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Biomedical subjects

N Woolf

Publications and source records attributed to N Woolf.

At least 37 records · Page 2Linked to original sources
PubMed1988

Effects of autologous mesothelial cell seeding on prostacyclin production within Dacron arterial prostheses.

Canine abdominal aortas have been replaced with Dacron arterial prostheses to assess the effects of mesothelial cell seeding on graft prostacyclin and thromboxane A2 release. At both 2 weeks and 6 weeks after surgery, three seeded and two unseeded control grafts were examined for prostacyclin release. In addition, thromboxane release was assessed in one seeded and one unseeded graft. Sections of aorta and graft were removed and incubated in PBS containing either 10 microM calcium ionophore A23187 or 20 microM arachidonic acid. The incubation mixture was sub-sampled at 5 min intervals over a 20 min period to assess the progressive release of prostacyclin and thromboxane A2 using a radioimmunoassay for 6-keto-prostaglandin F1 alpha and thromboxane B2 respectively. In seeded grafts, 6-keto-prostaglandin F1 alpha release averaged 15 per cent compared with aorta at 2 weeks and 45 per cent compared with aorta at 6 weeks. By contrast, release from unseeded grafts was undetectable at 2 weeks; however, by 6 weeks there was some release amounting to 15 per cent compared with aorta. There was a statistically significant increase in the release of 6-keto-prostaglandin F1 alpha from mesothelial cell seeded grafts at 6 weeks compared with unseeded grafts (P less than 0.01). Thromboxane release from the graft sections was variable and unrelated to whether the grafts had been seeded or not. These preliminary results, showing that grafts seeded with autologous peritoneal mesothelial cells release more prostacyclin than unseeded grafts, further highlight the role of the mesothelial cell as an alternative to the endothelial cell for improving the patency of arterial Dacron prostheses in the early postoperative days.

Animals↗
PubMed1988

Morphology of the endothelium over atherosclerotic plaques in human coronary arteries.

The right coronary arteries of six hearts removed from patients with atherosclerosis, who were undergoing cardiac transplantation, were perfused with 2% buffered glutaraldehyde for 20 minutes before preparation for scanning electron microscopy. Perfusion was started within five minutes of explanation. In two patients the artery was angiographically normal, in one it was irregular in outline, and three had focal segments with significant stenosis. None of the patients had concentrations of plasma lipids above 5.5 mmol/l. The endothelial surface showed widespread focal abnormalities ranging from adhesion and migration of monocytes to loss of individual endothelial cells. Larger areas of endothelial denudation with exposure of underlying collagen were also seen consistently. Loss of endothelial cells was associated with accumulation of monocytes, on and deep to the surface, as well as adhesion of platelets to the exposed subendothelial tissue. These results accord with the endothelial damage and platelet adhesion seen in hyperlipidaemic animals fed a high lipid diet.

Blood Platelets↗
PubMed1988

Interaction of lipoproteins with the artery wall.

Atherosclerosis can be defined in terms of the processes involved rather than in morphological terms, and there is evidence for possible roles of the macrophage in atherogenesis. The relevance of hyperlipidaemia to the morphogenesis of the atherosclerotic plaque is important, and this has been described in animal models including a strain of rabbit with a genetically determined hyperlipidaemia resembling familial combined hyperlipidaemia. Treatment of these animals with the HMG CoA reductase inhibitor lovastatin from the time of weaning results in a significant degree of inhibition of lesion formation.

Animals↗
PubMed1988

The effect of nicotine on human endothelial cell release of prostaglandins and ultrastructure.

The acute and sub-acute effects of nicotine at concentrations between 10(-9)M and 10(-2)M on human umbilical vein endothelial cell release of prostacyclin and prostaglandin E2 and the sub-acute effect on the endothelial cell ultrastructure have been examined. The acute effect of nicotine on prostaglandin release has been assessed by measuring release of prostacyclin and prostaglandin E2 following stimulation of confluent monolayers of endothelial cells with A23187 in the presence of nicotine. The sub-acute effect has been assessed by measuring A23187 stimulated release of prostacyclin and prostaglandin E2 from endothelial cells grown to confluence in the presence of nicotine. The cell monolayers were also examined for morphological and ultrastructural changes using light and electron microscopy. Nicotine treated and untreated cells released minimal amounts of prostaglandin E2. Concentrations of nicotine between 10(-9)M and 10(-4)M did not inhibit release of prostacyclin or induce morphological changes. Acute exposure to 10(-3)M nicotine resulted in a statistically significant inhibition of prostacyclin release, however, sub-acute exposure did not inhibit prostaglandin release or effect the cell morphology. Acute and sub-acute exposure to 10(-2)M nicotine resulted in a statistically significant inhibition of prostacyclin release. This was accompanied by the appearance of large translucent cytoplasmic inclusions which did not appear to be lipid rich as indicated by the negative uptake of oil-red-O and osmium tetroxide. This study shows that concentrations of nicotine comparable to the plasma levels of smokers (10(-9)-10(-6)M) do not induce morphological changes or effect the release of endothelial prostaglandins.

Calcimycin↗
PubMed1988

Epinephrine-induced cytotoxicity of rat plasma. Its effects on isolated cardiac myocytes.

The plasma from rats injected with epinephrine (5 mg/kg) (epinephrine plasma) was found to be cytotoxic when incubated with isolated heart cells. This cytotoxicity was apparent 60 minutes after the start of the incubation due to the appearance at this time of membrane microblebs and microvilli as seen by scanning electron microscopy and the start of a fall in intracellular concentrations of ATP. The membrane blebs increased in size with time and the cells became contracted. Incubation of the cells for 90 minutes with epinephrine plasma, caused an increase in permeability of plasma membrane to 86Rb+. Incubation with alpha-tocopherol prevent this change. After 180 minutes incubation, these cells no longer retained carboxyfluorescein indicating that extensive membrane damage had occurred. It has been suggested that the presence of membrane blebs are evidence that lipid peroxidation is occurring in the cell membrane. Accordingly, glutathione, which is used by the cell against free radical attack and membrane lipid peroxidation, was measured. Glutathione levels started to fall after 60 minutes incubation, the time when the ultrastructural cell membrane changes started to occur. Pretreatment of cells with 100 microM 1,3-bis(2-chloroethyl)-1-nitrosourea which inhibits glutathione reductase, before the addition of plasma, increased the sensitivity of these cells to the epinephrine plasma, as measured by fall in intracellular ATP. Cells treated with control plasma did not show the changes described above. The nature of the cytotoxic factor in the plasma is still unknown, although the evidence presented suggests that a free radical may be involved.

Adenosine Triphosphate↗
PubMed1987

Dysplasia of the colon after jejuno-ileal bypass.

Colonoscopic biopsies were performed on 38 patients, 10-13 years after jejuno-ileal bypass. No significant dysplasia or premalignant change was seen in 371 biopsies. In one patient two tubulovillous adenomata were found in an otherwise normal colon, which is likely to be a chance finding. Although it will take another 10-20 years to establish whether jejuno-ileal bypass is associated with an increased risk of large bowel cancer in humans, there is at present no indication for regular colonoscopic surveillance.

Colon↗
PubMed1987

The pathology of atherosclerosis with particular reference to the effects of hyperlipidaemia.

A brief description has been given of the major processes involved in the genesis of atherosclerosis, and of the morphological features of fatty streaks, gelatinous elevations and fibrolipid plaques. The effects of hyperlipidaemia, genetically and dietarily determined, are described, with special reference to the possible role of macrophages in the development of arterial lesions caused by such hyperlipidaemias. The administration of a competitive inhibitor of HMG-CoA reductase (lovastatin) to genetically hyperlipidaemic rabbits markedly reduced the extent of intimal surface involvement by lipid-rich lesions.

Animals↗
PubMed1985

The effects of nicotine on PGI2 production by rat aortic endothelium.

The production of prostacyclin by rat aortic rings was measured following administration of nicotine by a single subcutaneous injection and after continuous subcutaneous infusion over 7 days. Single subcutaneous injections of nicotine at 1, 5, 10 or 20 mg/kg had no effect on prostacyclin production by rat aortic rings in comparison with controls. However, aortic rings obtained after 7 days continuous subcutaneous infusion of 0.54 g/ml of nicotine at the rate of 1 microliter per hour produced significantly less prostacyclin than control animals.

Animals↗
PubMed1985

The correlation between catecholamine and lipid peroxidation induced damage in heart cells.

Cardiocytes incubated with isoprenaline plasma showed an initial rise in the intracellular ATP levels followed by a steady fall; after two hours the ATP levels of the cells treated with the plasma were less than half that of the control cells. This fall in intracellular ATP was accompanied by morphological changes, in particular the formation of both large and small membrane blebs.

Adenosine Triphosphate↗
PubMed1985

Cigarette smoke-induced injury of peritoneal mesothelial cells.

Cultured rat peritoneal mesothelial cells have been exposed to plasma obtained from healthy adult male volunteers before and after the smoking of two medium-tar cigarettes. The pre-smoking plasma had little effect on the mesothelial cells as observed by scanning electron microscopy. Post-smoking plasma produced extensive cellular damage evidenced by the production of blebs and microvillus-like structures on the cell surface. Some cells were also found to have a perforated luminal membrane. These results suggest that factors cytotoxic for these cells are present in plasma following exposure of humans to cigarette smoke.

Adult↗
PubMed1984

The mesothelial cell as a non-thrombogenic surface.

A technique for harvesting mesothelial cells is described. This entails collagenase digestion of omentum after which the cells can be cultured. The technique has been developed using the rat, but has also been successfully applied to human tissue. Cultured rat mesothelial cells obtained in this way have been examined by scanning electron microscopy. Rat mesothelial cells grown on plastic film have been exposed to blood in an in vitro system using a Baumgartner chamber and have been demonstrated to support blood flow. No adhering platelets were observed on the mesothelial cell surface. Fibroblasts similarly exposed to blood as a control were washed off the plastic.

Animals↗
PubMed1984

A study of the possible role of mesothelium as a surface for flowing blood.

Mouse mesothelium has been examined as a surface for supporting blood flow. We have examined ten pieces of intact mesothelium and ten pieces of damaged mesothelium following 10 min exposure to flowing blood in a Baumgartner chamber. Scanning electron microscopy of the intact specimens demonstrated no adhering blood platelets, whereas the damaged specimens were found to be covered with large numbers of adhering platelets. In addition we have demonstrated that undamaged mesothelium does not appear to be morphologically altered after exposure to blood, and that undamaged mesothelium produces significantly more prostacyclin than damaged control. These findings support that mesothelial cells hold promise as a lining for prosthetic vascular implants.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Seeding Dacron arterial prostheses with peritoneal mesothelial cells: a preliminary morphological study.

A preliminary laboratory study has been undertaken using dogs, in which porous Dacron arterial prostheses have been seeded with autologous peritoneal mesothelial cells before implantation into the arterial system. These cells were harvested from omentum by collagenase digestion and were introduced into the graft at the time of preclotting. Examination of the grafts by scanning and transmission electron microscopy one month after insertion showed no organized cellular lining in the control graft. In three seeded grafts there was a lining of mesothelial cells which extended over the whole surface of the grafts up to 1 cm from the suture lines. Selected areas of the grafts have been analysed morphometrically. In the seeded grafts there is a cellular layer which on average covers 94 per cent of the luminal surface. These results suggest that mesothelial cells, which both secrete prostacyclin and possess fibrinolytic activity, present a possible alternative to endothelium as a cellular lining for prosthetic grafts.

Animals↗
PubMed1984

Cigarette smoking and platelet adhesion.

Non-abraded rabbit endothelium has been exposed to human blood taken from male non-smoking volunteers before and after the smoking of two medium tar cigarettes, in an in vitro system using a Baumgartner chamber. In each case the blood was allowed to circulate for 10 min at a constant flow rate. Blood from 10 volunteers has been tested in this way. Scanning electron microscopy of the endothelial surfaces demonstrates large numbers of adherent platelets when 'post-smoking blood' is used, but very few and in some cases none with the 'pre-smoking' blood. As a further control to ensure that this phenomenon did not occur as a result from changes in the vessel related to the time during which it had been removed from its normal physiological environment, blood from further non-smoking volunteers was passed over seven of the remaining pieces of vessel at the completion of these runs. Platelets were either absent or very few in number, as with the pre-smoking samples.

Animals↗
PubMed1984

The early changes induced by isoproterenol in the endocardium and adjacent myocardium.

The acute phase of isoproterenol cardiotoxicity in the rat heart was studied by both scanning and transmission electron microscopy. The endocardium and immediate adjacent myocardium of the left ventricle and septum were chosen for examination because this area should be less affected by myocardial underperfusion. The initial damage, which was mainly to the endocardium, was well defined by 30 minutes; this damage consisted of endocardial cell contraction and separation with activated platelets adhering to the exposed subendocardium. Myocardial cell changes were present at 1 hour and always included those cells adjacent to the endocardium; frequently the damage did not extend to involve the deeper tissue layers. Polymorphonuclear leukocytes were present but not in large numbers before three hours. These results suggest that myocardial ischemia due to the action of isoproterenol is not a major factor in isoproterenol cardiotoxicity.

Animals↗