The myocardium and its vasculature: a histochemical comparison of the normal and chronically sympathectomized dog heart

Summary Using histochemical techniques, the reactivities of selected enzymes and other metabolic components were examined in the myocardium, coronary arteries, and coronary arterioles of normal, two-week-sympathectomized, and sham-operated canine hearts. There were no differences in the histochemistry of coronary arteries in any of the hearts, but important differences were noted in the myocardium and especially in the arterioles. The reactivities of the enzyme glucose-6-phosphate dehydrogenase and the nucleic acids were increased in arterioles of the sympathectomized heart, possibly indicating an increased protein synthesis. The reactivities of succinate dehydrogenase, NAD-isocitrate dehydrogenase, and cytochrome oxidase were reduced in myocardium and arterioles of sympathectomized hearts as well as in arterioles of sham-operated hearts; the changes were greater in the sympathectomized arterioles where there was also observed an increase in reactivity of lactate dehydrogenase. These findings suggest a depression in aerobic metabolic capacity and, in the case of the sympathectomized arteriole, imply a possible shift in adaptation from aerobic to anaerobic metabolism.     

Variables of myocardial backdiffusion,determined with 17-IODO-131 heptadecanoic acid in the normal dog heart

Summary Under normal and ischemic conditions backdiffusion of radiolabeled non-esterified fatty acids (NEFA) has been demonstrated. In the fasted normal canine heart the extraction fraction (EF) during interventions with glucose or lactate loading, vasodilation, and metabolic level augmentation was determined, and compared with the control EF. Backdiffusion alterations were deduced from the EF changes. After iv injection of 17-iodo-131 heptadecanoic acid (IHDA), 11 blood samples were drawn from aorta and coronary sinus in a time period of 60 minutes. In the control and vasodilation group the EF slowly decreased from 40 to 10%. In contrast, the EF in the noradrenaline group was constant. During glucose and lactate infusion the EF became negative within 10 min and remained negative. These results suggest that during physiological circumstances backdiffusion is determined by the metabolic level of the heart and its substrate availability.     

Alterations in intrinsic neuronal excitability during normal aging

Normal aging subjects, including humans, have difficulty learning hippocampus-dependent tasks. For example, at least 50% of normal aging rabbits and rats fail to meet a learning criterion in trace eyeblink conditioning. Many factors may contribute to this age-related learning impairment. An important cause is the reduced intrinsic excitability observed in hippocampal pyramidal neurons from normal aging subjects, as reflected by an enlarged postburst afterhyperpolarization (AHP) and an increased spike-frequency adaptation (accommodation). In this review, we will focus on the alterations in the AHP and accommodation during learning and normal aging. We propose that age-related increases in the postburst AHP and accommodation in hippocampal pyramidal neurons play an integral role in the learning impairment observed in normal aging subjects.     

Protection of the ischaemic dog heart by oxfenicine

Myocardial ischaemia was produced in closed-chest anaesthetised dogs by coronary embolisation with Sephadex microspheres. Myocardial enzyme release and lactate production were used to quantitate the severity of ischaemia. In dogs pretreated with oxfenicine (S-4-hydroxyphenylglycine; 0.1mmol.kg^?1) 1h prior to embolisation, peak lactate production (extraction ratio ?25±13%) was significantly less than in control dogs (?72±5%; p < 0.01), and the time post-embolisation at which nett lactate uptake became re-established was reduced from 1.4h to 0.4h. Myocardial release of lactate dehydrogenase isoenzyme 1 (HBDH) up to 5h post-embolisation was reduced by 40% in oxfenicine pretreated dogs and there was a similar reduction in the HBDH arterio-coronary sinus difference. Since oxfenicine pretreatment did not modify the major haemodynamic determinants of myocardial oxygen consumption, we conclude that these beneficial effects result from the ability of oxfenicine to divert myocardial metabolism from fatty acid to carbohydrate oxidation, with a consequent reduction in oxygen demand.