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Biomedical subjects

L Garvey

Publications and source records attributed to L Garvey.

7 recordsLinked to original sources
PubMed2001

Cocaine, ethanol, and cocaethylene cardiotoxity in an animal model of cocaine and ethanol abuse.

OBJECTIVES: Simultaneous abuse of cocaine and ethanol affects 12 million Americans annually. In combination, these substances are substantially more toxic than either drug alone. Their combined cardiac toxicity may be due to independent effects of each drug; however, they may also be due to cocaethylene (CE), a cocaine metabolite formed only in the presence of ethanol. The purpose of this study was to delineate the role of CE in the combined cardiotoxicity of cocaine and ethanol in a model simulating their abuse. METHODS: Twenty-three dogs were randomized to receive either 1) three intravenous (IV) boluses of cocaine 7.5 mg/kg with ethanol (1 g/kg) as an IV infusion (C+E, n = 8), 2) three cocaine boluses only (C, n = 6), 3) ethanol infusion only (E, n = 5), or 4) placebo boluses and infusion (n = 4). Hemodynamic measurements, electrocardiograms, and serum drug concentrations were obtained at baseline, and then at fixed time intervals after each drug was administered. RESULTS: Two of eight dogs in the C+E group experienced cardiovascular collapse. The most dramatic hemodynamic changes occurred after each cocaine bolus in the C+E and C only groups; however, persistent hemodynamic changes occurred in the C+E group. Peak CE levels were associated with a 45% (SD +/- 22%, 95% CI = 22% to 69%) decrease in cardiac output (p < 0.05), a 56% (SD +/- 23%, 95% CI = 32% to 80%) decrease in dP/dt(max) (p <.006), and a 23% (SD +/- 15%, 95% CI = 7% to 49%) decrease in SVO(2) (p < 0.025). Ventricular arrhythmias were primarily observed in the C+E group, in which four of eight dogs experienced ventricular tachycardia. CONCLUSIONS: Cocaine and ethanol in combination were more toxic than either substance alone. Co-administration resulted in prolonged cardiac toxicity and was dysrhythmogenic. Peak serum cocaethylene concentrations were associated with prolonged myocardial depression.

Alcoholism↗
PubMed2000

Etiologic factors in progression of carotid stenosis: a 10-year study in 905 patients.

PURPOSE: The purpose of this study was to determine the etiologic factors in the progression of carotid stenosis. METHODS: We performed prospective serial duplex scan surveillance of 1470 carotid arteries in 905 asymptomatic patients during a 10-year period, with an average follow-up interval of 29 months and an average of 3.0 scans per carotid artery. Vascular laboratory and hospital records were used to collect risk factor information. The data were analyzed with proportional hazards modeling. RESULTS: We examined several demographic, clinical, and laboratory risk factors that were chosen because of their potential relevance to atherosclerotic disease. These factors were analyzed with univariate proportional hazards modeling, in which time to progression of stenosis was the outcome variable. The six significant predictors (P <.05) were age, sex, systolic pressure, pulse pressure (systolic pressure - diastolic pressure), total cholesterol, and high-density lipoprotein (HDL). All, except HDL, were positive predictors of time to disease progression. With multivariate modeling, only pulse pressure and HDL remained as significant independent predictors of stenosis progression. The risk ratio for a 10-mm Hg rise in pulse pressure was 1.12, and the risk ratio for a 10-mg/dL decrease in HDL was 1.20. CONCLUSION: In this large cohort of patients who were followed prospectively for carotid stenosis, pulse pressure and HDL were found to be the key risk factors for carotid stenosis progression. The fact that pulse pressure superseded systolic pressure in multivariate modeling may shed light on the biology of carotid plaque progression. Further, our identification of these modifiable risk factors may help in the design of therapeutic trials for the prevention of progression of carotid atherosclerosis.

Age Factors↗
PubMed1996

Adjuvant hormonal treatment with peptide YY or its analog decreases human pancreatic carcinoma growth.

BACKGROUND: Recent studies have revealed decreased pancreatic cancer cell growth upon administration of peptide YY (PYY). We examined whether adjuvant treatment with PYY or its synthetic analog, BIM-43004, would decrease human pancreatic adenocarcinoma growth. MATERIALS AND METHODS: Human pancreatic ductal adenocarcinomas, MiaPaCa-2 and BxPC-3, were cultured and assessed for growth by MTT assay. Pancreatic cancer cells received 500 pmol of PYY or BIM-43004 for 24 hours prior to 5-fluorouracil (5-FU; 10 micrograms/mL) and leucovorin (40 micrograms/mL) administration. Cell membrane epidermal growth factor (EGF) receptors were analyzed by Western blotting after exposure to peptides and chemotherapy. RESULTS: Cancer cell growth was reduced in all groups receiving hormonal pretreatment (23% PYY/5-FU/leucovorin versus control; 27% BIM-43004/5-FU/leucovorin versus control) as compared with groups receiving 5-FU and leucovorin only (16% versus control). The EGF receptor expression was reduced by 30% in cells treated with PYY/5-FU/leucovorin and by 45% in cells treated with BIM/5-FU/leucovorin as compared with control cells without treatment. CONCLUSION: Human pancreatic cancer cell growth is further decreased when pretreated with PYY or its synthetic analog prior to chemotherapy.

Carcinoma, Ductal, Breast↗
PubMed1990

Assay of apolipoproteins A-1 and B by immunoturbidimetry: detection of individuals at risk for atherosclerotic artery disease.

Recent evidence has suggested that the levels of Apolipoprotein A-1 and B in plasma are better indicators of the risk of atherosclerotic artery disease than plasma lipids. This study describes the measurement of plasma Apolipoprotein A-1 and B by immunoturbidimetry in patients with atherosclerotic artery disease and in normal controls. Apoprotein B and the ratio of Apoprotein A-1/Apoprotein B were found to be the best discriminators between the two groups.

Adult↗
PubMedDate not supplied

Cocaine-induced wide complex dysrhythmia.

Cocaine is a local anesthetic with the potential to induce dysrhythmia due to direct myocardial sodium channel antagonism similar to class I antidysrhythmic drugs. The hallmark of myocardial sodium channel poisoning is wide complex dysrhythmia, and the current accepted treatment is intravenous bicarbonate. Wide complex dysrhythmio due to cocaine in the absence of myocardial infarction is rare, and optimum management is undefined. We report three cases of acute cocaine intoxicating during which patients developed wide complex dysrhythmia consistent with sodium channel poisoning. In one case, wide complex tachycardia resolved without direct treatment. In the other cases, wide complex dysrhythmia resolved following intravenous bicarbonate therapy directed at reversing sodium channel blockade.

Adult↗