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Biomedical subjects

L D Ferrell

Publications and source records attributed to L D Ferrell.

99 records · Page 6Linked to original sources
PubMed1983

Vessel wall and indium-111-labelled platelet response to carotid endarterectomy.

Postendarterectomy platelet deposition and thrombus formation may play an important role not only in vessel wall healing but also in the small incidence of postoperative cerebral ischemia and postoperative stenosis. A study has been performed using a canine model to investigate the healing response to carotid endarterectomy and the validity of an in vivo indium-111 (In-111) radiotracer technique in the assessment of postendarterectomy deposition of autologous labelled platelets. Sixteen endarterectomized carotid arteries showed uptake of autologous In-111 platelets immediately after infusion, reaching a maximum by 1 hour with little increase at 24 or 48 hours. No uptake was seen in ten control vessels following platelet infusion (P less than 0.05). At autopsy, seven vessels were demonstrated to have In-111 platelet deposition immediately prior to sacrifice of the animals. Postmortem scanning confirmed the localization to the vessel lumens, and microscopy revealed thrombus formation with or without partial endothelialization. Complete reendothelialization had occurred in the vessels that failed to show platelet deposition. Delayed healing was associated with continuing platelet deposition, excessive thrombus formation, and luminal stenosis. Arteriotomy closure with a vein patch altered the healing characteristics of the vessel with segmental thrombus formation over the vein patch. A preliminary study of the postendarterectomy in vivo In-111 platelet response in humans demonstrated platelet deposition that was not influenced by the administration of antiplatelet drugs at currently prescribed levels.

Animals↗
PubMed1982

Carotid plaque hemorrhage. Its role in production of cerebral ischemia.

A prospective study of carotid endarterectomy specimens showed an acute or recent intraplaque hemorrhage in 49 of 53 plaques (92.5%) from symptomatic patients, compared with seven of 26 plaques (27%) from nonsymptomatic patients. Luminal stenosis of greater than 50% was noted in 46 of 53 symptomatic patients (75%), 43 of whose plaques had evidence of multiple hemorrhages. Intimal disruption (ulceration) occurred over protruding mounds of intraplaque hemorrhage and was associated with retinal cholesterol emboli and prolonged neurologic deficits. Mural recesses with the angiographic appearance of ulceration seldom showed intimal breakdown. Eighteen patients continued to have symptoms while receiving aspirin, 13 of whom had had multiple intraplaque hemorrhages. Angioneogenesis occurred within the plaques in response to hemorrhage, creating vascular lesions vulnerable to mechanical stress and capable of producing further hemorrhage or intimal disruption.

Animals↗
PubMed1982

Transient ischaemic attacks: the static and dynamic morphology of the carotid artery bifurcation.

Studies evaluating the static and dynamic characteristics of the common carotid bifurcation are described. Slow motion angiographic frames, real time B-mode images and time position M-mode tracings have demonstrated appreciable vessel wall motion with an increase in distensibility at the carotid bulb compared to the proximal common carotid artery. Histopathological studies suggest that changes in the carotid artery elastin and collagen structure may contribute to the increased distensibility at the carotid bulb. The presence or absence of a cervical bruit did not correlate with the ultrasonic demonstration of plaque or blood flow turbulence. Mechanical factors relating to the development of symptoms of cerebral ischaemia are discussed.

Auscultation↗
PubMedDate not supplied

Histopathologic study of stenotic and occluded transjugular intrahepatic portosystemic shunts.

PURPOSE: A detailed histopathologic analysis of three stenotic and two occluded transjugular intrahepatic portosystemic shunts was performed to evaluate the nature and cause of each shunt abnormality. PATIENTS AND METHODS: The study group consists of five patients who developed a shunt stenosis or occlusion and subsequently underwent liver transplantation or autopsy. Shunt specimens were examined grossly and microscopically. RESULTS: The pseudointima was composed of granulation tissue, which was generally denser and more cellular near the luminal surface. Pseudointima was thicker in the parenchymal portion of the shunt than at the venous ends. A contiguous single layer of endothelial-like cells lined the majority of the luminal surface of each shunt. Scattered debris and clot covered 10%-15% of the luminal surfaces. Transected bile ducts were noted in three cases. Bile staining was detected around the transected ducts, and bile pigment was incorporated into the developing pseudointima. CONCLUSIONS: Pseudointimal hyperplasia appears to be the causative lesion in these obstructions. An inflammatory reaction incited by bile extravasation may have contributed to pseudointimal proliferation in three cases.

Adult↗
PubMedDate not supplied

Utility of CD34 reactivity in evaluating focal nodular hepatocellular lesions sampled by fine needle aspiration biopsy.

OBJECTIVE: To determine the patterns of CD34 reactivity in hepatocellular adenoma and focal nodular hyperplasia and to evaluate the utility of CD34 reactivity in the diagnosis of hepatocellular carcinoma. STUDY DESIGN: Seventeen cases of well-differentiated hepatocellular carcinoma, 14 cases of cirrhosis, 9 cases of focal nodular hyperplasia and 7 cases of hepatocellular adenoma were stained with immunoperoxidase antibodies to CD34. The slides were scored according to the degree of lesional reactivity. RESULTS: Fourteen of 17 cell blocks with hepatocellular carcinoma showed unequivocal sinusoidal or peripheral reactivity for CD34. Five of seven cases of hepatocellular adenoma and four of nine cases of focal nodular hyperplasia showed > 50% sinusoidal reactivity for CD34. All 14 cases of cirrhosis showed peripheral to no sinusoidal reactivity. CONCLUSION: CD34 reactivity in a diffuse sinusoidal pattern can be helpful in the diagnosis of hepatocellular carcinoma. However, consideration should be given to the possibility of hepatocellular adenoma and focal nodular hyperplasia, which can also exhibit significant diffuse CD34 reactivity. In these cases, a reticulin stain may be helpful with the differential diagnosis.

Adenoma, Liver Cell↗
PubMedDate not supplied

Myospherulosis of the breast. Diagnosis by fine needle aspiration.

A case of myospherulosis of the breast diagnosed by fine needle aspiration biopsy is reported. The characteristic spherules and "endobodies" stained red by the Papanicolaou stain and brown by the Wright stain. In this case, human fat may have been an endogenous inducing agent for the spherule formation from erythrocyte products.

Adult↗
PubMedDate not supplied

Effect of hypergastrinemia and blockade of gastrin-receptors on pancreatic growth in the mouse.

BACKGROUND/AIM: The present study evaluates whether endogenous gastrin regulates pancreatic growth in the mouse. MATERIALS AND METHODS: Male NMRI mice weighing 12-15 g were assigned to six groups (10 mice/group) which were treated with different combinations of 0.9% NaCl, omeprazole, a CCK-A antagonist, a CCK-B antagonist, loxiglumide, and L365, 260 for 10 days each according to different protocols. RESULTS: Omeprazole caused a marked, 10-fold increase in serum gastrin which was not affected by the gastrin antagonist, but markedly reduced by the CCK-A antagonist. The marked increase in endogenous gastrin caused by omeprazole did not promote pancreatic growth in any way. Similarly, the gastrin antagonist did not inhibit pancreatic growth. In contrast, the CCK-A antagonist significantly decreased pancreatic weight and protein content. CONCLUSIONS: The present results strongly suggest that endogenous gastrin--in contrast to CCK--does not regulate pancreatic growth in the mouse. The inhibitory effect of loxiglumide on omeprazole-induced increase in serum gastrin might be explained by recent findings which showed that CCK-A antagonists can stimulate gastric acid secretion probably due to a reduction of the inhibitory effect of basal CCK on the D-cell and its somatostatin release. Probably such a slight stimulation of gastric acid secretion caused by the CCK-A antagonist might reduce the gastrin increase caused by omeprazole's abolishment of acid secretion.

Animals↗