Biomedical subjects

B J Rah

Publications and source records attributed to B J Rah.

6 recordsLinked to original sources

PubMed1998

Evidence of protein kinase C translocation by ischemic preconditioning in global ischemia model.

We tested recent evidence that ischemic preconditioning (PC) involves in translocation of protein kinase C (PKC) from the cytosol to myocyte membrane. Isolated Langendorff-perfused rabbit hearts (n=96) were subjected to 60 or 45 min of ischemia (I) and 120 min of reperfusion (R) with or without PC (4 cycles of 5 min I and 5 min R; or single dose of 5 min I and 10 min R), respectively. Left ventricular function and infarct size (IS) were measured; myocardial cytosolic and membrane PKC activity were determined by 32P-gamma-ATP incorporation into PKC-specific peptide. PC enhanced improvement of functional recovery and reduced IS (26.9+/-1.4% versus 15.3+/-1.9%, p<0.01, in 60 min of I; 18.3+/-2.6% versus 8.6+/-2.5%, p<0.05, in 45 min of I); cytosolic PKC activity decreased 74% of total activity (p<0.05) both in 60 and 45 min of I; membrane PKC activity increased (1.7-fold of baseline, p<0.01, in 60 min of I; 1.8-fold, p<0.01, in 45 min of I; 1.5-fold, p<0.05, in 60 of min I and 120 min of R). From these results, it is concluded that translocation of PKC from the cytosol to myocyte membranes is an important mechanism responsible for PC effect.

Animals↗

PubMed1995

Relation between ischemic preconditioning and the duration of sustained ischemia.

It has been reported that repetitive brief periods of ischemia and reperfusion (ischemic preconditioning, IP) cause a significant reduction in the extent of myocardial necrosis or in the incidence of reperfusion arrhythmias in rat heart. However, recent reports have stated that IP effect is diminished or lost in the canine or bovine heart if ischemia (mostly regional) is sustained for 40 min or longer. The main objective of this study is to assess whether IP provides myocardial protection in prolonged sustained ischemia under the condition of global ischemia in isolated rabbit heart. The hearts were subjected to 10-60 min sustained ischemia (SI) followed by 60 min reperfusion with (IP heart) or without IP (ISCH heart). IP was induced by 4 cycles of 5 min global ischemia and 5 min reperfusion. Left ventricular function (LVF), extent of infarction (EI) and ultrastructural changes were examined. As a whole, the LVF began to recover on reperfusion but there was no significant difference in the functional parameters. However, extracellular Ca2+ concentration was lower in the ISCH hearts (p < 0.05) and the EI was significantly different between the hearts which had received 60 min SI (67% in the ISCH versus 32% in the IP heart, p < 0.01). Ultrastructural changes were homogeneous in the ISCH hearts and became irreversible in accordance with increase of the duration of ischemia, while these changes were heterogeneous and restricted in the IP heart. These results suggest that IP does not attenuate the postischemic dysfunction in prolonged ischemia but it can provide an infarct size-limiting effect and delay ultrastructural changes. This cardioprotective effect may be related to calcium homeostasis.

Animals↗

PubMed1994

Quantitative study on the relation between structural and functional properties of the hearts from three different mammals.

The ultrastructural quantitative composition of left ventricular cardiac myocytes from isolated Langendorff-perfused hearts was studied in three different mammals (rabbit, guinea pig, and rat). Volume densities of mitochondria, myofibrils, and unspecified cytoplasm were determined using morphometry and were compared to functional parameters including left ventricular developed pressure (LVDP), contractility (dP/dt), heart rate, TTI (tension-time index, an index of oxygen consumption), and relative heart mass (H/B) obtained from these hearts. Each of the mammals was found to possess a very specific and characteristic quantitative composition of cardiac myocyte. Cardiac myocytes contained 26.8% mitochondria and 56.3% myofibrils in rabbits, 25.8% mitochondria and 60.9% myofibrils in guinea pigs, and 27.7% mitochondria and 58.1% myofibrils in rats. The LVDP, contractility, heart rate, and TTI were quite different among species. However, there were close correlations between the mitochondrial volume density and the LVDP (p < 0.05), and between the mitochondrial volume density and the TTI (p < 0.05), in any group of the animals. It is concluded that the mitochondrial volume density is a good indirect indicator of function of cardiac muscle related to oxidative capacity.

Animals↗

PubMed1994

Effect of pretreatment with diltiazem on left ventricular function and intracellular calcium distribution in postischemic reperfused guinea-pig hearts.

BACKGROUND: It has been previously demonstrated that pretreatment with diltiazem preserves mitochondrial function during postischemic reperfusion. AIM: The purpose of this study was to perform cytochemical and hemodynamical assessment to confirm this demonstration. METHODS: Isolated Langendorff-perfused guinea-pig hearts received 10 min of diltiazem (7.5 microM) treatment, were subjected to 10 min of global ischemia and to 20 min of reperfusion. Left ventricular function was monitored by connecting a balloon to a pressure transducer. Intracellular calcium was precipitated with potassium pyroantimonate and examined with a transmission electron microscope. RESULTS: Compared with the control and the ischemic hearts, the diltiazem-pretreated hearts showed a significant increase in the left ventricular developed pressure (LVDP), dP/dtmax (P < 0.01), and recovery rates of the LVDP (P < 0.01 versus ischemic hearts) and dP/dtmax (P < 0.05), and a decrease in the heart rate (P < 0.01). The left ventricular end-diastolic pressure (LVEDP) and leakage of creatine kinase were not significantly different. Calcium deposits were seen along the inner aspects of the sarcolemma and t-tubule membranes, and in the mitochondria of the control hearts. The number of these deposits was considerably reduced after ischemia. They reappeared principally in the mitochondria by reperfusion. In contrast, the calcium deposits reappeared along the sarcolemma, t-tubule membranes, and cell junctions, and in the mitochondria in the diltiazem-pretreated hearts. CONCLUSION: These results suggest that pretreatment with diltiazem may improve cardiac function during postischemic reperfusion, probably in part by maintenance of sarcolemmal integrity rather than by mitochondrial buffering function.

Animals↗

PubMed1992

Human fetal heart development after mid-term: morphometry and ultrastructural study.

A total of 44 normally developed human fetal hearts aged from 17 to 40 weeks gestation were provided for routine ultrastructural and morphometric studies. For morphometric analysis, the maximal thicknesses of the anterior, lateral and posterior wall of both ventricles and that of interventricular septum were measured and the left-to-right thickness ratios calculated. The cross-sectional areas of both ventricles in the plane of the greatest heart diameter were measured with computerized image analysis system. Data were analyzed using linear regression and one-way analysis of variance. Myofibril formation occurred by attachment of thin filaments into amorphous Z materials which were presented in sarcolemmal plaques, sarcoplasmic condensations, desmosomes and in Z lines. From these Z centers, myofibrils radiated many directions and branched and anastomosed with further development. This pattern of myofibrillar development continued throughout the whole fetal period. A transverse tubule system was clearly evident in later fetal development. It occurred by invagination of sarcolemma into myocardial cells and formation of subsarcolemmal caveolae. Mitochondria, well-developed Golgi complexes, glycogen granules and well-developed microvessels were found throughout the whole fetal period. Binucleated myocytes appeared by 32 weeks gestation and this suggests that myocyte hyperplasia may cease before birth in humans. The growth of both ventricular walls, the interventricular septum and that of both ventricular cross-sectional areas showed linear regression, and the left-to-right wall thickness ratios were nearly constant. Also, there were no differences in morphometric data between the left and right ventricles. In conclusion, development of the myocyte is an ongoing process which may be continued in the post-natal period in humans, and our statistical results do not support the theory of the right ventricular dominance during the fetal period.

Cell Differentiation↗

PubMed1988

Effects of diltiazem on isoproterenol- or Ca-induced ventricular myocardial cell injuries in isolated perfused rabbit heart: an electron microscopic study.

The ultrastructural changes of isoproterenol- and those of Ca-induced ventricular cell injuries were compared in rabbits and the effect of diltiazem on these injuries was studied by electron microscopy. In comparison with the controls, the isoproterenol-treated (Group A), the Ca-treated (Group B), and the diltiazem-posttreated (Groups E and F) showed severe myocardial cell damage, such as sarcolemmal disruption, mitochondrial swelling, intramitochondrial electron-dense granules, membranous structures along mitochondrial cristae, thickening or close packing of the Z-lines, separation of cell junctions, frayed myofibrils, clumping of chromatin, and intracellular fluid accumulation. These ultrastructural changes were more pronounced in the Ca-treated (Groups B and F) than in the isoproterenol-treated (Groups A and E) animals. In contrast, the diltiazem-pretreated groups (Groups C and D) showed relatively intact myocardial ultrastructure. However, intramitochondrial electron-dense granules could be frequently found, and particularly the diltiazem-pretreated and Ca-treated group (Group D) showed intracellular fluid accumulation. The results of this study could suggest the following: 1) isoproterenol-induced myocardial cell damage is similar to Ca overload, 2) pretreatment with diltiazem could reduce the deleterious effects of isoproterenol-induced myocardial cell damage, but it could not prevent the effects of Ca overload completely, and 3) posttreatment with diltiazem could not provide any beneficial effect either on the isoproterenol-induced or on the Ca-overloaded myocardial cell damage, and 4) the beneficial effects of diltiazem are probably derived from the enhanced buffering function of mitochondria to cytosolic Ca or from selective inhibition of transsarcolemmal Ca influx.

Animals↗