{"title":"Proteoglycans of cartilage.","authors":"H Muir","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"12 ","pages":"67-81"},"PeriodicalIF":0.0,"publicationDate":"1978-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1347125/pdf/jclinpath00432-0074.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11573768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chondrocytes.","authors":"R A Stockwell","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"12 ","pages":"7-13"},"PeriodicalIF":0.0,"publicationDate":"1978-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1347119/pdf/jclinpath00432-0014.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11573769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Diseases of the collagen molecule.","authors":"C I Levene","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"12 ","pages":"82-94"},"PeriodicalIF":0.0,"publicationDate":"1978-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1347126/pdf/jclinpath00432-0089.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11573771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fetal hypoxaemia may result from altered maternal PaO2 or a reduction in maternal placental or umbilical blood flow. It is also possible that reduction of gas exchange across the placenta could limit the oxygen supply to the fetus. In this review we will be concerned with the effects of hypoxaemia in fetal sheep during the latter half of pregnancy. At present it is not easy to reduce maternal placental blood flow experimentally in a controlled manner, while an acute restriction of umbilical blood flow results in asphyxia (Towell and Salvador, 1974). Fetal hypoxaemia can be induced reproducibly by lowering maternal inspired oxygen concentrations and hence PaO2. During such experiments, the fetal blood gas tensions take several minutes to equilibrate while the cardiovascular and plasma changes require up to 60 min to reach a relatively steady state (Boddy et al, 1974a; Cohn et al, 1974; Jones and Robinson, 1975; Rurak, 1976a and b; Jones, 1977). Although the acute episodes of hypoxaemia known to occur spontaneously last only a few minutes (Jones and Ritchie, 1976; Patrick et al, 1976), studying changes over a 60-min period provides more detailed information. A different approach has been used to produce long-term hypoxaemia in the fetus so as to minimize the effects on the mother. This has been either to reduce placental mass surgically (Alexander, 1964), to embolize the maternal placenta with microspheres (Creasy et al, 1972), or to reduce umbilical blood flow by umbilical artery ligation (Emmanouilides et al, 1968). It is important when investigating fetal hypoxaemia to avoid the effects of anaesthesia and surgery. Such acute experiments are associated with much higher hormone (at least 10 fold higher for ACTH, catecholamines and vasopressin) and metabolite concentrations than in chronically catheterized fetal preparations. For instance, the plasma catecholamine concentration in the exteriorized fetal sheep is higher than that normally seen during hypoxaemia in fetal sheep in utero (Jones and Robinson, 1975; Jones and Rurak, 1976a) and hypoxaemia causes a tachycardia in the exteriorized fetus compared with an initial bradycardia in utero. We will therefore concentrate on the cardiovascular, metabolic and endocrine changes observed with both short-term and chronic hypoxaemia in the conscious unrestrained sheep with implanted catheters.
{"title":"The effects of hypoxaemia in fetal sheep.","authors":"J S Robinson, C T Jones, G D Thorburn","doi":"10.1136/jcp.s3-11.1.127","DOIUrl":"https://doi.org/10.1136/jcp.s3-11.1.127","url":null,"abstract":"Fetal hypoxaemia may result from altered maternal PaO2 or a reduction in maternal placental or umbilical blood flow. It is also possible that reduction of gas exchange across the placenta could limit the oxygen supply to the fetus. In this review we will be concerned with the effects of hypoxaemia in fetal sheep during the latter half of pregnancy. At present it is not easy to reduce maternal placental blood flow experimentally in a controlled manner, while an acute restriction of umbilical blood flow results in asphyxia (Towell and Salvador, 1974). Fetal hypoxaemia can be induced reproducibly by lowering maternal inspired oxygen concentrations and hence PaO2. During such experiments, the fetal blood gas tensions take several minutes to equilibrate while the cardiovascular and plasma changes require up to 60 min to reach a relatively steady state (Boddy et al, 1974a; Cohn et al, 1974; Jones and Robinson, 1975; Rurak, 1976a and b; Jones, 1977). Although the acute episodes of hypoxaemia known to occur spontaneously last only a few minutes (Jones and Ritchie, 1976; Patrick et al, 1976), studying changes over a 60-min period provides more detailed information. A different approach has been used to produce long-term hypoxaemia in the fetus so as to minimize the effects on the mother. This has been either to reduce placental mass surgically (Alexander, 1964), to embolize the maternal placenta with microspheres (Creasy et al, 1972), or to reduce umbilical blood flow by umbilical artery ligation (Emmanouilides et al, 1968). It is important when investigating fetal hypoxaemia to avoid the effects of anaesthesia and surgery. Such acute experiments are associated with much higher hormone (at least 10 fold higher for ACTH, catecholamines and vasopressin) and metabolite concentrations than in chronically catheterized fetal preparations. For instance, the plasma catecholamine concentration in the exteriorized fetal sheep is higher than that normally seen during hypoxaemia in fetal sheep in utero (Jones and Robinson, 1975; Jones and Rurak, 1976a) and hypoxaemia causes a tachycardia in the exteriorized fetus compared with an initial bradycardia in utero. We will therefore concentrate on the cardiovascular, metabolic and endocrine changes observed with both short-term and chronic hypoxaemia in the conscious unrestrained sheep with implanted catheters.","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"11 ","pages":"127-33"},"PeriodicalIF":0.0,"publicationDate":"1977-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jcp.s3-11.1.127","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11414381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This review gives an account of some of the factors affecting the transport of oxygen from the lungs until its final discharge in the tissues. The sequence of physiological and metabolic processes to be described may be considered collectively as the 'coarse adjustment' of oxygen transport. The 'fine adjustment' will be discussed in the succeeding chapter which surveys the local factors influencing distribution of oxygen from the microcirculation. Three terms which will doubtless be used more than once during this Symposium are worthy of definition. 'Oxygen availability' consists of two main components: blood flow and oxygen content (which is the product of haemoglobin concentration and oxygen saturation). By means of the Fick equation it can be shown that 'oxygen consumption' equates with the product of blood flow and arteriovenous difference for oxygen. Finally, 'oxygen debt' is the term used to describe the ability of certain tissues, notably muscle, to survive for short periods in the absence of oxygen. This factor may be expressed quantitatively as the product of the reduction in oxygen consumption during a period of hypoxia or ischaemia and its duration.
{"title":"Factors influencing oxygen availability.","authors":"I M Ledingham","doi":"10.1136/jcp.s3-11.1.1","DOIUrl":"https://doi.org/10.1136/jcp.s3-11.1.1","url":null,"abstract":"This review gives an account of some of the factors affecting the transport of oxygen from the lungs until its final discharge in the tissues. The sequence of physiological and metabolic processes to be described may be considered collectively as the 'coarse adjustment' of oxygen transport. The 'fine adjustment' will be discussed in the succeeding chapter which surveys the local factors influencing distribution of oxygen from the microcirculation. Three terms which will doubtless be used more than once during this Symposium are worthy of definition. 'Oxygen availability' consists of two main components: blood flow and oxygen content (which is the product of haemoglobin concentration and oxygen saturation). By means of the Fick equation it can be shown that 'oxygen consumption' equates with the product of blood flow and arteriovenous difference for oxygen. Finally, 'oxygen debt' is the term used to describe the ability of certain tissues, notably muscle, to survive for short periods in the absence of oxygen. This factor may be expressed quantitatively as the product of the reduction in oxygen consumption during a period of hypoxia or ischaemia and its duration.","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"11 ","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"1977-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jcp.s3-11.1.1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11544752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The distribution of the cardiac output is conventionally shared between six major circulatory components, that is, to the brain, heart, kidneys, bone and skeletal muscle, skin and viscera. This last comprises the splanchnic circulation, which arrives through the three great visceral arteries (coeliac axis, superior and inferior mesenteric artery) and is drained, via the liver, into the hepatic veins. The organs supplied include the liver, spleen and pancreas, stomach, duodenum and small and large intestine. In practice, the one area in which deprivation of blood supply carries important physiological consequences is the alimentary tract, because the other territories are irrigated by a double circulation. This chapter will, therefore, be mainly concerned with events in the mesenteric circulation.
{"title":"Responses of the splanchnic circulation to ischaemia.","authors":"A Marston","doi":"10.1136/jcp.s3-11.1.59","DOIUrl":"https://doi.org/10.1136/jcp.s3-11.1.59","url":null,"abstract":"The distribution of the cardiac output is conventionally shared between six major circulatory components, that is, to the brain, heart, kidneys, bone and skeletal muscle, skin and viscera. This last comprises the splanchnic circulation, which arrives through the three great visceral arteries (coeliac axis, superior and inferior mesenteric artery) and is drained, via the liver, into the hepatic veins. The organs supplied include the liver, spleen and pancreas, stomach, duodenum and small and large intestine. In practice, the one area in which deprivation of blood supply carries important physiological consequences is the alimentary tract, because the other territories are irrigated by a double circulation. This chapter will, therefore, be mainly concerned with events in the mesenteric circulation.","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"11 ","pages":"59-67"},"PeriodicalIF":0.0,"publicationDate":"1977-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jcp.s3-11.1.59","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11544754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The objective of any satisfactory model of myocardial ischaemia in experimental animals must be to reproduce, as accurately as possible, the spectrum of ischaemic heart disease as seen in man. Since we are still, to a very considerable extent, ignorant of the pathophysiology of angina pectoris and of sudden death causally associated with coronary atherosclerosis and thrombosis, it is, in my view, impossible to construct valid models for these important clinical expressions of ischaemic heart disease. This brief review is, therefore, exclusively concerned with myocardial necrosis. In human disease, the various patterns ofischaemic myocardial necrosis (Davies, 1977) occur for the most part against the background of a coronary circulation widely compromised by stenosing atherosclerosis. In regional infarction arterial occlusion, either by thrombus or by a mixture of thrombus and atheromatous debris, is present in the majority of cases (Davies et al, 1976) and the occlusions are usually related to splits or tears in the connective tissue caps of atherosclerotic plaques. These pathogenetic factors should certainly be subsumed in any experimental model which attempts to mimic the human disease. At present, it must be admitted that we cannot economically devise models which meet these requirements. Nevertheless our attitude, though critical, need not be totally nihilistic. Although the models we have are inherently unsatisfactory, they can provide some useful information on a variety of matters such as mapping infarcts, metabolic and structural changes in underperfused regions of the myocardium and the effects of various forms of intervention on these changes.
{"title":"Animal models of myocardial ischaemia.","authors":"N Woolf","doi":"10.1136/jcp.s3-11.1.53","DOIUrl":"https://doi.org/10.1136/jcp.s3-11.1.53","url":null,"abstract":"The objective of any satisfactory model of myocardial ischaemia in experimental animals must be to reproduce, as accurately as possible, the spectrum of ischaemic heart disease as seen in man. Since we are still, to a very considerable extent, ignorant of the pathophysiology of angina pectoris and of sudden death causally associated with coronary atherosclerosis and thrombosis, it is, in my view, impossible to construct valid models for these important clinical expressions of ischaemic heart disease. This brief review is, therefore, exclusively concerned with myocardial necrosis. In human disease, the various patterns ofischaemic myocardial necrosis (Davies, 1977) occur for the most part against the background of a coronary circulation widely compromised by stenosing atherosclerosis. In regional infarction arterial occlusion, either by thrombus or by a mixture of thrombus and atheromatous debris, is present in the majority of cases (Davies et al, 1976) and the occlusions are usually related to splits or tears in the connective tissue caps of atherosclerotic plaques. These pathogenetic factors should certainly be subsumed in any experimental model which attempts to mimic the human disease. At present, it must be admitted that we cannot economically devise models which meet these requirements. Nevertheless our attitude, though critical, need not be totally nihilistic. Although the models we have are inherently unsatisfactory, they can provide some useful information on a variety of matters such as mapping infarcts, metabolic and structural changes in underperfused regions of the myocardium and the effects of various forms of intervention on these changes.","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"11 ","pages":"53-8"},"PeriodicalIF":0.0,"publicationDate":"1977-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jcp.s3-11.1.53","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11483332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A supply of oxygenated blood appropriate to the tissue needs of the gut is essential to the maintenance of its vital functions. The splanchnic vascular system serves this purpose and much of our knowledge of ischaemic bowel disease has developed from studies of radiological and pathological abnormalities of this system. The purpose of this paper is to summarize current information concerning the histopathology of intestinal ischaemia in the light of our better understanding of the micro-circulation of the gut in health and disease; also to describe the difficulties we have in understanding the pathogenesis of ischaemic bowel disease because of the growing spectrum of systemic disorders with which it is associated
{"title":"Ischaemic bowel disease.","authors":"T Alschibaja, B C Morson","doi":"10.1136/jcp.s3-11.1.68","DOIUrl":"https://doi.org/10.1136/jcp.s3-11.1.68","url":null,"abstract":"A supply of oxygenated blood appropriate to the tissue needs of the gut is essential to the maintenance of its vital functions. The splanchnic vascular system serves this purpose and much of our knowledge of ischaemic bowel disease has developed from studies of radiological and pathological abnormalities of this system. The purpose of this paper is to summarize current information concerning the histopathology of intestinal ischaemia in the light of our better understanding of the micro-circulation of the gut in health and disease; also to describe the difficulties we have in understanding the pathogenesis of ischaemic bowel disease because of the growing spectrum of systemic disorders with which it is associated","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"11 ","pages":"68-77"},"PeriodicalIF":0.0,"publicationDate":"1977-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jcp.s3-11.1.68","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11483333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hypoxia in newborn infants is becoming much easier to prevent, detect and treat. Nevertheless the successful management of potentially hypoxic fetuses and newborn infants remains the major challenge to all physicians concerned with perinatal care. What is at stake is not only that sick infants should survive, but equally or more importantly that the survivors should be normal children. Recent follow-up studies show that this aim can, with few exceptions, now be achieved (Stewart and Reynolds, 1974; Davies and Stewart, 1975; Durbin et al, 1976).
新生儿缺氧正变得越来越容易预防、发现和治疗。然而，成功地管理潜在的缺氧胎儿和新生儿仍然是所有关注围产期护理的医生面临的主要挑战。生死攸关的不仅是生病的婴儿能否活下来，更重要的是幸存下来的应该是正常的孩子。最近的后续研究表明，除了少数例外，这一目标现在可以实现(Stewart和Reynolds, 1974;戴维斯和斯图尔特，1975;Durbin et al, 1976)。
{"title":"Hypoxia in the newborn infant.","authors":"E O Reynolds","doi":"10.1136/jcp.s3-11.1.134","DOIUrl":"https://doi.org/10.1136/jcp.s3-11.1.134","url":null,"abstract":"<p><p>Hypoxia in newborn infants is becoming much easier to prevent, detect and treat. Nevertheless the successful management of potentially hypoxic fetuses and newborn infants remains the major challenge to all physicians concerned with perinatal care. What is at stake is not only that sick infants should survive, but equally or more importantly that the survivors should be normal children. Recent follow-up studies show that this aim can, with few exceptions, now be achieved (Stewart and Reynolds, 1974; Davies and Stewart, 1975; Durbin et al, 1976).</p>","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"11 ","pages":"134-41"},"PeriodicalIF":0.0,"publicationDate":"1977-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jcp.s3-11.1.134","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11483328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
At birth the newborn infant is required to make an abrupt adjustment to a new environment. The most immediate changes required to support extrauterine life are concerned with respiration and the circulation. The infant must be able to expand its lungs fully and at the same time the pulmonary circulation must be adequate for gaseous exchange to occur between the air spaces and the pulmonary capillaries. Even the mature infant may have some difficulty in making the adjustment and this becomes an even greater problem in the case of the premature baby. In many instances there may be no apparent cause for the interruption of the pregnancy and the infant is inherently healthy but is under 2500g birthweight. In some pregnancies, however, maternal factors such
{"title":"Pathology of perinatal hypoxia.","authors":"A E Claireaux","doi":"10.1136/jcp.s3-11.1.142","DOIUrl":"https://doi.org/10.1136/jcp.s3-11.1.142","url":null,"abstract":"At birth the newborn infant is required to make an abrupt adjustment to a new environment. The most immediate changes required to support extrauterine life are concerned with respiration and the circulation. The infant must be able to expand its lungs fully and at the same time the pulmonary circulation must be adequate for gaseous exchange to occur between the air spaces and the pulmonary capillaries. Even the mature infant may have some difficulty in making the adjustment and this becomes an even greater problem in the case of the premature baby. In many instances there may be no apparent cause for the interruption of the pregnancy and the infant is inherently healthy but is under 2500g birthweight. In some pregnancies, however, maternal factors such","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"11 ","pages":"142-8"},"PeriodicalIF":0.0,"publicationDate":"1977-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jcp.s3-11.1.142","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11483329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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