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Biomedical subjects

J R Handy

Publications and source records attributed to J R Handy.

28 records · Page 2Linked to original sources
PubMed1996

Use of the gastroepiploic artery for coronary revascularization.

In summary, use of the gastroepiploic artery for coronary revascularization provides a reliable arterial conduit without increasing post-operative length of hospitalization, peri-operative morbidity or mortality. Reported mid-term patency rates exceed those of saphenous vein grafts and are comparable to internal thoracic artery grafts. Thus, the gastroepiploic artery is exceeded only by the internal thoracic artery as the preferable conduit in coronary revascularization.

Arteries↗
PubMed1995

Postinfarction cardiac rupture after coronary revascularization.

Rupture of the myocardium is a catastrophic complication of acute myocardial infarction. Coronary revascularization has been increasingly utilized for the treatment of postinfarction angina. Further, myocardial infarction is a well known complication of coronary revascularization. Nonetheless, cardiac rupture after coronary revascularization has been rarely described. Described herein are three such cases with a review of the literature.

Aged↗
PubMed1994

Pacemaker failure due to pocket emphysema.

Pocket emphysema is an unusual cause of failure of a permanent pacemaker. Reported herein is temporary failure of a unipolar DDD pacemaker caused by pocket emphysema in a pediatric patient.

Equipment Failure↗
PubMed1994

Hypothermic potassium cardioplegia impairs myocyte recovery of contractility and inotropy.

Acute postoperative left ventricular dysfunction after hypothermic, crystalloid potassium cardioplegia occasionally occurs. This project examined myocyte contractility and inotropic responsiveness after hypothermic arrest with and without potassium cardioplegia. Isolated swine left ventricular myocytes were placed in a thermostatically controlled chamber (37 degrees C) that contained a standard cell medium, pulse stimulated at 1 Hz, and steady-state contractions were measured by computer-assisted video microscopy with and without isoproterenol (25 nmol/L). After baseline measurements were taken the myocytes were randomly assigned to the following treatments: (1) control group with infusion of 37 degrees C crystalloid solution and maintained at 37 degrees C for 3 hours (n = 23), (2) hypothermia group with infusion of 4 degrees C crystalloid without potassium and stored at 4 degrees C for 3 hours (n = 22), (3) hypothermic cardioplegia group with infusion of a crystalloid cardioplegia (oxygenated, buffered 4 degrees C Ringer's solution with 24 mEq/L K+) and then stored at 4 degrees C for 3 hours (n = 35). After treatment the myocytes were then rewarmed to 37 degrees C by infusion of medium, and contractile measurements were repeated. In the control group, the percent and velocity of shortening were identical to those in baseline measurements: 6.4% +/- 0.4% and 53 +/- 5 microns/sec, respectively, and these values remained unchanged in the hypothermia group: 6.5% +/- 0.4% and 51 +/- 3 microns/sec, respectively. However, in the hypothermic cardioplegia group, the percent and velocity of shortening were significantly lower with rewarming: 4.8% +/- 0.4% and 35 +/- 3 microns/sec, respectively, p < 0.05). Isoproterenol caused increased percent and velocity of shortening in both the control and hypothermia groups: 10.0% +/- 0.6% and 9.5% +/- 0.9% and 81.6 +/- 8 microns/sec and 71.4 +/- 8 microns/sec, respectively. This response was significantly blunted in the cardioplegia group (8.9% +/- 0.8% and 56.9 +/- 7 microns/sec, p < 0.05). With an isolated myocyte system that is independent of extracellular and perfusion effects, hyperkalemic cardioplegic solution resulted in depressed myocyte contractile performance after rewarming. Potassium cardioplegia also caused a blunted inotropic responsiveness on rewarming. A potential contributory factor for the depressed left ventricular function after the use of potassium cardioplegia is a direct depression in myocyte contractility.

Analysis of Variance↗
PubMed1986

Thromboxane A2 mediates hemodynamic and respiratory dysfunction in graded bacteremia.

Thromboxane A2 has been implicated as a mediator of cardiorespiratory dysfunction in sepsis. This study evaluated whether or not thromboxane A2 was necessary or sufficient for these adverse effects to occur during bacteremia. Fourteen adult swine under barbiturate anesthesia and breathing room air were monitored with arterial and pulmonary artery catheters. Animals were studied for 4 hours in three groups: group I, graded infusion of 10(9)/ml Aeromonas hydrophila; group II, Aeromonas hydrophila infusion plus SQ 29,548 (thromboxane A2 antagonist); and group III, U46619 (thromboxane A2 agonist) infusion in normal swine to pulmonary artery pressures observed in group I. Hemodynamic parameters, arterial and mixed venous blood gases, and plasma thromboxane B2 and prostaglandin 6-keto-F1 were measured. At sacrifice after 4 hours, wet-to-dry lung weights were calculated. Results indicated that thromboxane A2 was necessary and sufficient for the development of pulmonary hypertension and impaired alveolar-capillary oxygen diffusion in graded bacteremia. It was necessary but not sufficient for increased lung water to occur and sufficient but not necessary for decreased cardiac index and stroke volume index. Thromboxane A2 was neither sufficient nor necessary to the pathophysiology of systemic hypotension during graded bacteremia. Plasma prostaglandin 6-keto-F1 levels were increased in hypotensive animals with sepsis, suggesting its involvement in hypotension during sepsis.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗