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G J Whitman

Publications and source records attributed to G J Whitman.

At least 73 records · Page 4Linked 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↗
PubMed1995

The phosphocreatine overshoot occurs independent of myocardial work.

Although the exact mechanism(s) responsible for the phosphocreatine/ATP overshoot have not been completely elucidated, our data demonstrate that the overshoot does not stem from reduced myocardial work, and consequently, reduced utilization of phosphocreatine (PCr). Additionally, we highlight a basic difference in the physiologic responses of skeletal and cardial muscle to work demands. By understanding the bioenergetic derangements which accompany reperfusion injury, one may hope to better salvage post-ischemic myocardium.

Adenosine Triphosphate↗
PubMed1994

Ischemic preconditioning preserves end-ischemic ATP, enhancing functional recovery and coronary flow during reperfusion.

The mechanisms by which ischemic preconditioning (IPC) protects against reperfusion (RP) injury are unknown. The purpose of this study was to relate IPC to postischemic mechanical function, vascular reactivity, and bioenergetics. Isolated perfused rat hearts were randomized to two groups. Control (CTRL) hearts underwent 25 min of global, 37 degrees C ischemia and 40 min RP. IPC hearts underwent 2.5 min ischemia and 10 min RP followed by 25 min ischemia and 40 min RP (RP40). Left ventricular developed pressure (DP) and coronary flow were continuously measured. 31P NMR spectra determined phosphocreatine and ATP concentrations in parallel hearts every 5 min. Results are means +/- SEM; n = 6/group. Significance was assumed for P < 0.05 by paired (within groups) and unpaired (between groups) t test. CTRL heart DP recovered to 35 +/- 4% of preischemic (PI) DP by RP40 (P < 0.001), while IPC heart DP reached 99 +/- 4% (P = NS vs PI; P < 0.001 vs CTRL). CTRL coronary flow recovered to only 75 +/- 3% of PI (P < 0.001) by RP40. IPC coronary flow exceeded baseline during RP (RP40 = 118 +/- 3%, P < 0.001 vs CTRL; P < 0.05 vs PI). After 25 min ischemia, CTRL heart ATP fell to 40 +/- 4% of PI (P < 0.001) while the IPC group fell to only 60 +/- 4% (P < 0.05 IPC vs CTRL; P < 0.001 vs PI). IPC preserves more end-ischemic ATP compared to CTRL hearts with a resultant improvement in mechanical function during reperfusion. Only preconditioned hearts preserve the adaptive mechanism(s) responsible for postischemic vasodilatation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1994

Infected biatrial myxoma: transesophageal echocardiography-guided surgical resection.

We identified a biatrial myxoma using transesophageal echocardiography whose right atrial component was missed with conventional transthoracic techniques. Identifying the biatrial component directs a safer approach to right heart catheterization. Infected biatrial myxomas are both rare and successfully managed using prolonged intravenous antibiotic therapy followed by resection. Atrial septal defects created during the resection of an infected myxoma may be safely repaired using a prosthetic patch.

Anti-Bacterial Agents↗
PubMed1994

A simple device to assist in needle positioning procedures.

At breast biopsy, use of a simple disk that fits into the hub of the needle can facilitate accurate placement of the needle with conventional lesion localization techniques. This disk forms a surface onto which the shadows of the localization crosshairs project so that the operator can advance the needle and maintain its alignment in the direction of the mammography beam by using the field light. The insert has been used successfully in more than 100 procedures.

Biopsy, Needle↗