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Biomedical subjects

G F Tyers

Publications and source records attributed to G F Tyers.

At least 145 records · Page 8Linked to original sources
PubMed1975

Amelioration of the effects of ischemic cardiac arrest by the intracoronary administration of cardioplegic solutions.

Interruption of coronary flow during cardiac surgical procedures provides a bloodless flaccid heart and allows precise and rapid correction of complex cardiac defects. However, myocardial damage occurs in direct proportion to the duration of the ischemia. As the induction of cardioplegia simulataneous with the initiation of cardiac ischemia helps to preserve cardiac energy reserves and thus myocardial integrity, the identification of a consistently reliable cardioplegic technique is desirable. Isolated perfused working rat hearts were made ischemic for one hour by aortic cross-clamping and were compared with hearts rendered cardioplegic at the onset of ischemia by the intracoronary administration of 5 ml of a hypothermic solution: 1) Krebs-Henseleit buffer, 2) Ringer's lactate, 3) tetrodotoxin, 4) potassium chloride, or 5) potassium citrate. Cardiac output, heart rate, aortic pressure and coronary flow were determined pre and post-ischemia. When compared to time-matched controls and hearts arrested with potassium or tetrodotoxin, the ischemia and ischemia-Ringer's lactate groups showed significant post cross-clamp depression of all measured parameters. Intracoronary Ringer's lactate, although often used as an adjunct to ischemic arrest, was not of significant value. In contrast, hearts arrested with tetrodotoxin, potassium chloride or potassium citrate showed no significant post-ischemic functional or histologic deficit. Perfusion with hypothermic Krebs-Henseleit buffer protected the myocardium better than did Ringer's lactate but less well than the tetrodotoxin or isotonic high potassium solutions. The induction of hypothermic metabolic arrest of the heart by briefly perfusing the coronary arteries via the aortic root with isotonic buffered solutions results in markedly improved myocardial tolerance to one hour of ischemia and avoids the problems of low cardiac output and ventricular irritability previously reported with hypertonic potassium citrate arrest.

Animals↗
PubMed1975

The advantages of transthoracic placement of permanent cardiac pacemaker electrodes.

To determine the effect of stimulation site on cardiac pacing thresholds, identical, small-surface area, cathodal, Elgiloy electrodes were placed intramyocardially on the left and right ventricular apices and transvenously into the right ventricular apex of 20 dogs in complete heart block. At seven stimulus durations, threshold voltage and current were measured directly with an oscilloscope and current probe. Left ventricular intramyocardial pacing required less threshold stimulus energy than right ventricular intramyocardial or right ventricular endocardial pacing. Previous studies that determined lower thresholds with transvenous right ventricular endocardial leads than with directly placed myocardial leads used stimulating electrodes of differing configuration, surface area, and materials at the different sites and/or used epicardial rather than intramyocardial electrodes. These factors biased the results in favor of the endocardial site. When all clinical and electrophysiological facotrs are considered, direct intramyocardial placement of electrodes deserves a much wider acceptance and application than it now enjoys.

Animals↗
PubMed1975

The mechanism of myocardial protection from ischemic arrest by intracoronary tetrodotoxin administration.

Intracoronary injection of 14 mcg. of tetrodotoxin into the ischemic isolated rat heart resulted in immediate cessation of mechanical activity. Upon reperfusion with oxygenated, modified Krebs-Henseleit bicarbonate buffer in a modified Langendorff apparatus, all hearts recovered normal rate, rtythm, and contractile vigor after up to 60 minutes of ischemia. In contrast, all hearts not administered tetrodotoxin showed bradycardia, irregular rhythm, and weak contraction upon reperfusion after 30 and 45 minutes of ischemia; after 60 minutes, no mechanical activity was evident. The improved cardiac function following ischemia in the tetrodotoxin-treated hearts was associated with persistence of normal adenosine triphosphate (ATP) levels after up to 30 minutes of ischemia and normal or elevated creatine phosphate (CP) levels after up to 60 minutes of ischemia. On the other hand, ATP and CP levels progressively declined to reach 50 per cent of normal values after 30 minutes in the ischemic hearts without tetrodotoxin. These findings indicate that postarrest ATP and CP levels play an important role in myocardial recovery after ischemic arrest.

Adenosine Triphosphate↗
PubMed1975

Effects of acid-base imbalance on myocardial pacing thresholds.

The effects of acid-base imbalance on ventricular pacing thresholds were studied in anesthetized dogs with complete heart block with the use of an oscilloscope and current probe. Acidosis (base excess-15) and alkalosis (base excess + 15)both resulted in significant increases in threshold voltage and current requirements at all stimulus durations tested. Chronaxie, however, was not significantly affected by shifts in acid-base balance. Abnormalities of acid-base status may adversely affect the accuracy of threshold values obtained during evaluation of different electrode designs and during electrodes implantation for clinical cardiac pacing.

Acidosis↗
PubMed1975

The mechanism of myocardial damage following potassium citrate (Melrose) cardioplegia.

To determine the reasons for clinical failure of Melrose solution, potassium arrest was studied in isolated working rat hearts. Eight control hearts were stable for 2-1/2 hours. After 1/2 hour of work, 42 experimental hearts were subjected to 1 hour of ischemis by aortic cross-clamping with unmodified ischemia in eight hearts and ischemia with simultaneous intracoronary injection of 5 ml. of 4 degrees C. (1)Krebs-Henseleit buffer in seven hearts (2)potassium chloride buffer in six hearts, (3)potassium citrate buffer in eight hearts (both 26 mEq. per liter of K, approximately 300 mOsm. per liter), (4)Melrose solution in seven hearts (greater than 200 mEq. per liter of K, greater than 400 mOsm. per liter), (5)hypertonic potassium citrate buffer in six hearts (26 mEq. per liter of K, greater than 400 mOsm. per liter). The pH of all solutions was 7.8 plus or minus 0.1. After recovery isotonic potassium citrate- and potassium chloride-arrested hearts and time-matched control hearts showed no significant differences in cardiac output, coronary flow, systolic pressure, or heart rate. Hypertonic potassium citrate decreased the recovery of cardiac function after arrest and Melrose arrest was not significantly different from unmodified ischemia. Intracoronary cold isotonic Krebs-Henseleit buffer was better than Melrose arrest but inferior to 26 mEq. er liter of potassium arrest. Arrest with 26 mEq. per liter of potassium augments perfusion hypothermia and prevents significant functional and histologic myocardial damage during 1 hour of ischemis. Previous authors assumed that hypertonicity and citrate were responsible for poor results with Melrose solution, but high potassium concentration is the major deleterious factor with hypertonicity playing a contributory role.

Animals↗
PubMed1975

Nonmechanical factors affecting aortocoronary vein graft flow.

To study aortocoronary vein graft flow, hemodynamic measurements were made in 17 patients with 22 grafts while on cardiopulmonary bypass during ventricular fibrillation and sinus rhythm and 15 minutes after termination of cardiopulmonary bypass. When compared with graft flow to the stable working heart, flow to the nonworking heart in sinus rhythm was reduced 50%. When fibrillating, the nonworking heart received 33% more flow than when in sinus rhythm but still significantly less flow than the working heart. All hemodynamic parameters measured, including flow in 12 grafts, remained stable between 15 minutes and 60 minutes following cardiopulmonary bypass. In contrast, heart rate and flow in 10 grafts fell within five minutes after 1 mg of propranolol was given intravenously. Although it was still reduced, heart rate had begun to rise 30 minutes after propranolol, but graft flow did not begin to return toward predrug control levels until over 60 minutes after drug administration. Further reduction in aortocoronary vein graft flow after heart rate had started to increase supports the possibility of a direct propranolol action reducing myocardial oxygen consumption in addition to its bradycardiac effect. This study shows the sensitivity of intraoperative vein graft flow to physiological and pharmacological factors and the need to standardize the technique and timing of flow measurements if their value for predicting long-term graft patency is to be determined.

Blood Flow Velocity↗