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Biomedical subjects

J C Keith

Publications and source records attributed to J C Keith.

72 records · Page 4Linked to original sources
PubMed1984

The valium project: diagnostic restrictions as a utilization control in a Medicaid drug program.

This study examines the effectiveness of diagnosis restrictions as a drug utilization control in California's Medi-Cal (Medicaid) program. The numbers of Valium prescriptions dispensed, the numbers of Medi-Cal beneficiaries using Valium and the expenditures represented by those prescriptions were measured during application of a diagnosis restriction for a 33-month base period, followed by removal of the diagnosis restriction for a 14-month period.

California↗
PubMed1984

An aspirin-prednisolone combination to modify postadulticide lung disease in heartworm-infected dogs.

A combination of aspirin and prednisolone was used in an attempt to modify the pulmonary disease produced by thiacetarsamide treatment of heartworm-infected dogs. Results of 6 heartworm-infected dogs treated with prednisolone (1 mg/kg, daily for 4 weeks) and aspirin (10 mg/kg, daily for 4 weeks) after thiacetarsamide treatment were compared with previously published results of 3 groups of dogs (6 dogs/group). One of these 3 groups was a nontreated control group, another was treated with prednisolone, and the 3rd was treated with aspirin. All dogs, each with 9 adult heartworms transplanted, were treated with a 2-day, twice-a-day treatment of thiacetarsamide (1 mg/kg) 4 weeks after the transplant. Thoracic radiographs were taken before and at 1, 2, and 3 weeks after thiacetarsamide treatment to evaluate lung disease. Pulmonary arteriography was performed before and 3.5 weeks after thiacetarsamide treatment to evaluate pulmonary blood flow. After treatment, radiographs of the aspirin-prednisolone group were similar to radiographs of the prednisolone group, both with a marked attenuation of the parenchymal disease, as compared with the non-treated group. Addition of aspirin to prednisolone prevented the blood flow obstruction and intraluminal filling defects that were present in the groups not receiving aspirin. Sixteen of 54 transplanted heartworms survived thiacetarsamide treatment in both prednisolone-treated groups, in contrast to complete elimination of heartworms in the nontreated group. Aspirin may be considered for treatment of any heartworm-infected dog that does not have hemotypsis, but postthiacetarsamide use of prednisolone should be restricted to the dog that develops severe lung disease after the heartworms have been killed.

Animals↗
PubMed1984

Histologic examination of selected areas of canine pulmonary arteries.

Selected areas of pulmonary arteries from 18 healthy mixed-breed dogs were examined using histologic staining techniques. Smooth muscle cell, collagen, and elastin content of the tunica intima and tunica media were assessed. Fifteen dogs had abnormalities of tunica intima or tunica media in at least one arterial section examined. Of all arterial sections examined, 40% had histologic changes of the tunica intima or tunica media, and 42% of these vascular lesions were in the main pulmonary artery. The most commonly occurring pathologic change was loss of smooth muscle cells and elastin of the tunica media and replacement by collagen. This lesion is similar to cystic medionecrosis of the aorta. Seemingly, a high frequency of spontaneous vascular lesions exist in pulmonary arteries of young dogs.

Animals↗
PubMed1983

Aspirin and prednisolone modification of radiographic changes caused by adulticide treatment in dogs with heartworm infection.

The effects of aspirin and prednisolone in modifying the radiographic changes following adulticide treatment were studied in 3 groups of 6 dogs each. The dogs were radiographed and then 9 Dirofilaria immitis adults were surgically transplanted in each dog. All dogs were treated with thiacetarsamide 4 weeks later. One group received no additional treatment, the 2nd group received aspirin (10 mg/kg, daily for 4 weeks), and the 3rd group received prednisolone (1 mg/kg, daily for 4 weeks). Radiographs were taken at 1, 2, and 3 weeks after adulticide treatment, and the dogs were euthanatized at 4 weeks. The most consistent radiographic sign of pulmonary disease was a perivascular alveolar pattern in the caudal and accessory lung lobes. The right caudal lobe was the one most frequently affected. These parenchymal lesions were more frequent and more severe in the dogs given only adulticide treatment than in those given aspirin after adulticide treatment; the latter group in turn was more severely affected than the dogs given prednisolone after adulticide treatment. The radiographic evidence of pulmonary disease was resolving in most dogs at 3 weeks. The alveolar pattern on radiographs was distributed similarly to that observed at necropsy, using parenchymal uptake of Evan's blue as an indication of increased vascular permeability. Dissection of the perfusion-fixed lungs revealed that heartworms in 3 of the 6 dogs given prednisolone appeared to survive adulticide treatment.

Animals↗
PubMed1983

Early arterial injury-induced myointimal proliferation in canine pulmonary arteries.

Transmission electron microscopy was used to study the early vascular response induced by arterial damage with heartworm infection. The pulmonary arteries were examined in dogs 4 days after experimental transplantation of 6 to 8 Dirofilaria immitis adults. Evan's blue dye was given IV and followed in 60 minutes by perfusion fixation with 1% glutaraldehyde. Endothelial cell junctions were disrupted and rounded endothelial cells were observed. Macrophages and neutrophils adhered to abnormal endothelial cells. Focal areas had platelet aggregates adhered to exposed subendothelial structures. Platelets were activated and degranulated. Areas of the internal elastic lamina appeared to be disrupted, and smooth muscle cell processes from the tunica media extended through these regions of disruption. Smooth muscle cells were oriented toward the arterial lumen and some had migrated to the surface. These findings are compatible with the response to injury theory of myointimal proliferation.

Animals↗
PubMed1983

Effect of acetylsalicylic acid on vascular damage and myointimal proliferation in canine pulmonary arteries subjected to chronic injury by Dirofilaria immitis.

The effect of aspirin (ASA) on pulmonary artery response to chronic injury induced by Dirofilaria immitis was assessed in the dog. Eight dogs were studied for 30 days after adult heartworms were transplanted into the pulmonary arteries. Four dogs were treated with ASA (325 mg/day given orally) starting 3 days before the transplantation was done. Evan's blue dye was used to locate areas of vascular damage. Vascular morphology was assessed by scanning electron microscopy and light microscopy. According to results of the morphologic studies, nontreated dogs had extensive endothelial damage and significant adhesion of leukocytes and blood platelets. Blood vessels of ASA-treated dogs had less endothelial damage. Platelet adhesion on areas of vascular damage was less than that observed in nontreated dogs. Myointimal proliferative lesions were observed in both nontreated and ASA-treated dogs. However, the lesions in nontreated dogs were larger (means 68 +/- 7 mm2) and more complex than those in ASA-treated dogs (means 20 +/- 1 mm2). The results indicated that aspirin may protect against development of myointimal proliferation resulting from chronic vascular injury. The mechanism of the ASA protection may result from a combination of antiplatelet and anti-inflammatory effects, as well as a direct protective effect on vascular endothelium.

Animals↗
PubMed1983

Treatment of canine dirofilariasis: pulmonary thromboembolism caused by thiacetarsamide--microscopic changes.

Light and scanning electron microscopies were used to study the pulmonary embolism occurring in Dirofilaria immitis-infected dogs after treatment with thiacetarsamide. Lesions in control dogs (nontreated) which had been infected for 4 weeks with 9 Dirofilaria immitis adults were compared with lesions occurring in infected dogs at 2 weeks and at 4 weeks after they were treated with the adulticide. Extensive thromboembolism occurred in the caudal lobar pulmonary arteries of dogs at posttreatment weeks 2 and 4. Complicated villous proliferations were present at posttreatment week 2. The characteristic myointimal proliferation of dirofilariasis showed resolution in the large pulmonary arteries of the dogs at week 4. However, the caudal lobar pulmonary arterial and lung lesions were more severe in the later group. The pathophysiology of adulticide-induced thromboembolism and associated lung parenchymal changes were discussed.

Animals↗
PubMed1983

Pulmonary thromboembolism during therapy of dirofilariasis with thiacetarsamide: modification with aspirin or prednisolone.

The effects that 4 weeks of treatment of dirofilaria-infected dogs with either aspirin or prednisolone had on the pulmonary thromboembolism which occurs after they are given thiacetarsamide were determined, using light and electron microscopies. Pulmonary lesions in control dogs at 4 weeks after thiacetarsamide was given were compared with lesions in dogs which were treated with either aspirin (22 mg/kg daily) or prednisolone (1 mg/kg daily) during the 4-week period after adulticide was given. Pulmonary vascular and perivascular lesions were most severe in the prednisolone-treated dogs and least severe in the aspirin-treated dogs. The aspirin-treated dogs had greater resolution of pulmonary arterial proliferative disease, and prednisolone-treated dogs had the lesser resolution.

Animals↗
PubMed1982

Four types of occult Dirofilaria immitis infection in dogs.

Occult heartworm infection, ie, infection with adult Dirofilaria immitis in the absence of circulating microfilariae, was detected in dogs with prepatent infection, unisexual heartworm infection, drug-induced sterility of adult heartworms, and an immune-mediated infection. In the immune-mediate occult infection, female heartworms contained microfilariae that were antigenically similar to circulating microfilariae but were in a privileged site inasmuch as the intrauterine microfilariae were not coated with circulating antimicrofilarial immunoglobulin G. Transplantation of these female worm into heart-worm-negative dogs resulted in microfilaremia.

Animals↗
PubMed1981

Effect of long-term aspirin treatment on platelet adhesion to chronically damaged canine pulmonary arteries.

The effect of aspirin on platelet adhesion to chronically damaged pulmonary arteries was studied in 18 dogs. Chronic injury was produced in all dogs by infection with the canine heartworm Dirofilaria immitis (DI). Ten dogs were subjected to 4 days of chronic injury. Eight dogs were subjected to 30 days of chronic injury. Five of the 4 day injury and 4 of the 30 day injury dogs received aspirin daily; (325 mg/day orally). Aspirin was started 3 days prior to infection with DI. Pulmonary arteries were perfusion fixed in situ at physiologic pressure. The damaged pulmonary arteries were located by Evan's blue staining (2 ml/kg of 1% dye given one hr prior to perfusion) and prepared for scanning electron microscopy. Both groups of dogs with 4 day DI infection had monolayers of platelets adhered to exposed subendothelium. Aspirin treated dogs had enhanced platelet adhesion to damaged arteries. Aspirin treatment for 33 days reduced platelet adhesion. The damaged arteries of treated dogs infected with DI for 30 days had very few platelets adhering to the damaged surface. However, non-treated dogs subjected to 30 days of infection had platelet adhesion equivalent to the 4 day non-treated infection group. These results suggest that although aspirin is ineffective in preventing platelet adhesion in short term therapy it is effective when given for longer time periods. This inhibitory effect may occur due to platelet membrane changes rather than because of aspirin inhibition of cyclooxygenase.

Animals↗
PubMed1981

Platelet adhesion and myointimal proliferation in canine pulmonary arteries.

Pulmonary arteries were studied by scanning and transmission electron microscopy in 15 preconditioned dogs. Five dogs were control animals, while 10 dogs were studied 4 and 30 days following transplantation of adult heartworms into the pulmonary arteries. Evan's blue dye was used to locate areas of vascular damage. Pulmonary arteries from control dogs exhibited no Evan's blue staining. The surface and ultrastructural characteristics of these blood vessels were comparable to normal peripheral blood vessels. Pulmonary arteries removed from dogs after 4 days of heartworm infection exhibited extensive staining with Evan's blue. These stained areas had disrupted endothelium with many platelets adhered to the exposed subendothelium. In addition, leukocytes were attached to adjacent areas of damaged endothelium. Pulmonary arteries of dogs infected with heartworms for 30 days also exhibited extensive staining with Evan's blue. The blue-stained areas in this group had two typical responses. On some portions the lesions were similar to those seen at 4 days (ie, loss of endothelium with platelet and leukocyte adhesion), while other stained areas had complex lesions that projected from the surface into the lumen of the blood vessel. These lesions were endothelialized, and transmission electron microscopy revealed that they consisted of large numbers of smooth muscle cells that had migrated through the internal elastic lamina. The findings in the 30-day infection group suggest that the proliferative lesion formation was a result of an ongoing active process of endothelial loss and plateletleukocyte adhesion. The characteristic response of canine pulmonary arteries to the presence of heartworms (endothelial loss, platelet-leukocyte adhesion, and development of myoproliferative intimal lesions) suggests that this condition is a potential model for study of the early vascular changes that produce myointimal proliferation.

Animals↗
PubMedDate not supplied

Effect of acetylsalicylic acid on pulmonary arteriosclerosis induced by a one-year Dirofilaria immitis infection.

The ability of aspirin to block arteriosclerosis that developed in response to chronic, low-level injury to pulmonary arteries was evaluated in 21 dogs during their 1-year infection with Dirofilaria immitis. Three groups, with seven dogs in each group, were studied before and after sustained injury produced by the transplantation of 28 adult Dirofilaria immitis into each dog. Group A received no treatment and served as controls; Group B received no treatment for 6 months and then received 7 mg/kg of aspirin daily) for 6 months; Group C received 7 mg/kg of aspirin daily for the entire year. The pulmonary arterial response was evaluated by hemodynamic and arteriographic studies at 6 and 12 months and by scanning electron microscopy at the end of the 12-month study. All groups developed a similar, mild pulmonary hypertension. The arteriographic changes of dilation and flow obstruction were worse in Groups A and B than in Group C at 6 months, and at 12 months both Groups B and C were less obstructed than Group A. Scanning electron microscopy revealed large, complex myointimal proliferations in Group A, whereas the two aspirin-treated groups had smaller, less complex lesions that covered a much smaller surface area. We concluded that: 1) aspirin markedly reduced the microscopic and macroscopic arteriosclerosis in Groups B and C; 2) aspirin in Group B not only arrested further development but also permitted resolution of arteriosclerosis while the arteries were still being injured.

Angiography↗
PubMedDate not supplied

Preeclampsia.

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Animals↗