ABSTRACT
We tested the hypothesis that different anesthetic may produce different effects on the ability of the myocardium to recruit capillaries. The experiments were performed on the isolated hearts of five dogs anesthetized with sodium pentobarbital (Nembutal), and six dogs anesthetized with chloralose. The isolated hearts were perfused with heparinized blood at controlled flows from a support dog anesthetized with the same agent. The adaptive capacity of the heart to recruit capillaries in response to rising left ventricular pressure (LVP) was determined by measuring the permeability-surface area product. (PS) of 22Na and 51Cr-ethylenediamine tetraacetic acid (EDTA). The myocardial ability to recruit functional capillary perfusion and transport was estimated by the ratio of the PS-Na (and EDTA) obtained at a given LVP to the PS-Na (and EDTA) at LVP = 0. In chloralose-anesthetized dogs there was a gradual increase in PS as a function of LVP. At systolic LVP ranges of 60-120 mm Hg and 130-200 mm Hg, mean PS-Na ratios were 1.15 and 1.60, while mean PS-EDTA ratios were 1.10 and 1.50, respectively. In Nembutal-anesthetized dogs there was no increase in PS associated with the increases in LVP. For the same range of LVP, the mean PS ratios for both Na and EDTA varied between 1.05 and 1.18. The results show the inhibition of capillary recruitment in Nembutal anesthetized dogs for LVP of 130-200 mm Hg. They also support the concept that Nembutal inhibits the ability of the myocardium to increase blood tissue transport of nutrients in response to increased metabolic demands.
Subject(s)
Capillaries/drug effects , Coronary Vessels/drug effects , Pentobarbital/pharmacology , Adaptation, Physiological/drug effects , Animals , Biological Transport, Active/drug effects , Capillaries/metabolism , Capillary Permeability/drug effects , Chloralose/pharmacology , Coronary Vessels/metabolism , Dogs , Edetic Acid/metabolism , In Vitro Techniques , Myocardial Contraction , Perfusion , Sodium/metabolismSubject(s)
Cell Membrane Permeability/drug effects , Liver/metabolism , Phosphates/metabolism , Prostaglandins E , Adenosine Triphosphate/metabolism , Adenosine Triphosphate/therapeutic use , Animals , Lactates/antagonists & inhibitors , Liver/cytology , Liver/drug effects , Male , Phosphocreatine/metabolism , Prostaglandins E/pharmacology , Rats , Rats, Inbred Strains , Shock, Hemorrhagic/drug therapyABSTRACT
The ability of exogenous ATP-MgCl2 to reverse the inhibition of ATP-dependent intracellular reactions by hemorrhagic shock was studied. Levels of ornithine in the postperfusion fluid were lower in animals receiving ATP-MgCl2 than in placebo-treated control animals (338.6 +/- 167.0 versus 692.1 +/- 67.2 mumol). Arginine levels were higher (399.1 +/- 130.1 versus 34.3 +/- 59.1 mumol) in ATP-MgCl2-treated animals. Ability of in vitro ATP to enter the cell and inhibit lactate formation (Crabtree effect) was significantly less in those animals receiving in vivo ATP-MgCl2 (81.4 +/- 11.1% versus 57.7 +/- 10.1%). Glutamate levels were not decreased by shock but were significantly increased by treatment with ATP-MgCl2 compared to placebo (190.5 +/- 48.8 versus 122.6 +/- 36.3 mumol). These data indicate that exogenously administered ATP-MgCl2 can reverse the inhibition of ornithine metabolism and the changes in lactate inhibition seen in hemorrhagic shock. These are both intracellular ATP-dependent reactions.
