Biomedical subjects

G J Whitman

Publications and source records attributed to G J Whitman.

At least 55 records · Page 3Linked to original sources

PubMed1996

Impact of respiratory acid-base status in patients with pulmonary hypertension.

BACKGROUND: The perioperative management of patients undergoing mitral valve replacement (MVR) with pulmonary hypertension from mitral stenosis may be complicated by increased pulmonary vascular resistance. The purpose of this study was to examine the influence of respiratory acid-base status on the pulmonary hemodynamic indices of patients with pulmonary hypertension before and after MVR. METHODS: Ten patients with pulmonary hypertension from mitral stenosis (mean preoperative systolic pulmonary artery pressure, 73 +/- 8 mm Hg) undergoing MVR were studied in the operating room before and after MVR. Arterial partial pressure of carbon dioxide was manipulated by the addition of 5% carbon dioxide to the breathing circuit. Hemodynamic data were collected as the partial pressure of carbon dioxide rose from 30 mm Hg to 50 mm Hg and decreased back to 30 mm Hg. RESULTS: There were no differences in mean pulmonary artery pressure or pulmonary vascular resistance before and after MVR. Before MVR, mean pulmonary artery pressure increased from 32 +/- 1 mm Hg to 48 +/- 1 mm Hg as the partial pressure of carbon dioxide rose from 30 mm Hg to 50 mm Hg (p < 0.05), and pulmonary vascular resistance rose from 379 +/- 30 to 735 +/- 40 dynes.second.cm-5 (p < 0.05). These effects on mean pulmonary artery pressure and pulmonary vascular resistance were not different after MVR. CONCLUSION: Respiratory acid-base status has a profound impact upon pulmonary vascular resistance in patients with pulmonary hypertension from mitral stenosis undergoing MVR. This impact persists in the immediate postoperative period. We conclude that respiratory acidemia should be avoided in these patients, whereas respiratory alkalemia may be used to help minimize pulmonary vascular resistance.

Acid-Base Imbalance↗

PubMed1996

Elucidation of a tripartite mechanism underlying the improvement in cardiac tolerance to ischemia by coenzyme Q10 pretreatment.

Coenzyme Q10, which is involved in mitochondrial adenosine triphosphate production, is also a powerful antioxidant. We hypothesize that coenzyme Q10 pretreatment protects myocardium from ischemia reperfusion injury both by its ability to increase aerobic energy production and by protecting creatine kinase from oxidative inactivation during reperfusion. Isolated hearts (six per group) from rats pretreated with either coenzyme Q10, 20 mg/kg intramuscularly and 10 mg/kg intraperitoneally (treatment) or vehicle only (control) 24 and 2 hours before the experiment were subjected to 15 minutes of equilibration, 25 minutes of ischemia, and 40 minutes of reperfusion. Developed pressure, contractility, compliance, myocardial oxygen consumption, and myocardial aerobic efficiency were measured. Phosphorus 31 nuclear magnetic resonance (31P-NMR) spectroscopy was used to determine adenosine triphosphate and phosphocreatine concentrations as a percentage of a methylene diphosphonic acid standard. Hearts were assayed for myocardial coenzyme Q10 and myocardial creatine kinase activity at end equilibration and at reperfusion. Treated hearts showed higher myocardial coenzyme Q10 levels (133 +/- 5 micrograms/gm ventricle versus 117 +/- 4 micrograms/gm ventricle, p < 0.05). Developed pressure at end reperfusion was 62% +/- 2% of equilibration in treatment group versus 37% +/- 2% in control group, p < 0.005. Preischemic myocardial aerobic efficiency was preserved during reperfusion in treatment group (0.84 +/- 0.08 mm Hg/(microliter O2/min/gm ventricle) vs 1.00 +/- 0.08 mm Hg/(microliter O2/min/gm ventricle) at equilibration, p = not significant), whereas in the control group it fell to 0.62 +/- 0.07 mm Hg/(microliter O2/min/gm ventricle, p < 0.05 vs equilibration and vs the treatment group at reperfusion. Treated hearts showed higher adenosine triphosphate and phosphocreatine levels during both equilibration (adenosine triphosphate 49% +/- 2% for the treatment group vs 33% +/- 3% in the control group, p < 0.005; phosphocreatine 49% +/- 3% in the treatment group vs 35% +/- 3% in the control group, p < 0.005) and reperfusion (adenosine triphosphate 18% +/- 3% in the treatment group vs 11% +/- 2% in the control group, CTRL p < 0.05; phosphocreatine 45% +/- 2% in the treatment group vs 23% +/- 3% in the control group, p < 0.005). Creatine kinase activity in treated hearts at end reperfusion was 74% +/- 3% of equilibration activity vs 65% +/- 2% in the control group, p < 0.05). Coenzyme Q10 pretreatment improves myocardial function after ischemia and reperfusion. This results from a tripartite effect: (1) higher concentration of adenosine triphosphate and phosphocreatine, initially and during reperfusion, (2) improved myocardial aerobic efficiency during reperfusion, and (3) protection of creatine kinase from oxidative inactivation during reperfusion.

Animals↗

PubMed1996

Coenzyme Q10 protects coronary endothelial function from ischemia reperfusion injury via an antioxidant effect.

BACKGROUND: Cardiac ischemia reperfusion (I/R) injury causes coronary vascular dysfunction. Coenzyme Q10 (CoQ), which preserves cardiac mechanical function after I/R, recently has been recognized as a free radical scavenger. We hypothesized that CoQ protects coronary vascular reactivity after I/R via an antioxidant mechanism. METHODS: Rats were pretreated with either CoQ (20 mg/kg intramuscular and 10 mg/kg intraperitoneal [CoQ group]) or a vehicle (Control) before the experiment. Isolated perfused rat hearts were subjected to 25 minutes of global normothermic ischemia and 40 minutes of reperfusion. The reperfusion-induced oxidative burst was directly assessed by lucigenin enhanced chemiluminescence. Coronary flow was measured at equilibration and after reperfusion with or without bradykinin, an endothelium-dependent vasodilator, and sodium nitroprusside (SNP), an endothelium-independent vasodilator. The effect of intracoronary infusion of hydrogen peroxide (H2O2 0.1 mumol/gm body weight given over 5 minutes), simulating the free radical burst after I/R, also was evaluated. RESULTS: I/R decreased the bradykinin-induced change in coronary flow (-5% +/- 4% versus 26% +/- 3% at equilibration; p < 0.05) and the SNP-induced change (+20% +/- 6% versus +56% +/- 5% at equilibration; p < 0.05). The coronary vasculature after H2O2 infusion revealed a similar loss in vasodilatory responsiveness (+4% +/- 4% in response to bradykinin, +35% +/- 8% in response to SNP; p < 0.05 versus equilibration). Pretreatment with CoQ improved BK-induced vasorelaxation after I/R (+12% +/- 2%; p < 0.05 versus control I/R) or H2O2 infusion (18% +/- 4%; p < 0.05 versus control I/R) but failed to improve SNP-induced vasorelaxation. The CoQ pretreatment decreased the I/R-induced maximal free radical burst (9.3 +/- 0.8 x 10(3) cpm versus 11.5 +/- 1.1 x 10(3) cpm; p < 0.05) during the early period of reperfusion. CONCLUSIONS: Endothelium-dependent vasorelaxation is more sensitive than endothelium-independent relaxation to I/R injury. Via a direct antioxidant effect, CoQ preserved endothelium-dependent vasorelaxation by improving tolerance to I/R injury.

Acridines↗

PubMed1996

Computed tomography-guided needle localization of nonpalpable breast lesions: review of 24 cases.

RATIONALE AND OBJECTIVES: We examined the role of computed tomography (CT) in breast imaging, especially in guiding needle localization procedures. METHODS: We reviewed our institution's breast imaging database, from 1978 to 1994, for procedures in which CT scanning was used. Twenty-four CT-guided needle localizations were identified. Medical records, mammograms, CT scans, and pathology reports were reviewed for all patients. RESULTS: Twenty-four needle localizations were performed on 22 female patients. The average size of the lesions localized was 12 mm. The most common reason for CT scanning was the inability to image a suspicious density by conventional mammography on two orthogonal views. Nine malignant and 15 benign lesions were localized under CT guidance. One patient developed a postoperative hematoma. No other complications occurred. CONCLUSION: CT-guided breast localization is a reliable technique that may be used to define selected breast lesions that are difficult to triangulate or localize by conventional two-view mammography.

Aged↗

PubMed1996

Positive predictive value of breast biopsy performed as a result of mammography: there is no abrupt change at age 50 years.

PURPOSE: To determine if the positive predictive value (PPV) of a biopsy initiated because of an abnormal mammogram changes abruptly at age 50 years. MATERIALS AND METHODS: The PPV and its variation with age was analyzed for 4,778 women who underwent biopsy for a clinically occult abnormality detected at mammography. The relationship of the results to the patient's age was analyzed with age represented as a continuous and two-categorized (< 50, > 50) measure. The latter measure represented an abrupt change, which distinguished those aged 49 years and younger from those aged 50 years and over. With this measure, the patients in each of the two age groups were statistically indistinguishable. RESULTS: The results were consistent with a steady increase in PPV and the yield of cancers with age, and there was no abrupt change at age 50 years. The modeled PPV for all cancers for these 4,778 patients was approximately 12% for women aged 40 years and increased to 46% by age 79 years. CONCLUSION: The PPV did not change abruptly at any age for women aged 40-79 years but increased steadily, which reflects the prior probability of breast cancer at each age. Inappropriate grouping of data can lead to misinterpretation of results. Screening guidelines should not be predicated on the false assumption that this variable changes at age 50 years.

Adult↗

PubMed1996

The sternalis muscle: an unusual normal finding seen on mammography.

OBJECTIVE: We studied the appearance of the sternalis muscle on mammography and on CT and MR imaging. To our knowledge, this is the first description of this normal anatomic variant. An approach is provided that permits differentiation of the sternalis from significant pathology. SUBJECTS AND METHODS: Between January 1992 and December 1994, four women of an estimated 32,000 who had mammograms at the Massachusetts General Hospital had an unusual, irregular structure visible medially on the craniocaudal projection that posed a diagnostic dilemma. The records and imaging studies of these women and two others from the Deaconess Hospital breast imaging program were reviewed to determine the etiology of the findings seen by mammography and to establish a diagnostic approach. RESULTS: Surgery in one patient and cross-sectional imaging in the other five established that the structure was the sternalis muscle. Although it may be bilateral, the sternalis muscle was visible only unilaterally on the mammograms of these six women. The appearance of the muscle ranged from an irregularly rounded density at the sternal edge of the film to flame-shaped and almost completely surrounded by fat. CT and MR imaging are diagnostic when they show the longitudinal extent of the muscle, which lies anterior to the medial margin of the pectoralis major muscle. CONCLUSION: The sternalis muscle is an unusual variant of the chest wall musculature. It may be visible as a rounded or irregular density on the craniocaudal mammogram along the sternal edge of the film. With improved mammographic positioning it will be seen more frequently. The muscle has a variety of appearances that should be familiar to the radiologist to avoid confusion with a malignant lesion. The etiology can be confirmed and cancer excluded by CT or MR imaging.

Adult↗

PubMed1996