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PubMed2004

Oxygen sensing in the circulation: "cross talk" between red blood cells and the vasculature.

Oxygen (O(2)) sensing in blood and regulation of microvascular tone appear to involve hemoglobin (Hb) conformational changes resulting from O(2) desaturation. This observation has prompted the thought that Hb functions as both an O(2) sensor and regulator of microvasular blood flow to meet local tissue oxygen demand. The mechanism(s) by which this is accomplished has recently been the subject of increasing debate. Three primary hypotheses are described within the literature and include release of adenosine 5'-triphosphate by red blood cells (RBCs), release of S-nitrosylated molecules from RBCs originally bound to beta93 cysteine residues of oxyHb, and nitrite conversion and storage of nitric oxide by Hb at the site of ferric (Fe(3+)) and ferrous (Fe(2+)) Hb. Within extravascular cells, the global regulator of oxygen homeostasis is hypoxia-inducible factor-1 (HIF- 1). This transcriptional factor is tightly regulated by O(2) and cellular redox-sensitive mechanisms. HIF-1 activation is responsible for the up-regulation of proteins, which increase O(2) supply. We believe that there are important and yet unexplored mechanisms by which RBCs can directly or indirectly communicate via redox intermediates with extravascular sites as part of the global O(2) sensing mechanism.

Adenosine Triphosphate↗
PubMed1955

Cross-circulation.

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Blood Circulation↗
PubMed1995

Renal and haemodynamic effects of nitric oxide blockade in a Wistar assay rat during high pressure cross-circulation of an isolated denervated kidney.

Blockade of NO synthesis with N-omega-nitro-L-arginine (L-NNA) inhibits the vasodepressor response seen in intact Wistar assay rats in which isolated kidneys perfused via an extracorporeal circuit are perfused at high pressure. This study explores the renal and haemodynamic changes associated with this inhibition. Isolated kidneys (IK) were perfused at high pressure (175 mmHg) by a pump in series with intact Wistar assay rats in which blood pressure (BP), haemodynamics and renal function were studied. Nitric oxide (NO) synthesis was blocked by L-NNA (2.5 mg kg-1) in 13 experiments (175NO) while 14 control experiments (175C) were performed. IK was perfused at 90 mmHg in seven experiments (90C). The BP drop in the 175C assay rat was blocked by L-NNA in 175NO (P < 0.01). However, when the blockade was reversed with L-arginine infusion (20 mg kg-1 min-1) BP declined also in 175NO. Effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) fell dramatically after L-NNA in both the assay rat and in IK despite a high perfusion pressure. The marked increase in filtration fraction (FF) after L-NNA suggests a dominating postglomerular vasoconstriction. The natriuretic response in IK to 175 mmHg was also markedly blunted by L-NNA. We conclude that NO blockade inhibits the renomedullary depressor mechanism probably by restricting renal blood flow, and also blunts the pressure induced natriuretic response as a result of a reduced sodium filtration. Finally, the autoregulation of whole kidney blood flow seems to be more efficient although set at a higher level of vasoconstriction.

Animals↗
PubMed1967

Pulmonary vasoconstriction in asphyxia during cross-circulation between twin foetal lambs.

1. The effect of asphyxia on pulmonary vascular resistance was measured in anaesthetized foetal lambs whose left lung was supplied with arterial blood from a twin, both still being attached to their placentas by intact umbilical cords.2. In foetal lambs of 91-92 days gestation asphyxia of the recipient caused no pulmonary vasoconstriction so long as its left pulmonary artery was supplied with normal blood from a twin donor. Asphyxia of the donor caused pulmonary vasoconstriction in the unasphyxiated recipient; this was therefore wholly due to a local effect of the blood passing through the lung.3. In foetal lambs of 98-142 days gestation asphyxia of the recipient caused a small degree of pulmonary vasoconstriction, even though the left pulmonary artery was supplied with normal blood from the twin donor. This vasoconstriction was abolished by administration of hexamethonium or by cutting the sympathetic nerves to the left lung.4. In mature foetal lambs pulmonary arterial inflow and venous outflow were measured simultaneously. Broncho-pulmonary blood flow was less than 5% of total pulmonary flow. Pulmonary O(2) consumption was 0.75 +/- 0.11 ml./100 g.min, or about 5% of total foetal O(2) consumption.

Animals↗