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Kinematic analysis of ∼ 1500 fault-slip measurements from the Puna plateau and adjacent foreland of northwestern Argentina suggests that two regional kinematic regimes characterize late Cenozoic deformation: a thrust phase with ∼WNW-ESE shortening and subvertical extension followed by a strike-slip phase with ∼ENE-WSW shortening and ∼NNW-SSE extension. Radiometric dating combined with field relationships demonstrate that thrust faulting started by 13 Ma and lasted, at least locally, until 1 Ma, and that strike-slip faulting started by 2 Ma and is still active. The shortening direction of the thrust phase, which accounts for most of the Andean shortening, differs from the coeval plate tectonic convergence direction and probably cannot be explained by later oroclinal bending. Paleostructural control of deformation kinematics and/or strike-slip faulting along the thermally weakened volcanic arc might explain the Mio-Pliocene shortening direction. The subhorizontal extension direction of the strike-slip phase is evident at all elevations studied, suggesting that local body forces do not drive it. A decrease in South America-Nazca plate convergence rate and/or complex three-dimensional effects, possibly including kinematic variation with depth in the crust, might provide a satisfactory explanation.

We previously reported that the very act of cannulating a lung lymph vessel could alter the unique flow characteristics that existed within the lymphatic before cannulation. We postulated that this phenomenon could hold true for lymphatics draining any organ within the body. Since it is frequently important to know the relationship between the transmicrovascular fluid flux and true lymph flow rate, it would be critical that a cannulated lymphatic vessel have the same flow characteristics as those uncannulated vessels draining the same organ. In order to test our hypothesis we cannulated lymph vessels draining the heart, liver, small intestine, kidney, and skeletal muscle. By altering the lymphatic outflow pressure (normally related to systemic venous pressure) and by using lymphatic cannulas of various resistance, we were able to demonstrate that lymph flow varied linearly with lymphatic outflow pressure in every organ. By increasing transmicrovascular fluid flux and lymph flow rate in each organ we were also able to demonstrate that effective resistance of the lymphatic vessels and the effective pressure driving lymph flow varied as a function of the physical characteristics of the organ under investigation. Characteristic effective resistances of the heart, liver, skeletal muscle, kidney, and small intestine lymphatics decreased by 83, 40, 61, 36, and 50%, respectively. Along with these changes in effective resistance, the effective lymph driving pressure in the same organs varied by 49, 0, 257, 0, and 63%, respectively. We conclude that the lymph flow from all of the organs studied varies linearly with changes in lymphatic outflow pressure and that lymphatic resistance and lymph driving pressure vary in a unique manner in each organ depending on the physical characteristics of that organ.

The lung lymph flow rate ( Q L ) is increased in edema caused by an increase in lung microvascular permeability. This increase in Q L could be caused by either a decrease in the effective resistance of the lymph vessels (RL), or by an increase in the effective lymph driving pressure (PL), or by a change in both RL and PL. We estimated PL and RL from the linear relationship between Q L and the pressure at the outflow end (PO) of five cannulated dog lung lymph vessels ( R L = −ΔP O Δ Q L and PL = the PO at which Q L = 0 ). We increased lung microvascular permeability by giving the dogs 100 mg/kg of alloxan and found that Q L increased from 24.5 ± 8.9 μl/min to 112 ± 41 μl/min (mean ± SD). RL decreased from 0.35 ± 0.12 to 0.11 ± 0.04 cm H2O min/μl and PL increased from 8.5 ± 1.5 to 15.9 ± 2.7 cm H2O. We then increased the capillary pressures from 18.3 ± 3.8 to 41.3 ± 7.3 cm H2O and Q L increased to 169.9 ± 47.8 μl/min. PL increased by an additional 6.3 cm H2O but RL decreased by only an additional 0.02 cm H2O min/μl. These results show that the Q L vs PO relationship is changed in edema secondary to an increase in microvascular permeability, and that this change can be represented as changes in RL and PL. In terms of these parameters, Q L increased in edema as a result of a decrease in RL and an increase in PL.