Heart, in vivo

Weissenburger, J., Nesterenko, V.V. and Antzelevitch, C. (2000) Transmural heterogeneity of ventricular repolarization under baseline and long QTconditions in the canine heart in vivo torsades de pointes develops with halothane but not pentobarbital anesthesia. Journal of Cardiovascular Electrophysiology, 11, 290-304. 

Abai, A., Hobart, P. and Barnhart, K. (1999) Insulin delivery with plasmid DNA. Hum. Gem Ther., 10, 2637-2649. Acsadi, G., Jiao, S., Jani, A., Duke, D., Williams, P., Chong, W. et al (1991a) Direct gene transfer and expression into rat heart in vivo. New Biol., 3, 71-81. 

Byun, J. H., Huh, J. E., Park, S. J. et al. (2000). Myocardial injury-induced fibroblast proliferation facilitates retroviral-mediated gene transfer to the rat heart in vivo. J. Gene Med. 2(1), 2-10. 

Lange, M., Smul, T.M., Blomeyer, C.A., Redel, A., Klotz, K.N., Roewer, N., and Kehl, F. 2006. Role of the betal-adrenergic pathway in anesthetic and ischemic preconditioning against myocardial infarction in the rabbit heart in vivo. Anesthesiology 105 503-510. 

Piot, C.A., Martini, J.F., Bui, S.K., and Wolfe, C.L. 1999. Ischemic preconditioning attenuates ischemia/reperfusion-induced activation of caspases and subsequent cleavage of poly(ADP-ribose) polymerase in rat hearts in vivo. Cardiovasc. Res. 44 536-542. 

Bhuiyan MS, Fukunaga K. Inhibition of HtrA2/Omi ameliorates heart dysfunction following ischemia/reperfusion injury in rat heart in vivo. Eur. J. Pharmacol. 2007 557 168-177. 

C. Depre, G. L. Shipley, W. Chen, Q. Han, T. Doenst, M. L. Moore, S. Stepkowski, P. J. Davies and H. Taegtmeyer, Unloaded heart in vivo replicates fetal gene expression of cardiac hypertrophy, Nature Medicine 4, 1269-1275 (1998). 

W. Schlack, B. Preckel, H. Barthel, D. Obal and V. Thamer, Halothane reduces reperfusion injury after regional ischemia in the rabbit heart in vivo, Br. J. Anaesth. 79, 88-96 (1997). 

R. Schulz, P. Gres and A. Skyschally, Ischemic preconditioning preserves connexin 43 phosphorylation during sustained ischemia in pig hearts in vivo, FASEB. J. 17, 1355-1357 (2003). 

On top, an increased intracellular calcium concentration in the presence of some remaining or restored energy production can induce cardiomyocyte hypercontracture,69 and opening of gap junctions might be involved in the transmission of factors triggering hypercontracture between adjacent cells,32,87 such as sodium.87,88 Indeed, cell-cell transmission of hypercontracture can be attenuated in isolated rat cardiomyocytes, in rat hearts in vitro and in pig hearts in vivo by the gap junction uncoupler heptanol (1-2 mM) in pig hearts in vivo heptanol reduces myocardial shrinkage and infarct size as well.89 Similar results have been obtained with butanedione monoxime, another gap junction uncoupler,90 in pig hearts in vivo.91... 

C.A. Piot, D. Padmanaban, P.C. Ursell, R.E. Sievers, C.L. Wolfe, Ischemic preconditioning decreases apoptosis in rat hearts in vivo, Circulation 96, 1598-1604 (1997). 

In isolated rabbit heart preparations, pr-MDI and bu-MDI (3x10-5m) produced a negative inotropic action with no alteration in chronotropy (62). The negative inotropic action was sizably smaller than the increase in coronary flow produced by these agents (62). The decrease in force of contraction is beneficial for the purpose of conservation of oxygen in an ischemic heart. In-vivo studies in dogs (65) also demonstrated that the tertiary MDIs did not alter cardiac rate. 

Since ouabain decreased cation transport and yet stimulated phosphate exchange in phosphatidic acid over a short period, any relationship of this particular lipid to cation transport would be difficult to explain. Digitoxin also enhanced the uptake of labeled phosphate into the phospholipids of rat heart in vivo (Marinetti et al., 1%1) the effect was greatest with ethanolamine phospholipids, but in these experiments the possibility of an increased permeability of the tissue to phosphate was not eliminated. Recent studies have strongly suggested that ouabain inhibits the sodium- and potassimn-activated adenosinetriphosphatase (Chamock and Post, 1963). It may well do this by specifically inhibiting the potassium-dependent phosphorolysis reaction which leads to the release of orthophosphate (see also, McIIwain, 1963). 

The effect of insulin on the kinetics of glucose transport have been studied by Morgan et al. (1961a). They find that insulin increases the Km and Fm x of transport in the perfused isolated rat heart. Fisher and Zachariah (1961) have concluded that insulin increases the Km of L-arabinose and D-xylose transport. In peripheral tissues or in the heart, in vivo evidence has been obtained that insulin lowers the tissue threshold for glucose (i.e., permits uptake of glucose at lower concentration) (Butterfield et al., 1958 Hackcl, 1960). 

There is a strong structural resemblance of (116a) to the anorectic compound mazindol (117). This resemblance is also found in the NA-uptake inhibiting properties (117) is a potent blocker of NA-accumulation of the rat heart in vivo [301]. Compound (118), obtained by protonation of (117), is an even more potent NA uptake inhibitor, and also shows strong DA and 5-HT uptake blocking properties in vitro [106]. 

In an effort to identify those tetrahydroisoquinolines which will inhibit the action of COMT, but will not act as false neurotransmitters, a series of tetrahydroisoquinolines were evaluated as substrates and inhibitors of this enzyme, and were also tested for their ability to stimulate norepinephrine release from mouse hearts in vivo. Methyl substituents at C-2 and C-4 of 6,7-dihydroxytetrahydroisoquinolines had little effect in regard to COMT, but did eliminate the norepinephrine depleting activity. The interesting exception was 6,7-dihydroxy-2,2-dimethyltetrahydroisoquinolinium iodide which was an active depleter of norepinephrine from mouse hearts. ... 

Acsadi, G. et al., Direct gene transfer and expression into rat heart in vivo. New Biol, 3,71,1991. 

Rumsey WL, Pawlowski M, Lejavardi N, Wilson DF. Measurement of oxygen pressure in the heart in vivo using phosphorescence quenching. Adv Exp Med Biol 1994a 361 93-97. 

---