The role of dietary phytate in the pathogenesis of nutritional osteomalacia.
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Adolescent↗
Biomedical subjects
R Mathew
Publications and source records attributed to R Mathew.
The significance of right aortic arch in D-transposition of the great arteries.
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Aorta, Thoracic↗
Collateral circulation in coarctation of aorta in infancy and childhood.
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Age Factors↗
Polymer-supported tetrafluorophenol: a new activated resin for chemical library synthesis.
A new tetrafluorophenol activated resin that facilitates the use of 19F NMR to quantitate loading is presented. This new resin provides a useful tool for acylation, and a novel activated polymeric sulfonate ester to generate sulfonamides. This activated resin reacts with a wide scope of N-nucleophiles including primary and secondary amines, and anilines. This new activated resin methodology provides a powerful tool for pure single-compound library synthesis.
Journal Article↗
Effect of verapamil on monocrotaline-induced pulmonary artery hypertension and endothelial cell dysfunction in rats.
Verapamil, a calcium channel blocker has been used with partial success in cases of primary pulmonary hypertension, as well as to reduce hypoxia-induced pulmonary hypertension (PH) in rats. However, its effect on monocrotaline (MCT)-induced PH in rats is not known. We studied the effect of verapamil on MCT-induced PH. Three weeks after a single injection of MCT, significant PH was noted in the MCT-injected rats compared with control (44.35 +/- 3.5 vs. 22 +/- 2.5 mmHg). MCT-injected rats on daily verapamil showed significant reduction in PH (31.5 +/- 3.4 mmHg). The main pulmonary artery of MCT-injected rats revealed subendothelial thickening, thinning and fragmentation of elastic laminae, smooth muscle cell hypertrophy and necrosis or loss of smooth muscle cells, and increased amounts of collagen in media and adventitia. In contrast, the main pulmonary artery of MCT + VP-treated rats showed less intimal thickening, some smooth muscle cell hypertrophy, but little necrosis or loss of cells in addition to disappearance of outer elastic laminae. Smaller pulmonary arteries (less than 150 microns in diameter) in MCT + VP-treated rats showed less medial thickening than MCT groups. However, diminished lung angiotensin-converting enzyme activity suggestive of endothelial cell dysfunction was noted in both MCT and MCT + VP-treated rats. This study indicates that verapamil attenuates MCT-induced PH, but has no effect on pulmonary endothelial cell dysfunction.
Animals↗
Coronary stenting in diabetics: six months clinical and angiographic outcome.
The aim of this study was to assess the clinical and angiographic outcome of coronary stenting in diabetics as compared to non-diabetic patients. A total of 114 patients undergoing coronary angioplasty with stenting were prospectively evaluated. There were 30 diabetic (group A) and 84 non-diabetic (group B) patients. There were no significant differences in both the groups with respect to other risk factors and clinical characteristics. Both the groups were also comparable in terms of lesion morphology and stent types. The clinical endpoints were recurrent angina, reinfarction, cardiac death and need for target vessel revascularisation. The angiographic endpoint was angiographic restenosis at six months. There were 70 males and 44 female patients with a mean age of 55 +/- 12 years. Angiographic follow-up was completed in 85 (74.7%) patients which included 25 (83.3%) patients in group A and 60 (71.4%) in group B. Among clinical events at 30 days, the incidence of recurrent angina was 10.0 percent versus 8.3 percent (group A and B; p = NS) and incidence of reinfarction was 6.6 percent versus 5.9 percent (group A and B; p = NS), respectively. At six months, recurrent angina was seen in 16.6 percent versus 15.4 percent (p = NS) and reinfarction was seen in 10.0 percent versus 8.3 percent (p = NS) in group A and B, respectively. There were no deaths in either group. The angiographic restenosis rate was significantly higher in diabetics compared to non-diabetics (40.0% vs 23.3%; p = 0.02). The need for target vessel revascularisation was higher in diabetics as compared to non-diabetics (16.0% vs 6.6%; p = 0.03). We conclude that in spite of using coronary stents, the diabetics have higher restenosis rate and higher target vessel revascularisation rate than the non-diabetic patients.
Aged↗
Monocrotaline induces interleukin-6 mRNA expression in rat lungs.
Monocrotaline-induced pulmonary hypertension (PH) in rats is preceded by an inflammatory response in the lungs, and interleukin-6 (IL-6) is expressed in response to inflammation. To evaluate the role of IL-6 in monocrotaline-induced PH, rats received a single subcutaneous injection of monocrotaline (60 mg/kg) or an equivalent amount of normal saline. Pulmonary artery pressure (Ppa), right ventricular hypertrophy (RVH), expression of IL-6 mRNA, and bioactivity of IL-6 in the lungs of these rats were examined 48 hours and 1 and 2 weeks after administration of monocrotaline. The effects of dexamethasone treatment on monocrotaline-induced PH also were evaluated. Two weeks after administration of monocrotaline, significant PH and RVH developed in these rats. Reverse transcription-polymerase chain reaction (RT-PCR) revealed expression of IL-6 mRNA in the lungs 48 hours and 1 and 2 weeks after administration of monocrotaline. This was confirmed using ribonuclease protection assay. The bioactivity of IL-6 in lung extracts progressively increased. Dexamethasone markedly inhibited expression of IL-6 mRNA and IL-6 bioactivity in the lungs, with concomitant attenuation of monocrotaline-induced PH and RVH. Our data show that monocrotaline induces expression of IL-6 mRNA in rat lungs and that inhibition of IL-6 results in attenuation of PH. These findings indicate that IL-6 may play a role in the pathogenesis of PH.
Analysis of Variance↗
Pulmonary hypertension in infancy and childhood.
Abnormalities of pulmonary artery pressure and resistance continue to complicate many varieties of cardiovascular problems in childhood. Much recent effort has been devoted to understanding the cellular mechanisms underlying the pathophysiology of pulmonary hypertension, centering on endothelial cell dysfunction as a principal factor. Defects in the vasodilation machinery of the endothelial cell, such as overexpression of vasoconstrictor elements, have been implicated in various forms of pulmonary hypertension. This includes pulmonary hypertension that is secondary to congenital heart disease, and the primary forms that occur in older children and in neonates. In addition, experimental methods assessing cyclic adenosine monophosphate-mediated and cyclic guanosine monophosphate-mediated vasoreactivity suggest a possible genetic basis in the responses of the pulmonary microvasculature. This article reviews some of the current information that has been developed along these lines, and explores the implications of these data for therapeutic strategies to treat this complex problem.
Child↗
The role of magnesium in lung diseases: asthma, allergy and pulmonary hypertension.
Magnesium is the fourth most abundant metal found in the body. It plays a crucial role in numerous biological processes. It is a natural calcium blocker. It can block or compete with Ca2+ at voltage-dependent, receptor- or leak-operated channels and result in translocation of intracellular Ca2+. Mg2+ inhibits Ca2+ release from the sarcoplasmic reticulum. Intracellular Mg2+ is thought to modulate smooth muscle contractions and the rate of relaxation. Mg2+ is a cofactor of numerous enzymes and is coupled with cellular use of phosphate as an activator and energy source. cAMP-dependent protein and adenylate cyclase are among many enzymes that require Mg2+ for their function. Mg2+ has been used successfully in treating asthma. There is experimental evidence that Mg2+ is required for various immune responses, and in rats, Mg2+ treatment has been shown to attenuate chemically induced pulmonary hypertension. It is not clear if Mg2+ deficiency plays a role in development of some of these diseases, but Mg2+ salts appear to have therapeutic value and certainly it has a role as an adjunct to traditional therapy in various lung diseases.
Animals↗
Physiology and pathophysiology of pulmonary circulation.
The lungs provide not only respiratory function, but also are involved in metabolism and maintaining homeostasis. The lungs receive the entire cardiac output, circulating blood cells and hormones. The metabolically active vascular endothelial cell lining participates in degrading and synthesizing various hormones and vasoactive substances which affect the pulmonary as well as systemic circulation. The normal state is maintained through complex interaction of the circulating hormones, maturation of the system, the physiological state of the lung cells and metabolism. Any noxious stimulus can disrupt this delicate balance and adversely affect the metabolism of various substances, thus producing an abnormal state. In this review, some of these factors including therapeutic implications are discussed.
Animals↗
Pulmonary vasculature in monocrotaline-induced hypertensive rats on magnesium therapy.
We have previously demonstrated that magnesium therapy attenuates monocrotaline-induced pulmonary hypertension and right ventricular hypertrophy in rats. In this report we evaluate the effect of oral magnesium therapy on the pulmonary vasculature of monocrotaline-treated rats. Lung sections were prepared for light microscopic examination, and the medial wall thickness of pulmonary arteries of less than 100 microns in diameter was measured. The mean medial wall thickness of control rats was 6.98 +/- 1.16% of the external diameter of the pulmonary artery, the monocrotaline group had a significant increase in medial wall thickness (14.61 +/- 1.52%, p less than 0.005 vs control); in contrast 75% of MCT + magnesium group revealed a significant reduction in medial wall thickness (8.13 +/- 1.26%, p less than 0.02, vs monocrotaline group). Magnesium therapy alone had no effects on pulmonary vasculature. We conclude that magnesium has significant beneficial effects on monocrotaline-induced pulmonary hypertension and the accompanying vascular lesions.
Animals↗
Coronary artery stenting in acute myocardial infarction.
Little information is available on the use of coronary stents to treat suboptimal results during direct angioplasty in acute myocardial infarction (AMI). In this study, we report 16 cases of AMI who underwent stent implantation in infarct-related artery for suboptimal results and their 6 months angiographic follow-up. Immediate angiographic success was achieved in all patients. The minimal luminal diameter increased from 0.06 +/- 0.12 mm to 2.89 +/- 0.12 mm (p < 0.001). One patient died in the hospital on day 8 due to subacute stent thrombosis. No patient required emergency bypass surgery. Two patients required blood transfusion for groin haematoma and one required intracoronary thrombolysis. All patients underwent exercise stress test at 1 month and at 3 months and coronary angiography at 4 months or earlier it indicated. At the end of 6 months follow-up, 4 patients had a positive exercise test and coronary angiography revealed angiographic restenosis in 3 and progression of disease in other vessels in 1 patient. We conclude that stent deployment is a viable option to treat suboptimal results after direct angioplasty in AMI.
Adult↗
Adenosine-induced chest pain: is it due to myocardial ischaemia? Clinical, electrocardiographic, haemodynamic and metabolic study.
Adenosine has recently been demonstrated to be a mediator of angina in human beings. The present study was undertaken to document the presence or absence of myocardial ischaemia on clinical, haemodynamic, electrocardiographic and metabolic evidences after intracoronary administration of adenosine. Fifteen patients with chronic stable angina (12 males and 3 females), positive exercise stress test and documented significant stenosis of the left anterior descending coronary artery (LAD) were included in the study. The surface and intracoronary electrocardiograms (ECGs), pulmonary artery diastolic pressure and coronary sinus lactate levels were monitored at baseline and after intracoronary administration of adenosine in all patients. Adenosine was administered intracoronary in doses of 1000-8000 microgram depending on the provocation of chest pain. Typical angina was observed in all patients. There were no signs of ischaemia on surface or intracoronary ECG. There was no statistically significant difference between the pulmonary artery diastolic pressure and coronary sins lactate levels at baseline and post-adenosine administration (p > 0.05). It is concluded that intracoronary administration of adenosine produces chest pain in patients with chronic stable angina by mechanism other than myocardial ischaemia.
Adenosine↗
Thrombotic complications during coronary angiography associated with use of non-ionic contrast media.
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Adult↗