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

Techniques of postoperative blood flow monitoring after free tissue transfer: An overview

Microsurgery ◽  
1994 ◽  
Vol 15 (11) ◽  
pp. 778-786 ◽  
Author(s):  
Hans-Guenther Machens ◽  
Peter Mailaender ◽  
Bernd Rieck ◽  
Alfred Berger
Keyword(s):  
Blood Flow ◽  
Free Tissue Transfer ◽  
Flow Monitoring ◽  
Tissue Transfer

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

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.

Vasopressor-Dependent Recipient Vessel Blood Flow in Head and Neck Free Tissue Transfer: A Report of Two Cases

2015 ◽  
Vol 31 (06) ◽  
pp. 477-480
Author(s):  
Edward Swanson ◽  
Srinivas Susarla ◽  
Georgia Yalanis ◽  
Hsu-Tang Cheng ◽  
Denver Lough ◽  
...  
Keyword(s):  
Blood Flow ◽  
Head And Neck ◽  
Free Tissue Transfer ◽  
Recipient Vessel ◽  
Tissue Transfer

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.

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