Search PubMed⌕ Search

Biomedical subjects

T G Bell

Publications and source records attributed to T G Bell.

At least 37 records · Page 2Linked to original sources
PubMed1986

Canine essential hypertension: probable mode of inheritance.

Essential hypertension (EH) in dogs is a relatively recently reported phenomenon. In this colony the canine disorder follows family lines and has a probable polygenic mode of inheritance, although the specific mode of inheritance has not been defined since an autosomal dominant trait has not clearly been ruled out. Direct intra-arterial femoral punctures are used to monitor blood pressure elevations, which tend to increase with advancing age. As in man, there are dogs with blood pressures intermediate between affected and normal dogs.

Animals↗
PubMed1986

Streptokinase treatment of cats with experimentally induced aortic thrombosis.

An investigation was initiated to determine the dosage of streptokinase (given IV) that would consistently produce systemic fibrinolysis, as determined by laboratory evaluation, and to determine the relative safety of this drug in the cat. Results indicated that a loading dose of 90,000 IU of streptokinase (given by continuous infusion over 20 to 30 minutes) and a maintenance dosage (IV) of 45,000 IU of streptokinase/hr predictably produced systemic fibrinolysis in the cat. There were no detectable adverse affects seen on physical examination, necropsy, or histopathologic examination. Using the foregoing dosage regimen, investigation was begun to evaluate the use of streptokinase for treatment of feline thromboembolism. Aortic thrombosis was created experimentally in 15 cats. There was no clearly predictable improvement in nonspecific venous angiograms or thermal circulatory indices for the cats given streptokinase, compared with the values for the control cats. After a total of 180 minutes of treatment, the mean weight of remaining clot removed at necropsy from the aortic trifurcation was 7.3 mg in the streptokinase-treated cats, compared with 13.4 mg in the control cats.

Angiography↗
PubMed1985

Abnormal release of storage pool adenine nucleotides from platelets of dogs affected with basset hound hereditary thrombopathy.

Platelets from dogs affected with Basset Hound Hereditary Thrombopathy (BHT), have a thrombasthenia-like aggregation defect but release storage pool ATP in quantities not significantly different from normal controls or BHT heterozygotes when stimulated with 1 X 10(-5)M ADP and 0.22 U/ml thrombin. However, the release occurs so rapidly in the BHT platelets stimulated with ADP that it is complete in approximately one-sixth of the time required for release from normal control and heterozygote platelets. Sequential electron micrographs reveal early release of BHT dense body constituents 30 seconds after stimulation with 1 X 10(-5)M ADP while resting BHT morphology is indistinguishable from normal control animals.

Adenine Nucleotides↗
PubMed1985

Screening coagulation tests in the cat: reference values based on direct venipuncture and catheterized samples.

Platelet count, prothrombin time, activated partial thromboplastin time, fibrinogen degradation products, fibrinogen, and modified thrombin time were determined in 46 healthy adult cats. Samples were obtained by direct venipuncture (pet cats, n=20) or through an 18 gauge intravenous jugular catheter (laboratory conditioned cats, n=26). Range, mean, standard error, and 95% confidence interval were tabulated for the 2 samples. A statistically significant difference between the two groups of cats (Student's t test, p <.05) was found for fibrinogen. No statistical difference was detected between the two groups of cats for the other laboratory values.

Journal Article↗
PubMed1984

Effects of thrombocytopenia on monocrotaline pyrrole-induced pulmonary hypertension.

Monocrotaline pyrrole (MCTP) causes lung injury, pulmonary hypertension, and right ventricular hypertrophy in rats. To determine if platelets are involved in the cardiopulmonary effects of MCTP, the response to MCTP was determined in thrombocytopenic rats. Blood platelet count was reduced to 10-20% of normal for 48 h by ip administration of an antirat platelet serum (PAS) prepared in the goat. Rats were treated iv with either MCTP 5 mg/kg or dimethylformamide vehicle and with either PAS or preimmune serum. Fourteen days after MCTP, right ventricular hypertrophy and several indexes of lung injury were measured. MCTP treatment produced right ventricular hypertrophy, increased lactate dehydrogenase activity and protein concentration in bronchopulmonary lavage fluid, increased perfusion pressure in isolated lungs, and decreased pulmonary clearance and metabolism of perfused 5-hydroxytryptamine. Thrombocytopenia did not influence the changes in these indexes of lung injury produced by MCTP in this protocol. When PAS was given 12 h before MCTP, it did not affect right ventricular hypertrophy, but when PAS treatment was begun 3 or 6 days after MCTP, right ventricular hypertrophy was decreased by 19 or 41%, respectively. These results suggest that platelets help to mediate the development of pulmonary hypertension and the hypertrophic response of the right heart following MCTP administration.

Animals↗
PubMed1983

Monocrotaline pyrrole-induced pulmonary hypertension in fawn-hooded rats with platelet storage pool deficiency: 5-hydroxytryptamine uptake by isolated, perfused lungs.

Platelets are believed to be involved in the development of monocrotaline pyrrole (MCTP)-induced pulmonary hypertension. To help identify the role of the platelet, the cardiopulmonary toxicity of MCTP was examined in fawn-hooded (FH) rats, a strain with a platelet function defect. Both Sprague-Dawley (SD) and FH rats developed right ventricular hypertrophy and increased lung weights and exhibited decreased biogenic amine removal by isolated, perfused lung preparations after MCTP treatment. The responses of the FH rats were not significantly different from those of the SD rats, suggesting that platelet uptake and release of 5-hydroxytryptamine (5HT) are not the platelet functions involved in MCTP-induced pulmonary hypertension. The FH rats had an interesting strain-related difference from SD rats; isolated lungs from FH rats removed and metabolized a greater proportion of perfused 5HT than the SD rats.

Animals↗
PubMed1983

Aggregation of platelets from monocrotaline pyrrole-treated rats.

Aggregation responses of platelet-rich plasma (PRP) from monocrotaline pyrrole (MCTP)-treated rats were examined to help elucidate the role of platelets in MCTP-induced pulmonary hypertension. PRP from rats treated one or four days earlier with MCTP (5 mg/kg, i.v.) or vehicle exhibited the same slope and maximum aggregation to ADP (1 X 10(-5) M, 2 X 10(-6) M, 1 X 10(-6) M), 74 micrograms/ml dog collagen, or 500 micrograms/ml arachidonic acid. PRP collected 7 days after MCTP treatment had a 15% decrease in both slope and maximum aggregation to 1 X 10(-5) M ADP and a 25% decrease in response to 2 X 10(-6) M ADP relative to the control group. Fourteen days after MCTP treatment, the responses to all of the aggregating agents were decreased 18-71% from control values. These results indicate that MCTP treatment alters the responses of PRP to aggregating agents.

Adenosine Diphosphate↗
PubMed1982

Pneumotoxicity and thrombocytopenia after single injection of monocrotaline.

Adult Sprague-Dawley rats were treated once with 105 mg/kg monocrotaline (MCT) subcutaneously or an equivalent volume of isotonic saline and examined 2, 5, 10, and 14 days later. The earliest changes observed were in the platelet count, which was decreased in the MCT animals at 2, 5, and 10 days postinjection. Clearance of perfused 5-hydroxytryptamine, a function of pulmonary vascular endothelium, was unaltered in isolated lungs of treated rats until 5 days after dosing but decreased progressively thereafter in the MCT animals and was 24% less than controls by 14 days. The magnitude of this effect was dose related. Inflow perfusion pressure was elevated in perfused lungs of MCT-treated animals at day 14. Right heart hypertrophy, measured as an increase in the ratio of right ventricle to left ventricle plus septum weights, was not evident until 14 days after treatment. A larger dose of MCT (130 mg/kg) resulted in significant mortality, whereas a lower dose (60 mg/kg) did not result in right ventricular hypertrophy 2 wk after treatment. The treatment regimen described has advantages over administration of MCT by ingestion and may prove suitable for investigations of the mechanism by which MCT results in pulmonary hypertension.

Alanine Transaminase↗
PubMed1980

Prolonged bleeding time in Aleutian mink associated with a cyclo-oxygenase-independent aggregation defect and nucleotide deficit in blood platelets.

A prolonged mean template bleeding time of 13 minutes was present in nine Aleutian mink affected with Chediak-Higashi syndrome (CHS) compared with 4 minutes in dark control mink. The concentrations of blood platelets in normal and affected animals did not differ significantly. However, in mink with CHS, a marked disturbance of platelet response to collagen was present. Administration of aspirin and indomethacin completely blocked CH platelet response to collagen. Blood platelet adenosine triphosphate and adenosine diphosphate values from mink with CHS were significantly less than those of normal mink, and the platelet adenosine triphosphate/adenosine diphosphate ratios were 10.31 in affected mink and 2.74 in normal mink. These findings are consistent with our previous investigations in affectd cattle and persons and indicate that a "storage pool disease" of platelets exist in the mink with CHS.

Adenine Nucleotides↗
PubMed1979

Increased renal tubular synthesis of prostaglandins in the rabbit kidney in response to ureteral obstruction.

The hydronephrotic rabbit kidney exhibits elevated basal prostaglandin synthesis and supersensitivity to peptide stimulation of vascular prostaglandin and thromboxane formation. In this study the distribution of the prostaglandin-forming cyclooxygenase in hydronephrotic and contralateral rabbit kidneys following one and four day ureteral obstructions was compared using immunohistofluorescence. No alterasions were detected in the distribution or intensity of cyclooxygenase-positive fluorescence in the renal vasculature in response to ureteral obstructions. However, two significant differences were noted between hydronephrotic and contralateral kidneys in the staining of renal tubules: (a) the intensity of fluorescent staining in cortical and medullary collecting tubules of the hydronephrotic kidney was increased and (b) cyclooxygenase antigenicity appeared in the thin limbs of Henle's loop in the hydronephrotic organ. Although alterations in prostaglandin formation by the renal vasculature have been documented previously, our results indicate that ureteral obstruction also causes increased prostaglandin synthesis by renal tubules.

Animals↗
PubMed1978

Immunohistochemical localization of the prostaglandin-forming cyclooxygenase in renal cortex.

An immunohistofluorescence procedure for detecting prostaglandin-forming cyclooxygenase has been used to localize the enzyme in the renal cortex of the cow, guinea pig, rabbit, rat, and sheep. Cyclooxygenase antigenicity was found in endothelial cells lining all arteries and arterioles and in cortical collecting tubules in each species examined. The enzyme was also detected in epithelial cells of Bowman's capsule in the rabbit and in mesangial cells in both ovine and bovine glomerular tufts. That prostaglandins can be formed in renal resistance vessels suggests that it is the synthesis occurring in these vessels which is responsible for the effects of prostaglandins on renal blood flow. Of further note is the correlation that exists between the location of the cyclooxygenase and that of the antidiuretic hormone-responsive adenyl cyclase in the distal nephron.

Animals↗
PubMed1976

Decreased nucleotide and serotonin storage associated with defective function in Chediak-Higashi syndrome cattle and human platelets.

Prolonged mean template bleeding time of 14 min observed in seven cattle with the Chediak-Higashi syndrome (CHS) prompted the examination of platelet function in these animals. There was no distinguishable difference in concentration of circulating platelets between CHS and control cattle. CHS bovine platelets failed to aggregate in vitro in response to concentrations of acid-soluble collagen which induced aggregation in all normal samples. The primary platelet response to 5 muM ADP was normal in CHS cattle. A markedly decreased amount of serotonin (1.2% of normal) was detected in CHS bovine platelets. Bovine CHS platelet ATP and ADP contents were significantly less than normal, and the ATP/ADP ratios were 5.04 in normal and 29.38 in CHS platelets. Results of these animal investigations prompted a similar study of two patients with CHS. In humans, an increased bleeding time greater than 15 min and an in vitro impaired aggregation response to acid-soluble collagen and 5 muM adrenaline were discovered. Both ATP and ADP were reduced in CHS human platelets, and the ATP/ADP ratio was 3.96, compared to a ratio of 1.52 for platelets of two normal subjects. These findings suggested the presence of a "storage pool disease" of CHS platelets.

Adenosine Diphosphate↗
PubMed1975

Ataxia, depression, and dermatitis associated with the use of dichlorvos-impregnated collars in the laboratory cat.

Ataxia and depression developed in 21 of 50 (42%) laboratory cats wearing flea collars impregnated with 2,2-dichlorovinyl dimethyl phosphate (dichlorvos or DDVP) in a warm dry environment. Five (10%) of the cats died. Whole blood cholinesterase (ChE) activity was significantly (P smaller than 0.001) reduced in all cats and cervical dermatitis occurred in 37 (74%) of them.

Alanine Transaminase↗