Local Blood Flow Monitoring by Means of the Hydrogen Clearance Technique

1994 ◽  
Vol 19 (1_suppl) ◽  
pp. 5-5
Author(s):  
H. G. Machens ◽  
P. Mailaender ◽  
B. Rieck ◽  
A. Berger
Keyword(s):  
Blood Flow ◽  
Local Blood Flow ◽  
Flow Monitoring ◽  
Hydrogen Clearance ◽  
Clearance Technique

Postoperative Blood Flow Monitoring after Free-Tissue Transfer by Means of the Hydrogen Clearance Technique

1997 ◽  
Vol 99 (2) ◽  
pp. 493-505 ◽  
Author(s):  
Hans-Guenther Machens ◽  
Peter Mailaender ◽  
Ralf Reimer ◽  
Norbert Pallua ◽  
Yuan Lei ◽  
...  
Keyword(s):  
Blood Flow ◽  
Free Tissue Transfer ◽  
Flow Monitoring ◽  
Tissue Transfer ◽  
Hydrogen Clearance ◽  
Clearance Technique

Measurement of local blood flow of the intestine by hydrogen clearance method; Experimental study

1979 ◽  
Vol 9 (1) ◽  
pp. 63-70 ◽  
Author(s):  
Yoshio Mishima ◽  
Hiroshi Shigematsu ◽  
Yoshiaki Horie ◽  
Masanori Satoh
Keyword(s):  
Experimental Study ◽  
Blood Flow ◽  
Local Blood Flow ◽  
Hydrogen Clearance Method ◽  
Hydrogen Clearance

scholarly journals Quantitative Measurement of Cerebral Blood Flow and Cerebral Blood Volume after Cerebral Ischaemia

1986 ◽  
Vol 6 (3) ◽  
pp. 338-341 ◽  
Author(s):  
Nicholas V. Todd ◽  
Piero Picozzi ◽  
H. Alan Crockard
Keyword(s):  
Blood Flow ◽  
Surface Area ◽  
Blood Volume ◽  
Quantitative Measurement ◽  
Cerebral Blood Volume ◽  
Vessel Occlusion ◽  
Permeability Surface ◽  
Area Product ◽  
Hydrogen Clearance ◽  
Clearance Technique

CBF obtained by the hydrogen clearance technique and cerebral blood volume (CBV) calculated from the [14C]dextran space were measured in three groups of rats subjected to temporary four-vessel occlusion to produce 15 min of ischaemia, followed by 60 min of reperfusion. In the control animals, mean CBF was 93 ± 6 ml 100 g−1 min−1, which fell to 5.5 ± 0.5 ml 100 g−1 min−1 during ischaemia. There was a marked early postischaemic hyperaemia (262 ± 18 ml 100g−1 min−1), but 1 h after the onset of ischaemia, there was a significant hypoperfusion (51 ± 3 ml 100 g−1 min−1). Mean cortical dextran space was 1.58 ± 0.09 ml 100 g−1 prior to ischaemia. Early in reperfusion there was a significant increase in CBV (1.85 ± 0.24 ml 100 g−1) with a decrease during the period of hypoperfusion (1.33 ± 0.03 ml 100 g−1). Therefore, following a period of temporary ischaemia, there are commensurate changes in CBF and CBV, and alterations in the permeability–surface area product at this time may be due to variations in surface area and not necessarily permeability.

Use of the Hydrogen Clearance Technique for Measurements of Pancreatic Blood Flow

1993 ◽  
Vol 55 (2) ◽  
pp. 122-130 ◽  
Author(s):  
H.G. Machens ◽  
N. Senninger ◽  
N. Runkel ◽  
G. Frank ◽  
R.V. Kummer ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pancreatic Blood Flow ◽  
Hydrogen Clearance ◽  
Clearance Technique

Role of K+ in regulating hypoxic cerebral blood flow in the rat: effect of glibenclamide and ouabain

1996 ◽  
Vol 270 (1) ◽  
pp. H45-H52 ◽  
Author(s):  
J. M. Reid ◽  
D. J. Paterson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Extracellular Potassium ◽  
Hydrogen Electrode ◽  
Marked Rise ◽  
Arterial Blood ◽  
Arterial Po2 ◽  
Hydrogen Clearance ◽  
Clearance Technique

We assessed the role of extracellular potassium ([K+]e) on the increase in cerebral blood flow (CBF) during hypoxia, and we tested whether it was affected by glibenclamide or ouabain. Cortical CBF was measured using the hydrogen clearance technique in enflurane-anesthetized rats, and local [K+]e was measured with K+ microelectrodes adjacent to the hydrogen electrode. Eucapnic hypoxia (arterial Po2 approximately 35-40 Torr) increased CBF twofold and caused a modest rise in [K+]e (from 2.9 +/- 0.2 to 3.7 +/- 0.2 mM; mean arterial blood pressure, ABP, 86 +/- 5 mmHg). If ABP fell < 70 mmHg during hypoxia, no increase in CBF was seen, whereas [K+]e increased to > 20 mM. Glibenclamide (10-100 microM intracortically) attenuated [K+]e and CBF during hypoxia (ABP approximately 75 mmHg, P < 0.01). Ouabain (20-1,000 microM) increased [K+]e; however, it did not remove the hypoxic-induced rise in [K+]e. We conclude that glibenclamide-sensitive potassium channels contribute to the accumulation of [K+]e during hypoxia, although an increase in CBF during hypoxia can occur without a marked rise in [K+]e. Furthermore, if ABP falls below the lower limit of autoregulation during hypoxia, there is no increase in CBF, yet there is a large increase in [K+]e.

Effect of L-NMMA, cromakalim, and glibenclamide on cerebral blood flow in hypercapnia and hypoxia

1995 ◽  
Vol 269 (3) ◽  
pp. H916-H922 ◽  
Author(s):  
J. M. Reid ◽  
A. G. Davies ◽  
F. M. Ashcroft ◽  
D. J. Paterson
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Combined Effects ◽  
Arterial Pco2 ◽  
Anesthetized Rats ◽  
Adenosine Antagonist ◽  
Arterial Po2 ◽  
Hydrogen Clearance ◽  
Clearance Technique

Sulfonylureas reduce cerebral blood flow (CBF) during hypoxia but not during hypercapnia, whereas blockers of nitric oxide (NO) synthesis reduce hypercapnic CBF. However, the effect of NO blockers on hypoxic CBF is uncertain. CBF was measured in the cortex of 51 enflurane-anesthetized rats by the hydrogen clearance technique during eucapnia, hypercapnia (arterial PCO2 65 Torr), and hypoxia (arterial PO2 40 Torr). CBF increased twofold in both hypercapnia and hypoxia from eucapnia. Intracortical (ic) NG-monomethyl-L-arginine (L-NMMA, 100 microM-5 mM) attenuated both the hypercapnic and hypoxic dilations by 60-70%, and L-arginine (300 mg/kg iv) partially reversed these effects. Glibenclamide (10 microM ic) and L-NMMA gave no further attenuation of the hypoxic dilation than L-NMMA alone. Cromakalim (10 microM, ic) increased CBF in eucapnia, but this was not seen in the presence of glibenclamide. The adenosine antagonist 8-phenyl-theophylline did not attenuate the hypoxic dilation. This suggests that NO synthesis plays a major role in the regulation of CBF in hypercapnia and hypoxia. But the combined effects of glibenclamide and L-NMMA do not further attenuate CBF in hypoxia.

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