changes were observed, involving the formation of giant polykaryotic syncytia with chromosome pulverization. It is suggested that the development of giant cells in vivo and the damage to epithelial membranes characteristic of severe measles in the tropics are to be correlated with these changes.
A varying incidence of minor chromosome aberrations, mostly small gaps, was found in 15 cases of measles as well as in controls. The specific relationship of this type of aberration to the virus is questionable.
Mitotic activity was induced in two replicate lymphocyte cultures in the absence of phytohaemagglutinin.
The possible oncogenic potential of the measles virus is discussed in connection with the fusion-pulverization phenomenon.