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Biomedical subjects

O Poupa

Publications and source records attributed to O Poupa.

At least 37 records · Page 2Linked to original sources
PubMed1975

Adaptive tolerance of fish myocardium to hypercapnic acidosis.

Isometric, electrically paced strips of cardiac ventricle from two species of fish (plaice, Pleuronectes platessa; cod, Gadus morrhua) with different tolerance to hypoxia were compared with respect to effects of hypercapnic acidosis. Acidosis was induced by altering the equilibrating gas mixture for the muscle strip chamber from 3% CO2 in 97% 02 to 15% CO2 in 85% O2. The pH was varied further by changing the NaHCO3 content of the Cortland-Ringer solution used in the muscle chamber. After onset of acidosis with the highest buffer value of the Cortland-Ringer solution (35.7 mM NaHCO3), the force decay was similar for the initial 10 min of exposure to high Pco2. Subsequently the cod heart continued to lose force at the same rate, whereas the plaice heart regained a cardiac contractile force that after 40 min even exceeded prehypercapnic values. When buffer values were varied by changing the bicarbonate content of the Cortland-Ringer solution in steps from 0.0 to 35.7 mM NaHCO3, the cod heart showed steep force decays at all buffer values during hypercapnic acidosis. The plaice heart showed a similar decline at low buffer values but at a bicarbonate concentration above 23.8 mM NaHCO3, the initial force decline was reversed and prehypercapnic force restored.

Acid-Base Equilibrium↗
PubMed1975

Histochemical and electron microscopic studies of acute cardiomyopathy induced by restraint stress in pigs.

In 23 healthy crossbred pigs of Yorkshire and Swedish Landrace (body weight 85 to 90 kg), stress was produced by pharmacological restraint. Cardiac lesions were observed in all the experimental animals, but no alterations were seen in the 9 controls. The lesions consisted of focal myocardial necrosis with infiltration of mononuclear inflammatory cells. Histochemical stains for two dehydrogenases, cytochrome oxidase and unspecific esterase, were applied to fresh-frozen sections of heart muscle. The damaged muscle fibers exhibited initially an increase in formazan deposits, and then a decrease and total loss of enzymatic activity. A reduction or total loss of glycogen and accumulation of lipids were demonstrated in the damaged myocardium ultrastructurally. The mitochondria were swollen with focal loss of the cristae. They often exhibited electron-dense of diverse appearance. In degenerating cells, the myofilaments usually lacked the normal cross-striations whereas, in necrotic foci, the changes ranged from clumping to complete lysis of the myofilaments. The sarcoplasmic reticulum and the T system contained numerous dilated vesicles in cells with mitochondrial and myofibrillar damage. It was concluded that the myocardial alterations, following restraint stress, were caused by a reflex liberation of cardiotoxic catecholamines.

Animals↗
PubMed1975

Tissue water and pH in experimental primary cardiomyopathy induced by isoproterenol in frog.

Acute aneurysms and other morphologically defined cardiac lesions were produced in frogs by isoproterenol (IPR) as previously described. Samples from lesions verified in vivo and from macroscopically normal ventricular areas, together with samples from nontreated control animals, were analyzed for total water content, inulin space, pHe, and pHi by using DMO-14C and inulin-3H. Total cardiac tissue water content was increased in all types of lesions after IPR injection. The highest content was found in bulging, noncontractile aneurysms. Inulin space was enlarged in all heart muscle specimens from IPR-treated animals, including those without macroscopically visible lesions. Those specimens with aneurysms showed the greatest degree of enlargement. The (pHe-pHi) did not differ between injected and noninjected animals, and the noncontractile samples from aneurysms did not differ from other lesions and macroscopically intact areas. In IPR-injected animals, there was no difference in pHi between macroscopically damaged and nondamaged segments of ventricle wall. On comparing these animals to controls, however, a slight shift to the alkaline side for both pHi and pHe was observed. The (pHe-pHi) was higher in skeletal muscle than in heart muscle in both IPR-treated and nontreated animals. Tissue water increased in skeletal muscle after IPR injection, reflecting a change of intracellular water as inulin space was maintained.

Animals↗
PubMed1975

Effect of H+ on force development of the heart muscle under acute respiratory failure by cyanide.

Force decay of slowly paced (12/min) isometric ventricular strips of frog heart at low temperature (+12 degrees C) was studied under standard cellular respiratory failure (3 mM NaCN). An exponential force decay obtained at pH0 6.0 was transformed to two-step decline by increasing the pH0. The rapid phase of the force decline was pH insensitive. The slope of the second slow phase was regulated by pH0 between 6.0 and 7.7 (force reduction to 50 percent was 7 min at pH 6.0 and more than 60 min at 7.7). This effect was partially blocked by citrate (1.5-3.0 mM). Data obtained are compared with pH values measured within the normal and ischemic myocardium and are discussed with respect to the role of proton accumulation and diffusion within the ischemic ventricular wall.

Animals↗
PubMed1975

Force development of isoproterenol-damaged frog heart muscle in cyanide anoxia.

From recent experiments it is indicated that in frogs living at +25 degrees C the abnormal response to cyanide anoxia appears as soon as 4-5 hr after the first isoproterenol (IPR) injection, but the aneurysm does not appear until a few hours after the second injection of IPR. There is evidently a discrepancy between the biochemical and structural effects of IPR on the heart. The biochemical effects are probably transient as we have observed that a normal response to cyanide reappears a few weeks after the second IPR injection. It might thus be concluded that IPR causes derangement to the cells also in hearts without any visible lesions and demonstrated as a lowered resistance to histotixic anoxia. This effect precedes any structural damage if such should occur and is of a transient nature.

Animals↗
PubMed1975

The role of H+ in temporary hypoxic contractility failure: different effects of pH on the force decay and on the force recovery after reoxygenation.

The contractility of isolated ventricle strips of the frog heart (Rana pipiens) was studied under temporary N2 hypoxia and during subsequent recovery after reoxygenation under different extracellular H ion concentrations (pH 6.0-8.5). The recovery of contractile force was three times more pH-sensitive than force decay. Under slow pacing (12/min) at +12 degrees C there was almost complete recovery to control values within 60 min at pHe above 7.0. Under this pH level recovery was largely delayed (pH 6.5) or did not occur (pH 6.0). Prolongation of contraction during the reoxygenation phase, observed at low H ion concentrations, was largely delayed or absent under high concentrations of H ions.

Animals↗