1491: HEMODYNAMIC AND ECMO FLOW RESPONSE TO ALBUMIN VERSUS CRYSTALLOID THERAPY

Abstract. A large number of Himalayan glacier catchments are under the influence of humid climate with snowfall in winter (November–April) and south-west monsoon in summer (June–September) dominating the regional hydrology. Such catchments are defined as "Himalayan catchment", where the glacier meltwater contributes to the river flow during the period of annual high flows produced by the monsoon. The winter snow dominated Alpine catchments of the Kashmir and Karakoram region and cold-arid regions of the Ladakh mountain range are the other major glacio-hydrological regimes identified in the region. Factors influencing the river flow variations in a "Himalayan catchment" were studied in a micro-scale glacier catchment in the Garhwal Himalaya, covering an area of 77.8 km2. Three hydrometric stations were established at different altitudes along the Din Gad stream and discharge was monitored during the summer ablation period from 1998 to 2004, with an exception in 2002. These data have been analysed along with winter/summer precipitation, temperature and mass balance data of the Dokriani glacier to study the role of glacier and precipitation in determining runoff variations along the stream continuum from the glacier snout to 2360 m a.s.l. The study shows that the inter-annual runoff variation in a "Himalayan catchment" is linked with precipitation rather than mass balance changes of the glacier. This study also indicates that the warming induced an initial increase of glacier runoff and subsequent decline as suggested by the IPCC (2007) is restricted to the glacier degradation-derived component in a precipitation dominant Himalayan catchment and cannot be translated as river flow response. The preliminary assessment suggests that the "Himalayan catchment" could experience higher river flows and positive glacier mass balance regime together in association with strong monsoon. The important role of glaciers in this precipitation dominant system is to augment stream runoff during the years of low summer discharge. This paper intends to highlight the importance of creating credible knowledge on the Himalayan cryospheric processes to develop a more representative global view on river flow response to cryospheric changes and locally sustainable water resources management strategies.

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Myocardial blood flow response to isometric (handgrip) and treadmill exercise in coronary artery disease.

Circulation ◽

10.1161/01.cir.51.1.126 ◽

1975 ◽

Vol 51 (1) ◽

pp. 126-131 ◽

Cited By ~ 31

Author(s):

D K Lowe ◽

D A Rothbaum ◽

P L McHenry ◽

B C Corya ◽

S B Knoebel

Keyword(s):

Coronary Artery Disease ◽

Blood Flow ◽

Coronary Artery ◽

Myocardial Blood Flow ◽

Treadmill Exercise ◽

Isometric Handgrip ◽

Blood Flow Response ◽

Flow Response ◽

Artery Disease

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Hypoxia and Hypotension Transform the Blood Flow Response to Cortical Spreading Depression from Hyperemia into Hypoperfusion in the Rat

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.2008.35 ◽

2008 ◽

Vol 28 (7) ◽

pp. 1369-1376 ◽

Cited By ~ 56

Author(s):

Inna Sukhotinsky ◽

Ergin Dilekoz ◽

Michael A Moskowitz ◽

Cenk Ayata

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Cortical Spreading Depression ◽

Spreading Depression ◽

Ischemic Penumbra ◽

Doppler Flowmetry ◽

Blood Flow Response ◽

Flow Response ◽

Normal Rat ◽

Cortex Cérébral

Cortical spreading depression (CSD) evokes a large cerebral blood flow (CBF) increase in normal rat brain. In contrast, in focal ischemic penumbra, CSD-like periinfarct depolarizations (PID) are mainly associated with hypoperfusion. Because PIDs electrophysiologically closely resemble CSD, we tested whether conditions present in ischemic penumbra, such as tissue hypoxia or reduced perfusion pressure, transform the CSD-induced CBF response in nonischemic rat cortex. Cerebral blood flow changes were recorded using laser Doppler flowmetry in rats subjected to hypoxia, hypotension, or both. Under normoxic normotensive conditions, CSD caused a characteristic transient CBF increase (74 ± 7%) occasionally preceded by a small hypoperfusion (−4 ± 2%). Both hypoxia ( pO2 45 ± 3 mm Hg) and hypotension (blood pressure 42 ± 2 mm Hg) independently augmented this initial hypoperfusion (−14 ± 2% normoxic hypotension; −16 ± 6% hypoxic normotension; −21 ± 5% hypoxic hypotension) and diminished the magnitude of hyperemia (44 ± 10% normoxic hypotension; 43 ± 9% hypoxic normotension; 27 ± 6% hypoxic hypotension). Hypotension and, to a much lesser extent, hypoxia increased the duration of hypoperfusion and the DC shift, whereas CSD amplitude remained unchanged. These results suggest that hypoxia and/or hypotension unmask a vasoconstrictive response during CSD in the rat such that, under nonphysiologic conditions (i.e., mimicking ischemic penumbra), the hyperemic response to CSD becomes attenuated resembling the blood flow response during PIDs.

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Na delivery and ENaC mediate flow regulation of collecting duct endothelin-1 production

AJP Renal Physiology ◽

10.1152/ajprenal.00034.2012 ◽

2012 ◽

Vol 302 (10) ◽

pp. F1325-F1330 ◽

Cited By ~ 19

Author(s):

Meghana M. Pandit ◽

Kevin A. Strait ◽

Toshio Matsuda ◽

Donald E. Kohan

Keyword(s):

Plasma Membrane ◽

Collecting Duct ◽

Extracellular Fluid ◽

Na Channel ◽

Endothelin 1 ◽

Flow Response ◽

Mrna Content ◽

Static Conditions ◽

Biologic System

Collecting duct (CD) endothelin-1 (ET-1) is an important autocrine inhibitor of Na and water transport. CD ET-1 production is stimulated by extracellular fluid volume expansion and tubule fluid flow, suggesting a mechanism coupling CD Na delivery and ET-1 synthesis. A mouse cortical CD cell line, mpkCCDc14, was subjected to static or flow conditions for 2 h at 2 dyn/cm2, followed by determination of ET-1 mRNA content. Flow with 300 mosmol/l NaCl increased ET-1 mRNA to 65% above that observed under static conditions. Increasing perfusate osmolarity to 450 mosmol/l with NaCl or Na acetate increased ET-1 mRNA to ∼184% compared with no flow, which was not observed when osmolarity was increased using mannitol or urea. Reducing Na concentration to 150 mosmol/l while maintaining total osmolarity at 300 mosmol/l with urea or mannitol decreased the flow response. Inhibition of epithelial Na channel (ENaC) with amiloride or benzamil abolished the flow response, suggesting involvement of ENaC in flow-regulated ET-1 synthesis. Aldosterone almost doubled the flow response. Since Ca2+ enhances CD ET-1 production, the involvement of plasma membrane and mitochondrial Na/Ca2+ exchangers (NCX) was assessed. SEA0400 and KB-R7943, plasma membrane NCX inhibitors, did not affect the flow response. However, CGP37157, a mitochondrial NCX inhibitor, abolished the response. In summary, the current study indicates that increased Na delivery, leading to ENaC-mediated Na entry and mitochondrial NCX activity, is involved in flow-stimulated CD ET-1 synthesis. This constitutes the first report of either ENaC or mitochondrial NCX regulation of an autocrine factor in any biologic system.

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