Urinary excretion of sodium, potassium and some hormones influencing their transport was investigated before and after i.v. furosemide administration in 10 offsprings of normotensive subjects who had a normal Na(+)-K+ cotransport activity and in 26 normotensive men with a positive family history of essential hypertension. The latter group was divided into two subgroups with regard to the activity of red cell Na(+)-K+ cotransport. The Co[-] subjects with a decreased Na(+)-K+ cotransport activity had lower urinary excretion of sodium and vasodilators (kallikrein, dopamine, PGE2 and prostacyclin) after furosemide administration. The urinary excretion of vasopressor factors (PGF2 alpha, thromboxane) was unchanged as compared with that in the control group. There was a significant correlation between Na(+)-K+ cotransport activity and kallikrein excretion. These results suggest a deficit in the secretion of renal substances with vasodilating or natriuretic effects in Co[-] subjects. This could negatively affect their sodium excretion.
本文对10例Na(+)-K+共转运活性正常的血压正常者后代和26例高血压家族史阳性的血压正常者的尿钠、钾排泄及影响其转运的一些激素进行了静脉滴注速尿前后的研究。后一组红细胞Na(+)-K+共转运活性分为两个亚组。服用呋塞米后,Na(+)- k +共转运活性降低的Co[-]受试者尿中钠和血管扩张剂(kallikrein、多巴胺、PGE2和前列环素)的排泄量降低。与对照组相比,尿中血管加压因子(PGF2 α、血栓素)的排泄没有变化。Na(+)-K+共转运活性与钾激肽分泌有显著相关性。这些结果表明,在Co[-]受试者中,具有血管舒张或尿钠作用的肾脏物质分泌不足。这可能会对它们的钠排泄产生负面影响。
{"title":"Vasoactive humoral systems and sodium transport in erythrocytes of normotensive offsprings of essential hypertensive subjects.","authors":"V Janata, H Bultasová, P Pinsker","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Urinary excretion of sodium, potassium and some hormones influencing their transport was investigated before and after i.v. furosemide administration in 10 offsprings of normotensive subjects who had a normal Na(+)-K+ cotransport activity and in 26 normotensive men with a positive family history of essential hypertension. The latter group was divided into two subgroups with regard to the activity of red cell Na(+)-K+ cotransport. The Co[-] subjects with a decreased Na(+)-K+ cotransport activity had lower urinary excretion of sodium and vasodilators (kallikrein, dopamine, PGE2 and prostacyclin) after furosemide administration. The urinary excretion of vasopressor factors (PGF2 alpha, thromboxane) was unchanged as compared with that in the control group. There was a significant correlation between Na(+)-K+ cotransport activity and kallikrein excretion. These results suggest a deficit in the secretion of renal substances with vasodilating or natriuretic effects in Co[-] subjects. This could negatively affect their sodium excretion.</p>","PeriodicalId":20547,"journal":{"name":"Physiologia Bohemoslovaca","volume":"39 1","pages":"65-70"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13296950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N Tribulová, J Slezák, T Ravingerová, A Ziegelhöffer
The Ca paradox resulted in marked inhibition, up to disappearance, of histochemically studied enzyme activities (SDH, LDH, beta-HBDH, phosphorylase and ATPase) in the subepicardial layer of the myocardium. In the subendocardial region there was only a small decrease. These transmural differences correlated well with ultrastructural changes. It is assumed that the heterogeneity in transmural distribution of injury is the result of transmural differences in coronary flow.
{"title":"Transmural non-homogeneity of calcium-induced heart injury.","authors":"N Tribulová, J Slezák, T Ravingerová, A Ziegelhöffer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The Ca paradox resulted in marked inhibition, up to disappearance, of histochemically studied enzyme activities (SDH, LDH, beta-HBDH, phosphorylase and ATPase) in the subepicardial layer of the myocardium. In the subendocardial region there was only a small decrease. These transmural differences correlated well with ultrastructural changes. It is assumed that the heterogeneity in transmural distribution of injury is the result of transmural differences in coronary flow.</p>","PeriodicalId":20547,"journal":{"name":"Physiologia Bohemoslovaca","volume":"39 2","pages":"147-50"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13298876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
I Niedermayerová-Roucová, P Hude, V Strnadová, O Gulda
The delayed type hypersensitivity (DTH) was studied in guinea-pigs using the skin test. The mycobacterium tuberculosis (M. tbc)--was applied by various routes. The control group received ovalbumin in Freund's incomplete adjuvant (FIA) into the footpad. The first experimental group received ovalbumin in Freund's complete adjuvant (FCA) into the footpad. The other experimental groups always received, in addition to ovalbumin plus FIA into the footpad, the M. tbc. 1. intracisternally, 2. intramuscularly, 3. intraperitoneally, 4. orally. On the day of administration of the sensibilizing substance, the body temperature was monitored. The skin test was measured after 14 and 21 days. It was established that, for the study of the DTH, the 21-day interval was more significant than the 14-day interval. A 100 times smaller dose of M. tbc. given intracisternally had the same immunostimulating effect as the injection of ovalbumin with M. tbc into the footpad (p less than 0.01). The size of the skin reaction was not only significantly influenced by the intramuscular and oral administration of M. tbc. On the other hand, the intraperitoneal administration inhibited the DTH (p less than 0.01). The increase of body temperature after the administration of M. tbc. correlated with the influence on the DTH except for the intraperitoneal administration. The route of the M. tbc. administration was crucial for the development of the DTH.
{"title":"Intracisternal administration of Mycobacterium tuberculosis potentiates the delayed type hypersensitivity in guinea-pigs.","authors":"I Niedermayerová-Roucová, P Hude, V Strnadová, O Gulda","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The delayed type hypersensitivity (DTH) was studied in guinea-pigs using the skin test. The mycobacterium tuberculosis (M. tbc)--was applied by various routes. The control group received ovalbumin in Freund's incomplete adjuvant (FIA) into the footpad. The first experimental group received ovalbumin in Freund's complete adjuvant (FCA) into the footpad. The other experimental groups always received, in addition to ovalbumin plus FIA into the footpad, the M. tbc. 1. intracisternally, 2. intramuscularly, 3. intraperitoneally, 4. orally. On the day of administration of the sensibilizing substance, the body temperature was monitored. The skin test was measured after 14 and 21 days. It was established that, for the study of the DTH, the 21-day interval was more significant than the 14-day interval. A 100 times smaller dose of M. tbc. given intracisternally had the same immunostimulating effect as the injection of ovalbumin with M. tbc into the footpad (p less than 0.01). The size of the skin reaction was not only significantly influenced by the intramuscular and oral administration of M. tbc. On the other hand, the intraperitoneal administration inhibited the DTH (p less than 0.01). The increase of body temperature after the administration of M. tbc. correlated with the influence on the DTH except for the intraperitoneal administration. The route of the M. tbc. administration was crucial for the development of the DTH.</p>","PeriodicalId":20547,"journal":{"name":"Physiologia Bohemoslovaca","volume":"39 3","pages":"193-8"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13299608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The authors evaluated the migratory and proliferative properties and the chromosome number of cultivated male and female smooth muscle cells (SMC) obtained by the explanation method from the thoracic aorta of rats of a conventional and a specific pathogen-free (SPF) breed. It was found that male SMC, in most cases, began to migrate from the explants sooner than female SMC and that they migrated from a higher total number of explants. The time needed for the number of cells in the culture to double (doubling time) was practically the same for male and female SMC, but male SMC attained a higher maximum population density. Male SMC cultures (2nd passage) contained cells with a hyperploid chromosome number, whereas female SMC were diploid. It was also found that SMC from conventional rats, in which the presence of pathogens could be presumed, displayed higher migratory and proliferative capacity than the SMC of SPF rats. The capacity of the SMC of male rats for migration and proliferation could have been potentiated by the effect of a different composition of the intercellular matrix and a different chromosome number, and in conventional rats by the presence of pathogens.
{"title":"Vascular smooth muscle cells of male and female rats in culture, migration, proliferation and chromosome number.","authors":"L Bacáková, M Baudysová","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The authors evaluated the migratory and proliferative properties and the chromosome number of cultivated male and female smooth muscle cells (SMC) obtained by the explanation method from the thoracic aorta of rats of a conventional and a specific pathogen-free (SPF) breed. It was found that male SMC, in most cases, began to migrate from the explants sooner than female SMC and that they migrated from a higher total number of explants. The time needed for the number of cells in the culture to double (doubling time) was practically the same for male and female SMC, but male SMC attained a higher maximum population density. Male SMC cultures (2nd passage) contained cells with a hyperploid chromosome number, whereas female SMC were diploid. It was also found that SMC from conventional rats, in which the presence of pathogens could be presumed, displayed higher migratory and proliferative capacity than the SMC of SPF rats. The capacity of the SMC of male rats for migration and proliferation could have been potentiated by the effect of a different composition of the intercellular matrix and a different chromosome number, and in conventional rats by the presence of pathogens.</p>","PeriodicalId":20547,"journal":{"name":"Physiologia Bohemoslovaca","volume":"39 5","pages":"449-58"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13304856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A study of the numbers of pulmonary endocrine cells per cm2 of section of lung obtained at combined heart-lung transplantation in 25 cases of plexogenic pulmonary arteriopathy demonstrated that the peptide which may become unduly prominent in pulmonary arterial disease is bombesin. The type of vascular disease in which bombesin becomes prominent is plexogenic pulmonary arteriopathy, be this primary or secondary to congenital heart disease. The increased prominence of bombesin appears to be related to the stage reached in the arteriopathy. Increased numbers of pulmonary endocrine cells are found in association with classic cellular plexiform lesions with narrow vascular channels. Their numbers are within normal limits when the plexiform lesions are mature with wide vascular channels and narrow intervening septa. The pulmonary endocrine cells are most prominent in the pre-plexiform stage when smooth muscle cells in the inner half of the media of the pulmonary artery show increased electron density, and migrate through gaps in the inner elastic lamina to reach the intima. Here they are transformed into myofibroblasts and proliferate. The migration of muscle cells may be related in some way to long-acting trophic factors released from the pulmonary endocrine cells into the surrounding tissues from which they reach the blood and hence the pulmonary arteries.
{"title":"Pulmonary endocrine cells in plexogenic pulmonary arteriopathy.","authors":"D Heath, B Madden, M Yacoub","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A study of the numbers of pulmonary endocrine cells per cm2 of section of lung obtained at combined heart-lung transplantation in 25 cases of plexogenic pulmonary arteriopathy demonstrated that the peptide which may become unduly prominent in pulmonary arterial disease is bombesin. The type of vascular disease in which bombesin becomes prominent is plexogenic pulmonary arteriopathy, be this primary or secondary to congenital heart disease. The increased prominence of bombesin appears to be related to the stage reached in the arteriopathy. Increased numbers of pulmonary endocrine cells are found in association with classic cellular plexiform lesions with narrow vascular channels. Their numbers are within normal limits when the plexiform lesions are mature with wide vascular channels and narrow intervening septa. The pulmonary endocrine cells are most prominent in the pre-plexiform stage when smooth muscle cells in the inner half of the media of the pulmonary artery show increased electron density, and migrate through gaps in the inner elastic lamina to reach the intima. Here they are transformed into myofibroblasts and proliferate. The migration of muscle cells may be related in some way to long-acting trophic factors released from the pulmonary endocrine cells into the surrounding tissues from which they reach the blood and hence the pulmonary arteries.</p>","PeriodicalId":20547,"journal":{"name":"Physiologia Bohemoslovaca","volume":"39 4","pages":"309-13"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13305070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H Valtin, A K Coffey, D J O'Sullivan, S Homma, T P Dousa
In a strain of mice called DI +/+ Severe, nephrogenic (or vasopressin-resistant) diabetes insipidus is caused by an inability of the antidiuretic hormone (ADH, or vasopressin) to increase the water permeability of the renal collecting system. That inability, in turn, arises from abnormally high activity of the enzyme cAMP-phosphodiesterase, specifically of the isozyme type III (PDE-III), which hydrolyzes cAMP and prevents the intracellular buildup of this second messenger. Two rather specific inhibitors of PDE-III, rolipram and cilostamide, used either in vitro or in vivo, reverse the deficiencies in DI +/+ Severe mice by increasing intracellular cAMP and water permeability toward or to their normal values. These results have implications for the treatment of nephrogenic diabetes insipidus in human patients.
{"title":"Causes of the urinary concentrating defect in mice with nephrogenic diabetes insipidus.","authors":"H Valtin, A K Coffey, D J O'Sullivan, S Homma, T P Dousa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In a strain of mice called DI +/+ Severe, nephrogenic (or vasopressin-resistant) diabetes insipidus is caused by an inability of the antidiuretic hormone (ADH, or vasopressin) to increase the water permeability of the renal collecting system. That inability, in turn, arises from abnormally high activity of the enzyme cAMP-phosphodiesterase, specifically of the isozyme type III (PDE-III), which hydrolyzes cAMP and prevents the intracellular buildup of this second messenger. Two rather specific inhibitors of PDE-III, rolipram and cilostamide, used either in vitro or in vivo, reverse the deficiencies in DI +/+ Severe mice by increasing intracellular cAMP and water permeability toward or to their normal values. These results have implications for the treatment of nephrogenic diabetes insipidus in human patients.</p>","PeriodicalId":20547,"journal":{"name":"Physiologia Bohemoslovaca","volume":"39 1","pages":"103-11"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13318527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M A Devynck, M David-Dufilho, C Astarie, M Mazeaud, M G Pernollet, K H Le Quan Sang
Inhibition of the Na(+)-K+ pump by digitalis compounds has been reported to increase intracellular Na+ and Ca2+ concentrations and to stimulate Na(+)-H+ exchange. The activity of endogenous digitalis-like compounds, proposed to promote natriuresis and to raise blood pressure, has been found to be increased in volume expansion and hypertension. The enhanced cytosolic [Ca2+] present in platelets from hypertensive patients may thus originate from inhibition of the Na(+)-K+ pump by endogenous inhibitors, enhanced mobilization of internal Ca2+ stores due to phospholipase C activation and/or structural membrane defects. In unstimulated platelets from essential hypertensives, the increase in [Ca2+]i depends on external Ca2+, thereby underlining the importance of Ca2+ influx. The observation that [Ca2+]i was also enhanced in erythrocytes (p = 0.03) demonstrates that intracellular stores are not required for this rise. Plasma digitalis-like activity was positively correlated with platelet [Ca2+]i (inhibition of renal Na+,K(+)-ATPase, competition with ouabain binding, p less than 0.01). Platelet [Ca2+]i also rose during chronic digoxin administration (p less than 0.02) but not after acute in vitro ouabain treatment. The alkalinisation of platelet cytosol (p = 0.005) also agrees with the stimulation of the Na(+)-H(+)-exchange. In conclusion, these results are compatible with a participation of endogenous Na(+)-K+ pump inhibitors in the control of cytoplasmic [Ca2+] and cell excitability.
{"title":"Endogenous inhibitors of the Na+, K(+)-pump and platelet Ca2+ handling in hypertension.","authors":"M A Devynck, M David-Dufilho, C Astarie, M Mazeaud, M G Pernollet, K H Le Quan Sang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Inhibition of the Na(+)-K+ pump by digitalis compounds has been reported to increase intracellular Na+ and Ca2+ concentrations and to stimulate Na(+)-H+ exchange. The activity of endogenous digitalis-like compounds, proposed to promote natriuresis and to raise blood pressure, has been found to be increased in volume expansion and hypertension. The enhanced cytosolic [Ca2+] present in platelets from hypertensive patients may thus originate from inhibition of the Na(+)-K+ pump by endogenous inhibitors, enhanced mobilization of internal Ca2+ stores due to phospholipase C activation and/or structural membrane defects. In unstimulated platelets from essential hypertensives, the increase in [Ca2+]i depends on external Ca2+, thereby underlining the importance of Ca2+ influx. The observation that [Ca2+]i was also enhanced in erythrocytes (p = 0.03) demonstrates that intracellular stores are not required for this rise. Plasma digitalis-like activity was positively correlated with platelet [Ca2+]i (inhibition of renal Na+,K(+)-ATPase, competition with ouabain binding, p less than 0.01). Platelet [Ca2+]i also rose during chronic digoxin administration (p less than 0.02) but not after acute in vitro ouabain treatment. The alkalinisation of platelet cytosol (p = 0.005) also agrees with the stimulation of the Na(+)-H(+)-exchange. In conclusion, these results are compatible with a participation of endogenous Na(+)-K+ pump inhibitors in the control of cytoplasmic [Ca2+] and cell excitability.</p>","PeriodicalId":20547,"journal":{"name":"Physiologia Bohemoslovaca","volume":"39 1","pages":"71-8"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13318530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The authors studied the effect of administration of thyroid hormones on the beta-adrenergic receptors of rat adenohypophyseal cells. The administration of triiodothyronine and thyroxine was followed by an increase in specific binding for 3H-dihydroalprenolol. No significant differences were found in cyclic adenosine monophosphate levels before and after isoprenaline stimulation. The significance of changes in these receptors for the hyperplastic reaction after oestrogens is discussed with reference to the inhibitory effect of the thyroid hormones on hyperplasia of the adenohypophyseal cells after the administration of oestradiol.
{"title":"Increased number of beta-adrenergic receptors on cells of the rat adenohypophysis after thyroid hormone administration.","authors":"K Pacák, J Nedvídková, P Stolba, V Schreiber","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The authors studied the effect of administration of thyroid hormones on the beta-adrenergic receptors of rat adenohypophyseal cells. The administration of triiodothyronine and thyroxine was followed by an increase in specific binding for 3H-dihydroalprenolol. No significant differences were found in cyclic adenosine monophosphate levels before and after isoprenaline stimulation. The significance of changes in these receptors for the hyperplastic reaction after oestrogens is discussed with reference to the inhibitory effect of the thyroid hormones on hyperplasia of the adenohypophyseal cells after the administration of oestradiol.</p>","PeriodicalId":20547,"journal":{"name":"Physiologia Bohemoslovaca","volume":"39 3","pages":"249-52"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13323789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The problem of space flights called for the need to construct ground-base models which imitate or simulate some reactions of the organism to the complex of spaceflight factors, mainly to microgravity. In this review the processes and models simulating flight factors and their advantages and disadvantages are described. The authors have supplemented the models used until now by a new modification of suspension hypokinesia, so-called safety-pin suspension. This model appears to be simple and inexpensive. It causes relatively weak traumatic stress and this may be demonstrated by daily weighing of the animals.
{"title":"New modification of suspension hypokinesia in rats.","authors":"P Noskovic, I Ahlers, L Racek","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The problem of space flights called for the need to construct ground-base models which imitate or simulate some reactions of the organism to the complex of spaceflight factors, mainly to microgravity. In this review the processes and models simulating flight factors and their advantages and disadvantages are described. The authors have supplemented the models used until now by a new modification of suspension hypokinesia, so-called safety-pin suspension. This model appears to be simple and inexpensive. It causes relatively weak traumatic stress and this may be demonstrated by daily weighing of the animals.</p>","PeriodicalId":20547,"journal":{"name":"Physiologia Bohemoslovaca","volume":"39 5","pages":"471-4"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13304858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The rôle of the endocrine cells which populate the airways of the lung is uncertain, although it has been suggested that one of their functions might be to regulate the pulmonary vasculature. We have studied the number, content and distribution of these cells in 26 pairs of lungs removed during heart-lung transplantation for the treatment of pulmonary hypertension of various causes, none of which were characterized by plexogenic arteriopathy. In comparison with the controls, there were no differences in the number, content or distribution of these cells, although in two cases of recurrent pulmonary thromboembolism they were aggregated into abnormal disorderly clusters.
{"title":"Pulmonary endocrine cells in different varieties of pulmonary vascular disease.","authors":"J Gosney, M Yacoub, B Madden","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The rôle of the endocrine cells which populate the airways of the lung is uncertain, although it has been suggested that one of their functions might be to regulate the pulmonary vasculature. We have studied the number, content and distribution of these cells in 26 pairs of lungs removed during heart-lung transplantation for the treatment of pulmonary hypertension of various causes, none of which were characterized by plexogenic arteriopathy. In comparison with the controls, there were no differences in the number, content or distribution of these cells, although in two cases of recurrent pulmonary thromboembolism they were aggregated into abnormal disorderly clusters.</p>","PeriodicalId":20547,"journal":{"name":"Physiologia Bohemoslovaca","volume":"39 4","pages":"301-3"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13305067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}