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Biomedical subjects

G J Whitman

Publications and source records attributed to G J Whitman.

At least 19 recordsLinked to original sources
PubMed1995

The cumulative nature of pyruvate's dual mechanism for myocardial protection.

Pyruvate (PYR) supplementation protects myocardium from ischemia reperfusion injury. This study was designed to characterize and quantify the mechanism underlying this protection: specifically whether this ability resides in PYR's metabolic effect or in its antioxidant effect. Isolated perfused rat hearts (n = 6/group) were subjected to 15 min of equilibration (EQ), 25 min of ischemia, and 10 min of reperfusion (RP). Glucose was the sole metabolic substrate (Control) or was supplemented with PYR (5 mM) during (a) EQ only (PYREQ group), (b) RP only (PYRRP group), or (c) EQ and RP (PYREQ-RP group). Left ventricular developed pressure (DP) and +/- dP/dt were recorded throughout the experiment. ATP concentrations and intracellular pH were determined by 31P NMR spectroscopy. Myocardial creatinine kinase (CK) activity was assayed at end EQ and end RP. In vitro, purified CK was assayed and, after exposure to H2O2 (200 microM) and increasing concentrations of PYR (0-6 mM) for 10 min, reassayed to determine the antioxidant effect of PYR. In all cases PYR improved recovery of mechanical function at end RP (DP: Control, 11 +/- 1%; PRYRP, 23 +/- 6%; PYREQ, 34 +/- 8%; PRYEQ&RP, 53 +/- 7%; P < 0.05 between all groups and Control). Ischemic contracture was delayed in hearts that received PYR during EQ (PYREQ and PYREQ&RP: 17.8 +/- 0.2 vs 12.5 +/- 0.3 min, P < 0.001). PYR during EQ (PYREQ and PYREQ&RP) led to higher end ischemic ATP levels (32 +/- 4% vs 14 +/- 3%, P < 0.001) and a more acidic end ischemic pH (5.92 +/- 0.02 vs 5.98 +/- 0.03 in Control and PYRRP, P < 0.05). PYREQ&RP showed the highest end reperfusion ATP levels (55 +/- 7% vs 38 +/- 4%, P < 0.05 vs other groups).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1995

Nitric oxide as a positive inotropic agent in isolated rat hearts.

The purpose of this study was to examine the inotropic effects of nitroprusside (NP), a direct nitric oxide (NO) donor, in isolated rat hearts. Langendorff-perfused hearts (n = 5), paced at 6 Hz, were subjected to 15 min of equilibration (EQ) followed by infusion of NP, producing a coronary artery concentration of 1 x 10(-5) M. Coronary flow, left ventricular developed pressure (DP), end-diastolic pressure, and contractility and compliance (+/- dP/dt) were monitored throughout the experiment by a computerized data acquisition system. Myocardial oxygen consumption (MVO2) was measured at the end of EQ and after 2 1/2 min of NP infusion. Myocardial efficiency was calculated as the quotient of DP divided by MVO2. Values are expressed as the mean +/- SEM. Paired t tests were used to calculate statistical significance. Values for parameters monitored at end EQ and at 2 1/2 min NP infusion showed that there was a 93% increase in coronary flow, 18, 17, and 16% increases in developed pressure, contractility, and compliance, respectively, no significant change in end-diastolic pressure, a 49% increase in myocardial oxygen consumption, and a 21% decline in myocardial efficiency (P < 0.05 for all differences). We conclude that in the isolated rat heart, NO behaves as a positive inotrope.

Animals↗
PubMed1995

Superior vena cava syndrome caused by aneurysm of the innominate artery.

Isolated aneurysms or ruptures of the innominate artery are rare causes of the superior vena cava syndrome. We report on a patient who suffered an isolated acute expansion and rupture of an innominate artery aneurysm that precipitated a dramatic superior vena cava syndrome. Immediate repair using modern surgical techniques, cardiopulmonary bypass, profound hypothermia, circulatory arrest, and a Dacron graft rapidly cured the patient of this deadly syndrome.

Aged↗
PubMed1994

Protection of the patent internal mammary artery by-pass graft from subsequent sternotomy.

OBJECTIVE: We describe a technique to protect the patent internal mammary artery graft from injury by repeat sternotomy. INTERVENTIONS: The internal mammary artery is dissected as far proximally as possible. The left pleural space is opened widely thus allowing the left lung to protrude through the pleural defect once mechanical ventilation is resumed. The left lung is then interposed between the internal mammary graft and the sternum. The internal mammary artery is thereby protected from adherence to the sternum and injury upon resternotomy. RESULTS: In two patients in whom this technique was employed repeat sternotomy was easily performed without injury to the internal mammary artery. CONCLUSIONS: This simple technique effectively protects the patent internal mammary artery bypass graft from injury at subsequent sternotomy.

Humans↗
PubMed1992

Breast cancer survival among women under age 50: is mammography detrimental?

Great uncertainty exists about the benefit of detecting breast cancer by mammography in women under 50 years of age. We have reviewed the survival of patients aged 49 years or less whose cancers were detected by mammography alone. 117 women under the age of 50 years were diagnosed with breast cancer between 1978 and 1991 based only on an abnormal mammogram. Ductal carcinoma in-situ (DCIS) was found in 47 (40%) of these women, whilst 70 (60%) had infiltrating ductal or infiltrating lobular carcinomas. During the same interval, 928 women in this age group presented with palpable breast cancer. DCIS was diagnosed in 82 (9%) of these women, whilst 846 (91%) had infiltrating carcinoma. Among the infiltrating cancers detected by mammography alone, 50% were stage I, whilst only 30% of the women with palpable cancers were stage I. Five-year survival for all mammographically detected cancer patients was 95%, whereas for women with palpable cancers the survival was 74% (p < 0.00005). If DCIS is not included, the corresponding survivals are 91% for mammographically detected infiltrating cancers and 72% for palpable infiltrating cancers. Only 1 woman who died among those with palpable cancer had had a mammogram before diagnosis. Our data contradict the suggestion that women under 50 are put at a survival disadvantage by undergoing mammography. We believe that investigators who have reported negative results in this age group must examine other causes for their results.

Actuarial Analysis↗
PubMed1992

Safe intraaortic balloon pump placement through the ascending aorta using transesophageal ultrasound.

Intraaortic balloon pumping salvages a substantial number of patients who fail to be weaned from cardiopulmonary bypass after an open heart operation. Patients with severe peripheral vascular disease may require ascending aortic balloon pump insertion. We describe a simple method of direct aortic puncture for intraaortic balloon pump placement using transesophageal ultrasound as a means of avoiding complications during insertion and documenting correct balloon position.

Aorta↗
PubMed1991

Primed neutrophils injure rat lung through a platelet-activating factor-dependent mechanism.

Bacterial lipopolysaccharide (LPS) promotes transient lung neutrophil sequestration. These LPS-primed neutrophils, when stimulated by an N-formyl peptide (FNLP), promote lung injury. We hypothesized that LPS-primed, FNLP-stimulated neutrophils promote lung injury through a platelet-activating factor (PAF)-dependent mechanism. Rats were pretreated with either saline or WEB2170, a PAF receptor antagonist (10 mg/kg po). One hour after pretreatment, rats were administered intraperitoneal LPS (salmonella typhimurium lipopolysaccharide, 500 micrograms/kg) followed 6 hr later by intravenous FNLP (250 micrograms/kg infused over 30 min). Two hours after the initiation of FNLP infusion, rats were sacrificed and assays were performed to measure: (1) lung neutrophil sequestration with myeloperoxidase (MPO) activity; (2) circulating neutrophil activation with nitroblue tetrazolium (NBT) staining, and (3) lung microvascular leak with 125I-albumin flux. We found that lung myeloperoxidase, circulating neutrophil NBT staining, and lung 125I-albumin flux were increased (P less than 0.05) in saline-pretreated LPS/FNLP rats, relative to control. While lung MPO remained increased (P less than 0.05) in WEB2170-pretreated LPS/FNLP rats, circulating neutrophil NBT and lung 125I-albumin flux were decreased (P less than 0.05) relative to those in saline-pretreated rats. We conclude that PAF mediates LPS/FNLP-induced neutrophil activation and lung injury, but is independent from lung neutrophil sequestration. Thus, lung neutrophil sequestration does not inevitably produce lung injury. Rather, neutrophils can accumulate in the lung without causing lung injury if neutrophil activation can be blocked.

Animals↗
PubMed1991

Oxygen metabolite effects on creatine kinase and cardiac energetics after reperfusion.

Noninvasive 31P nuclear magnetic resonance measurements indicate that during the initial reperfusion phase myocardial tissue contents of phosphocreatine (PCr) recover rapidly, while ATP levels remain low and recover slowly. There is also a burst of H2O2 during the first 10 min of reperfusion, as indicated by the in vivo inactivation of catalase that occurs only when H2O2, and the inactivator 3-aminotriazole (AMT), are simultaneously present. Neither H2O2 production nor CK inactivation was discernable after ischemia alone. In excitable tissue the PCr and ATP pools are equilibrated by the enzyme creatine kinase (CK), but myocardial CK activity is decreased by 20% after reperfusion, though not by simple washout. Extrapolating from the well-known air sensitivity of CK, we find that limited exposure in vitro to small concentrations of H2O2 can markedly diminish CK activity. We postulate that failure of certain CK isoenzymes at energy-using termini may decouple the relative rates of PCr production and ATP regeneration and hence cause elevated PCr-to-ATP ratios. The assumptions of 1) CK equilibrium during the reperfusion period to calculate free ADP levels and 2) cardiac recovery deduced from the elevation of PCr levels may require reexamination.

Adenosine Triphosphate↗