Biomedical subjects

J R Hinton

Publications and source records attributed to J R Hinton.

3 recordsLinked to original sources

PubMed1997

Acute intensive interval training and in vitro t-lymphocyte function.

Five male endurance-trained runners completed an interval running session of 15 x 1-min intervals at 95% VO2 max. Venous blood samples were collected pre-exercise and then immediately, 30- and 60-minutes post-exercise. The response of cultures of total lymphocytes to mitogen (phytohaemagglutinin) were significantly reduced immediately after exercise, but returned to resting levels by 30-min of recovery. Conversely, the mitogen response of cultures of pure T-lymphocytes (CD4+ and CD8+ cells), separated using a magnetic separation technique, showed no significant change during the exercise and recovery periods. These data showed directly that there was no apparent change in the functional capability of T-lymphocytes following an intensive interval training session. Furthermore, there were significant changes in the composition of the total lymphocyte cultures immediately post-exercise; increased numbers of natural killer (NK) cells (CD56+) and T-suppressor cells (CD8+) and decreased numbers of T-helper cells (CD4+). There were also significant correlations between total mitogen response and the composition of the cultured lymphocytes. These data indicated that the large increases in NK cells, relative to T-cells, following intensive exercise, were the most likely cause of the reduced mitogen response of total lymphocyte cultures.

Adult↗

PubMed1976

Site of myocardial infarction. A determinant of the cardiovascular changes induced in the cat by coronary occlusion.

The influence of site of acute myocardial infarction on heart rate, blood pressure, cardiac output, total peripheral resistance (TPR), cardiac rhythm, and mortality was determined in 58 anesthetized cats by occlusion of either the left anterior descending (LAD), left circumflex or right coronary artery. LAD occlusion resulted in immediate decrease in cardiac output, heart rate, and blood pressure, an increase in TPR, and cardiac rhythm changes including premature ventricular beats, ventricular tachycardia, and occasionally ventricular fibrillation. The decrease in cardiac output and increase in TPR persisted in the cats surviving a ventricular arrhythmia. In contrast, right coronary occlusion resulted in a considerably smaller decrease in cardiac output. TPR did not increase, atrioventricular condition disturbances were common, and sinus bradycardia and hypotension persisted in the cats recovering from an arrhythmia. Left circumflex ligation resulted in cardiovascular changes intermediate between those produced by occlusion of the LAD or the right coronary artery. Mortality was similar in each of the three groups. We studied the coronary artery anatomy in 12 cats. In 10, the blood supply to the sinus node was from the right coronary artery and in 2, from the left circumflex coronary artery. The atrioventricular node artery arose from the right in 9 cats, and from the left circumflex in 3. The right coronary artery was dominant in 9 cats and the left in 3. In conclusion, the site of experimental coronary occlusion in cats is a major determinant of the hemodynamic and cardiac rhythm changes occurring after acute myocardial infarction. The cardiovascular responses evoked by ligation are related in part to the anatomical distribution of the occluded artery.

Animals↗

PubMedDate not supplied

Deleterious effects of taurine in cats with digitalis-induced arrhythmias.

An established model of digitalis toxicity was used to investigate the antiarrhythmic properties of taurine. I.v. doses of taurine ranging from 0.01 to 4.0 mmole/kg were ineffective in converting a deslanoside-induced arrhythmia to sinus rhythm. Indeed, taurine was found to aggravate the arrhythmia and in three experiments precipitated ventricular fibrillation. In addition, pretreatment with 5 mmole/kg taurine i.v. had no significant effect on the doses of deslanoside to produce ventricular arrhythmia and fibrillation.

Animals↗