Biomedical subjects

K Zmudka

Publications and source records attributed to K Zmudka.

38 records · Page 3Linked to original sources

PubMedDate not supplied

Ischemic and reperfusive release of the endogenous purines and its influence on the myocardial viability during beta-adrenergic blockade.

The aim of this study was to estimate ischemic and reperfusive release of myocardial adenosine degradation products (MADP) during beta-adrenergic blockade and its relation to infarct size (IS) and viable myocardium size (VM). In a group of 24 shepherd-mongrel dogs, randomly assigned to a metoprolol (M-) and placebo-group (P-group), occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion with recombinant tissue plasminogen activator was performed. Regional myocardial blood flow (MBF) was measured by the radiolabelled microsphere technique. Blood samples from aorta and great cardiac vein were collected to evaluate the concentrations of MADP. The triphenyltetrazolium chloride perfusion and fixation technique was used for infarct size measurement. MBF in the area at risk decreased in both groups during ischemia, but it was significantly higher (p = 0.013) in M-group. Recanalization of LAD was associated with an increase in flow in postischemic vascular bed. MBF was significantly higher (p = 0.024) in P-group during late reperfusion. In M-group IS was smaller (p = 0.007) and VM was bigger (p = 0.007). The correlation between arterial adenosine concentration during early reperfusion and IS (p = 0.044, r = -0.588) or VM (p = 0.036, r = 0.607) in M-group was noted. Values of net MADP balances significantly increased during early reperfusion. The correlation between reperfusive net MADP balance and IS (p = 0.00005, r = 0.906) or VM (p = 0.016, r = -0.675) in M-group was observed. The amount of MADP released during reperfusion correlates with the IS and is inversely proportional to the area of VM. The endogenously released adenosine may have additional cardioprotective effect during beta-adrenergic blockade.

Adenosine↗

PubMedDate not supplied

[Lack of additional action of oxygen on pulmonary artery pressure at the peak of verapamil or captopril action in pulmonary hypertension secondary to mitral stenosis].

The aim of the study was to investigate whether oxygen causes a further decrease in pulmonary artery pressure after administration of calcium channel blocker-verapamil-or angiotensin converting enzyme inhibitor-captopril-in the secondary pulmonary hypertension. We studied 37 patients with the secondary pulmonary hypertension (mean pulmonary artery systolic pressure = 56.1 mm Hg) due to mitral stenosis. After having completed hemodynamic diagnostic procedures, basal oxygen test was performed and pulmonary artery pressure was recorded at 10 min of oxygen breathing. Then, 10 mg of verapamil was injected into the pulmonary artery of 16 patients and 21 patients received 75 mg of oral captopril. At the peak of vasodilation, 30 min after verapamil and 90 min after captopril administration, pulmonary artery pressure was recorded and oxygen test was repeated. Baseline oxygen test produced a statistically significant decrease in pulmonary artery pressure. Verapamil and captopril also lowered pulmonary artery systolic and diastolic pressures. The second oxygen test did not cause a further decrease in the pulmonary artery pressure; mean pulmonary artery systolic pressure was 52.3 +/- 23.7 mm Hg, pulmonary artery diastolic pressure 22.7 +/- 10.6 mm Hg before and 49.1 +/- 23.8 mm Hg and 23.0 +/- 13.5 mm Hg, respectively after the test in verapamil group, and 47.0 +/- 15.5 mm Hg and 21.7 +/- 8.4 mm Hg before and 46.6 +/- 15.4 mm Hg, respectively in captopril subset. The results may support the thesis that vasodilating effect depends rather on the degree of pulmonary vascular changes than on the vasodilatory mechanism of particular drugs.

Adult↗