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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although there is increasing evidence that mineral dust exposure will produce obstructive lung disease, there is little information on the effects of mineral dust on the pulmonary vascular system. To examine whether exposure to amosite asbestos would affect the pulmonary vasculature and produce pulmonary hypertension, we instilled 5 mg amosite asbestor intratracheally into guinea pigs. After periods of 3 and 6 months, we examined their pulmonary and pulmonary vascular function, and compared these data to those obtained from groups of control animals. We found that, at both time periods, there was pulmonary arterial hypertension, with alteration of the vascular pressure-flow relationships. This was accompanied by abnormalities in the structure of the small pulmonary arterioles. The animals also showed airflow obstruction, with air trapping and an upward shift of the pressure-volume curve. There was evidence of emphysema, and the animals were moderately hypoxic. We found no consistent increase in inflammatory cells either in lavage or peripheral blood, and the histamine dose-response curves were similar in control and asbestos-exposed animals at 6 months. We conclude that intratracheal instillation of asbestos in the guinea pig produces pulmonary hypertension associated with modest hypoxia, emphysema, and airflow obstruction. Whether pulmonary hypertension reflects emphysema-induced hypoxia and loss of vascular bed, or is related to the brief but intense inflammatory infiltrate induced by asbestos, is unclear.
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PMID:Pulmonary hypertension induced by amosite asbestos: a physiological and morphologic study in the guinea pig. 184 13

Single lung transplantation was performed in several steps: laparotomy to prepare an omentopexy, followed by pneumonectomy and implantation of a pulmonary graft, both by postero-lateral thoracotomy. The patients suffered from lymphangiomyomatosis (1), panacinar emphysema (2) and idiopathic pulmonary fibrosis (1). Immunosuppressive treatment was started before surgery. Anaesthesia was induced and maintained with alfentanil, midazolam and vecuronium. The patients were intubated with a Carlens endotracheal tube. Ventilation was carried out using an oxygen-air mixture, without any nitrous oxide or halogenated anaesthetic agent. Besides the usual parameters, expired CO2 concentrations, and oxygen saturation in the pulmonary artery were monitored. Partial femoro-femoral cardiopulmonary bypass was not required. Three major problems were encountered: hypoxia, hypercapnia, and pulmonary arterial hypertension. Hypoxia first occurred during the period of one-lung ventilation, during pneumonectomy, and again after unclamping of the graft vessels before the bronchus had been anastomosed. It was treated either by increasing the FiO2, inflating the lungs with pure oxygen, or partial clamping of the homolateral pulmonary artery. Hypercapnia occurred in three of the four patients until the graft was ventilated again. Except in one patient with preoperative pulmonary hypertension, the increase in pulmonary vascular resistances remained moderate after clamping of the pulmonary artery. Sufficient oxygen delivery, with more than 50% venous oxygen saturation, was maintained at this time by the infusion of dopamine and dobutamine. Two other specific problems were encountered in the emphysematous patients: severe hypotension following the start of artificial ventilation and after placing the patient in lateral position; thoracic asymetry with overdistension of the emphysematous lung, and mediastinal shift.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anesthesia in unilateral pulmonary transplantation]. 185 49

Pulmonary hypertension was diagnosed in 97 elderly patients (age 60-79) using electrokymography of the heart and vessels, ECG and rheography of the lungs. All the patients suffered from chronic cor pulmonale (CCP). Electrokymography proved an effective diagnostic tool in detection of pulmonary hypertension in CCP patients, whereas quantitation of the hypertension was successful at electrokymography with application of L. Burstin nomogram and electrocardiography according to S. A. Dushanin. ECG according to R. Bernar et al. appeared poorly sensitive, especially at early CCP stages. A. M. Novikov's rheopulmonography technique can provide only an approximate value of mean pressure in the pulmonary artery of elderly CCP patients.
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PMID:[Noninvasive diagnosis of pulmonary hypertension in aged and elderly patients with chronic pulmonary heart disease]. 185 88

To determine the hemodynamic effects of endothelin-1 (ET-1) in the fetal pulmonary circulation, we studied pulmonary vascular responses to brief and prolonged intrapulmonary infusions of the peptide in nine chronically prepared late-gestation fetal sheep. Left pulmonary artery (LPA) blood flow was measured with an electromagnetic flow transducer, and a catheter placed in the LPA allowed ET-1 infusion directly into the left lung. Brief (10-min) infusions of ET-1 (12.5-100 ng/min) increased flow up to 212% of baseline without changing pulmonary artery pressure. With prolonged (120-min) infusion of ET-1 (50 ng/min), flow increased from 69 +/- 8 to 164 +/- 23 ml/min at 10 min (P less than 0.05) but then declined and was not different from baseline at 120 min. The gradient between mean pulmonary artery and aortic pressures did not change, suggesting no constriction of the ductus arteriosus. Systemic (vena caval) infusion of ET-1 (100 ng/min for 30 min) caused systemic and pulmonary hypertension, as mean pulmonary artery pressure increased from 43 +/- 1 to 51 +/- 2 mmHg (P less than 0.05) and remained elevated for 30 min after cessation of the ET-1 infusion. We conclude that intrapulmonary ET-1 is a potent fetal pulmonary vasodilator, but its dilator effect is transient during prolonged infusion. In contrast, systemic infusion causes sustained hypertension, suggesting differential effects of ET-1 on the pulmonary and systemic circulations. These findings demonstrate marked vasoactivity of ET-1 in the fetus, suggesting a potential role in the normal or abnormal transitional circulation.
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PMID:Hemodynamic effects of endothelin-1 on ovine fetal pulmonary circulation. 185 46

The long-term results of pediatric heart transplantation were evaluated in 53 patients, aged 0.25 to 18.94 years, who received transplants at Stanford University Medical Center between 1974 and 1989. Indications for transplantation were idiopathic cardiomyopathy (68%), congenital heart disease (21%), endocardial fibroelastosis (8%), and doxorubicin cardiomyopathy (3%). Immunosuppression was achieved with combinations of cyclosporine, prednisone, and azathioprine. Thirty-seven of 42 recipients leaving the hospital after transplantation were alive and in New York Heart Association class I at study's end. Cumulative survival was 79% at 1 year, 76% at 3 years, and 69% at 5 years. Fourteen recipients have survived more than 5 years (5.1 to 12.4 years). Hospital readmission for illness has been infrequent, decreasing from 6.8 days to 0.9 days per year over 5 years. Eleven patients have required no rehospitalization. Posttransplant deaths were due to infection (19%), rejection (4%), pulmonary hypertension (4%), coronary artery disease (2%), and lymphoproliferative disease (2%). Retransplantation was required for intractable rejection in 4 patients and advanced coronary artery disease in 2. Hypertension and elevated blood urea nitrogen and creatinine levels were common in individuals receiving cyclosporine. Growth was often impaired in prepubertal children receiving daily prednisone. Based on this 15-year experience, it is concluded that heart transplantation represents a reasonable alternative for selected young patients with end-stage cardiac disease.
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PMID:Pediatric heart transplantation at Stanford: results of a 15-year experience. 186 16

Prostacyclin is a critical mediator of structure and function in the pulmonary circulation, causing both the inhibition of vascular smooth muscle growth and vasodilation via the stimulation of adenylate cyclase. To examine the potential role of alterations in prostacyclin production or mechanism of action in chronic hypoxic pulmonary hypertension, we determined the effects of prolonged (7 d) in vivo hypoxia on in vitro prostacyclin synthesis and mediation of adenylate cyclase activity in rat main pulmonary arteries. In control arteries prostacyclin production exceeded that of prostaglandin (PG) E2 by 25-fold, with 42% originating from the endothelium. Studies utilizing indomethacin revealed that endogenous prostaglandins mediate at least 69% of basal adenylate cyclase activity. Prostacyclin-stimulated enzyme activity was enhanced by exogenous GTP, indicating that this is a receptor-mediated process involving G protein amplification. Comparable dose-related responses to prostacyclin and PGE2 suggest that these agents may activate a common receptor. After 7 d of in vivo hypoxia there was a 2.7-fold increase in in vitro prostacyclin production, with equivalent increases in synthesis in the endothelium and vascular smooth muscle. However, despite this increase there was no change in basal adenylate cyclase activity, and this was associated with attenuated sensitivity of the enzyme to prostacyclin stimulation. Concomitant diminution of the response to beta-adrenergic stimulation, with previously-demonstrated beta receptor downregulation and unaltered postreceptor-mediated activity, suggests that the blunted response to prostacyclin is due to receptor downregulation. Parallel studies of the thoracic aorta indicated that these changes are specific to the pulmonary artery. It is postulated that attenuation of the response of adenylate cyclase to prostacyclin may contribute to the structural changes and hypertension observed in the pulmonary vasculature of the rat with chronic hypoxia.
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PMID:Prostacyclin production and mediation of adenylate cyclase activity in the pulmonary artery. Alterations after prolonged hypoxia in the rat. 186 58

EDRF is a potent, endogenous vasodilator that is produced and released from endothelial cells and subsequently causes the relaxation of VSM through the activation of soluble guanylate cyclase and an increase in VSM cyclic GMP. Structurally, EDRF is likely to be NO or a related nitrogen oxide-containing compound. It is synthesized in endothelial and other cell types from L-arginine by a calcium-calmodulin and NADPH-dependent enzyme. Its action is very similar to the nitrovasodilators that act directly on VSM. EDRF is present in all vascular beds, large and small vessels, and in a wide range of species. Its role in human vascular physiology and pathophysiology is just beginning to be understood. EDRF is a potent endogenous vasodilator and inhibitor of platelet aggregation and adhesion. Its activity is impaired in hypertension and atherosclerosis, and its absence due to endothelial damage may play a role in cerebral and coronary vasospasm. It is a mediator of flow-dependent vasodilation, and its inhibition by hypoxia may contribute to the hypoxic pulmonary vasoconstrictor response. Endothelial cell damage and impairment of EDRF production may also contribute to acute and chronic pulmonary hypertension. A further understanding of the chemical nature and synthetic pathways of EDRF should lead to the production of analogs and antagonists, which may play an important role in future treatments for atherosclerosis, myocardial infarction, angina, hypertension, and other vascular diseases. The recent realization that EDRF serves as the second messenger for guanylate cyclase activation and cyclic GMP production in a variety of cell types outside of the cardiovascular system, including renal and respiratory epithelium, cerebellar neurons, macrophages, and adrenocytes, suggests even broader implications. The importance of EDRF to the anesthesiologist may go beyond an understanding of its role in cardiovascular physiological and pathophysiological states. Initial studies have shown that the endothelium may play a role in mediating the vascular actions of anesthetics, and that anesthetics can inhibit the production, release, or action of EDRF. How are these interactions mediated? Are there significant differences between anesthetics with regard to their effects on EDRF? Is there a clinically significant effect of anesthetics on basal activity of EDRF, or only in response to exogenous stimulation? Conversely, it is important to determine if alterations in endothelial cell function by various disease states such as hypertension, atherosclerosis, adult respiratory distress syndrome, cerebral vasospasm, and others cause changes in the vascular actions of anesthetics. The potential interactions of anesthetics with EDRF production and action in cell types other than the endothelium have not yet been explored.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Endothelium-derived relaxing factor: basic review and clinical implications. 186 89

Two-dimensional and Doppler echocardiographies were used to examine 102 hypertensive patients who were found to have pulmonary hypertension, whose manifestation was determined by the degree of arterial hypertension, cardiac contractile insufficiency and diminished left heart pump function. The degree of pulmonary hypertension was related to the hemodynamic type and maximal with hypokinetic circulation when the pump function of the heart was minimal. Obsidan caused a decrease in pulmonary and systemic arterial hypertension, producing higher effects with hypokinetic hemodynamics. Corinfar was demonstrated to attenuate pulmonary hypertension to a greater extent. Its action on systemic arterial hypertension was highest in patients with hyperkinetic circulation. Heterodirectional hemodynamic effects of these drugs make it expedient to study their combined action on the hemodynamic of hypertensive patients.
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PMID:[Pulmonary hemodynamics in patients with hypertension during acute drug tests using obsidan and corinfar]. 187 2

Newborn animals develop more severe hypoxic pulmonary hypertension than do adults, their vascular changes are greater, and both the hypertension and vascular changes occur more rapidly. We hypothesize that this differential developmentally controlled response may arise from either a difference in the type or quantity of endogenously secreted mediators in response to a given injury or a difference in the replicative and/or matrix-producing response of the vascular cells to physical or chemical stimuli. We investigated the effect of chronic hypoxia (14 days) on the proliferative and matrix-producing phenotype of the neonatal (14-day-old) pulmonary artery smooth muscle cell (SMC) and examined the heterogeneity and potential mechanisms responsible for this response. In situ hybridization studies demonstrated a remarkable change in the distribution of cells hybridizing with a tropoelastin cRNA probe after 14 days of hypoxia. Studies also demonstrated a population of SMC that did not hybridize with the elastin or collagen probes, indicating that the pulmonary artery contains SMC of multiple phenotypes and that the response to hypoxic and hemodynamic stress is not uniform for the various types. Bromodeoxyuridine labeling experiments indicated a large increase in DNA synthesis in hypertensive vessels, which, again, was not uniform either across or along the arterial wall. In vitro experiments with neonatal SMC suggested that hypoxia alone could not be responsible for the proliferative or matrix changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cellular adaptation during chronic neonatal hypoxic pulmonary hypertension. 192 59

In this open pilot study, the potential therapeutic efficacy of Cyclosporin A (CsA) in systemic sclerosis (scleroderma) was investigated. Eight patients with severe scleroderma (skin manifestation and at least three organ manifestations such as pulmonary, intestinal, cardiac, renal, and severe hypertension) were included in the study. CsA administration was started at a dose of 5 mg per kg body weight per day and then, to obtain whole blood levels of 300-500 ng/ml, adjusted to a mean dosage of 4.3 mg/kg/day. Therapeutic effects were evaluated by monitoring the measures of cutaneous, pulmonary, cardiac, gastrointestinal, and renal involvement as well as laboratory parameters. After 6 to 12 months of CsA-administration, cutaneous abnormalities improved in seven, arterial oxygen tension slightly increased in four, pulmonary hypertension decreased in five, and smooth muscle esophageal contraction amplitudes improved in three patients. However, the disease progressed in one patient. No serious side effects were observed, and occurring renal side effects were mild. Taken together, these observations indicate that CsA administration may be effective mainly in the skin involvement, but also in some organ manifestations of scleroderma. The results of this pilot investigation therefore indicate that a controlled study of the efficacy of CsA in scleroderma is needed and ought to be performed.
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PMID:Efficacy of cyclosporin A in systemic sclerosis. 193 87


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