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349 results on '"Haworth, S. G."'

25. Newborn intrapulmonary veins are more reactive than arteries in normal and hypertensive piglets

Author

ARRIGONI, F. I., HISLOP, A. A., HAWORTH, S. G., and MITCHELL, J. A.

Subjects
Pulmonary veins -- Physiological aspects, Acetylcholine -- Research, Hypoxia -- Research, Biological sciences
Abstract

Arrigoni, F. I., A. A. Hislop, S. G. Haworth, and J. A. Mitchell. Newborn intrapulmonary veins are more reactive than arteries in normal and hypertensive piglets. Am. J. Physiol. 277 (Lung Cell. Mol. Physiol. 21): L887-L892, 1999.--The reactivity of pulmonary veins during adaptation from pre- to postnatal life is not well characterized. With an in vitro organ bath technique, the responses to the contractile and relaxant agonists U-46619 ([10.sup.-10] to 3 x [10.sup.-6] M) and acetylcholine ([10.sup.-9] to [10.sup.-4] M) were compared in adjacent conduit pulmonary vein and artery rings from 66 piglets aged 1 wk preterm to 14 days of postnatal life and from adult tissue. Five additional piglets were made hypertensive by exposure to chronic hypoxia for 3 days after birth. Both arteries and veins showed smaller contractile and relaxant responses before birth than after. By 5 min after birth, the contraction by arteries and relaxation by veins had increased (P [is less than] 0.05). By 3 days of age, arterial relaxation increased, but in all animals, venous relaxation exceeded that in arteries (P [is less than] 0.05). Veins contracted more than arteries in animals aged 3-14 days. Neonatal hypoxia diminished the responses to both agonists in the veins (P [is less than] 0.05), whereas the response in the arteries remained similar to that in the normal newborn. We speculate that veins may be more important in postnatal adaptation than previously suggested. development; U-46619; hypoxia; acetylcholine

Published
1999

26. Pulmonary Hypertension - ECAB

Author

Kumar, R. Krishna, Haworth, S. G., Arif, Ehtesham, Kumar, R. Krishna, Haworth, S. G., and Arif, Ehtesham

Subjects
Pulmonary hypertension
Abstract

Pulmonary hypertension is defined as a mean pulmonary artery pressure (mPAP) ≥25 mmHg, with Pulmonary Capillary Wedge Pressure ≤ 15 mmHg, measured by cardiac catheterization. The etiology of PH has a varied spectrum extending right from Drugs, toxins and portal hypertension to HIV, Collagen Vascular Diseases and Persistent Pulmonary Hypertension of Newborn, etc. The estimation of disease prevalence has been nearly impossible owing to the geographic distribution and economic diversity, along with significant regional variations in human development and healthcare infrastructure. A large number of patients with PH never reach the health centers capable of diagnosing the disease condition correctly. Advance pulmonary vascular disease as a result of uncorrected CHD is a major health challenge in the developing world. PH exists as a major component of many forms of cardiac and pulmonary disease. While breathlessness is the most common feature of PH, patients often also present with chest pain, syncope, fatigue, weakness and abdominal distension. The precordial signs include a right ventricular lift, accentuated pulmonary component of S2, a pansystolic murmur of Tricuspid regurgitation, a diastolic murmur of pulmonary regurgitation and a right ventricular S3. The standard diagnostic workup in developed countries includes a series of investigations to rule out the secondary causes. Additional tests are required to estimate the disease severity and plan the appropriate treatment. These include the cardiac catheterization, selective pulmonary angiography by direct injection of pulmonary arteries, high resolution CT scan, cardiac magnetic resonance, ABGs, nocturnal O2 saturation, etc. While most of the basic management is feasible in the Indian conditions, most of the newly introduced drugs are either not available or are available at costs that far exceed the paying capacity of an average citizen of a developing economy. An underdeveloped health insurance system adds further to the financial burden of the treatment. Measures like formulation of guidelines for diagnosis and treatment of PAH, educating clinicians and scientists and making medications affordable to poor patients might ensue a breakthrough in the overall management of pulmonary hypertension.

Published
2009

27. Vasodilatation of intrapulmonary arteries to P2-receptor nucleotides in normal and pulmonary hypertensive newborn piglets

Author

McMillan, M R, Burnstock, G, and Haworth, S G

Subjects
Vasodilation, Organ Culture Techniques, Animals, Newborn, Adenine Nucleotides, Receptors, Purinergic P2, Swine, Hypertension, Pulmonary, Papers, Animals, Uridine Triphosphate, Pulmonary Artery
Abstract

1. The vasodilator responses of isolated intrapulmonary arteries (IPA) to P2-receptor agonists were investigated during adaptation to extrauterine life in the piglet. The effect of pulmonary hypertension on the normal response was determined after exposing newborn animals to chronic hypobaric hypoxia (51 kPa) for 3 days. 2. Adenosine 5'-triphosphate (ATP), 2-methylthioATP (2-meSATP), adenosine 5-O-(2-thiodiphos-phate) (ADPbetaS) and uridine 5'-triphosphate (UTP) induced a relaxation in normal newborn piglet IPA pre-contracted with prostaglandin F2alpha (PGF2alpha). The relaxations were not affected by removal of the endothelium. The responses to ATP and ADPbetaS increased significantly with age. 3. The relaxation responses of IPA to ATP, 2-meSATP and ADPbetaS continued to increase normally after birth in an hypoxic environment. 4. The results of the study show that vasodilatation of porcine intrapulmonary vessels to nucleotides increased during development from foetus to adult; that the vasodilatation to purines was mediated by P2Y-receptors on the vascular smooth muscle rather than on the endothelium; and that the P2Y-receptor mediated relaxation of IPA remained normal in the pulmonary hypertensive neonate.

Published
1999

36. Changes in pulmonary circulation in severe bronchopulmonary dysplasia

Author

Bush, A, Busst, C M, Knight, W B, Hislop, A A, Haworth, S G, and Shinebourne, E A

Subjects
Research Article
Abstract

Eight patients with severe bronchopulmonary dysplasia underwent cardiac catheterisation. Seven had a pulmonary vascular resistance greater than 3 mm Hg.l-1 min.m2 (mean 8.9, range 2.2-13.8). All had raised intrapulmonary shunts (mean 25.6%, range 5.4-50%, normal less than 5%). Two had a high alveolar dead space, and two had unsuspected congenital heart disease. Epoprostenol (prostacyclin), but not 100% oxygen, caused a significant fall in pulmonary vascular resistance. Death was associated with a high pulmonary vascular resistance and a high shunt. Morphometric studies in three cases showed normal numbers of airways, but increased thickness of bronchial muscle. The numbers of alveoli were reduced and the walls thickened. There was increased medial thickness in small pulmonary arteries with distal extension of muscle. In the oldest child some vessels were obliterated by fibrosis. We speculate that measurements of pulmonary vascular resistance and shunt may have prognostic value; that a trial of pulmonary vasodilators other than oxygen might be worthwhile in patients with poor prognosis; and that abnormalities of the pulmonary circulation contribute to the difficulties of managing patients with bronchopulmonary dysplasia.

Published
1990

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