Ralph J P M Franken

Publications (3)6.59 Total impact

• Article: Effect of HTK on the microcirculation in the rat cremaster muscle during warm ischemia and reperfusion.

  Jacqueline Bastiaanse, Gary L Anderson, Ralph J P M Franken, Brigitte E P A van der Heijden, Mirjam G A Oude Egbrink, Dick W Slaaf, Moshe Kon
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  ABSTRACT: Histidine-tryptophan-ketoglutarate (HTK) preserves rat muscle function during cold storage. We examined the effect of HTK perfusion on preservation of microvascular function during 4 h of warm ischemia and subsequent reperfusion (I/R) in the rat cremaster muscle. Leukocyte-endothelium interactions, capillary perfusion, and arteriole diameters were quantified prior to HTK-perfusion and/or ischemia, and at 0, 1, and 2 h after restoration of blood flow. In all groups, the number of rolling leukocytes increased with time, whereas I/R induced a slight increase in leukocyte adhesion. After ischemia, capillary perfusion rapidly recovered to about 50% and returned to near normal (90%) after 2 h. HTK at 22 degrees C did not affect the assessed microcirculation variables, whereas HTK at 4 degrees C reduced leukocyte rolling, but not adhesion. Therefore, microvascular function of HTK-perfused muscles was not better preserved during warm I/R than that of nonperfused muscles. Contrary to other preservation solutions, HTK perfusion in itself was not detrimental to the microcirculation.
  Microsurgery 02/2005; 25(2):174-80. · 1.61 Impact Factor
• Article: Can angiogenesis induced by chronic electrical stimulation enhance latissimus dorsi muscle flap survival for application in cardiomyoplasty?

  Max L E Overgoor, Sean M Carroll, George Papanicolau, Camilla M A Carroll, Tuncay E T Ustüner, Richard W Stremel, Gary L Anderson, Ralph J P M Franken, Moshe Kon, John H Barker
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  ABSTRACT: In cardiomyoplasty, the latissimus dorsi muscle is lifted on its primary neurovascular pedicle and wrapped around a failing heart. After 2 weeks, it is trained for 6 weeks using chronic electrical stimulation, which transforms the latissimus dorsi muscle into a fatigue-resistant muscle that can contract in synchrony with the beating heart without tiring. In over 600 cardiomyoplasty procedures performed clinically to date, the outcomes have varied. Given the data obtained in animal experiments, the authors believe these variable outcomes are attributable to distal latissimus dorsi muscle flap necrosis. The aim of the present study was to investigate whether the chronic electrical stimulation training used to transform the latissimus dorsi muscle into fatigue-resistant muscle could also be used to induce angiogenesis, increase perfusion, and thus protect the latissimus dorsi muscle flap from distal necrosis. After 14 days of chronic electrical stimulation (10 Hz, 330 microsec, 4 to 6 V continuous, 8 hours/day) of the right or left latissimus dorsi muscle (randomly selected) in 11 rats, both latissimus dorsi muscles were lifted on their thoracodorsal pedicles and returned to their anatomical beds. Four days later, the resulting amount of distal flap necrosis was measured. Also, at predetermined time intervals throughout the experiment, muscle surface blood perfusion was measured using scanning laser Doppler flowmetry. Finally, latissimus dorsi muscles were excised in four additional stimulated rats, to measure angiogenesis (capillary-to-fiber ratio), fiber type (oxidative or glycolytic), and fiber size using histologic specimens. The authors found that chronic electrical stimulation (1) significantly (p < 0.05) increased angiogenesis (mean capillary-to-fiber ratio) by 82 percent and blood perfusion by 36 percent; (2) did not reduce the amount of distal flap necrosis compared with nonchronic electrical stimulation controls (29 +/- 5.3 percent versus 26.6 +/- 5.1 percent); (3) completely transformed the normally mixed (oxidative and glycolytic) fiber type distribution into all oxidative fibers; and (4) reduced fiber size in the proximal and middle but not in the distal segments of the flap. Despite the significant increase in angiogenesis and blood perfusion, distal latissimus dorsi muscle flap necrosis did not decrease. This might be because of three reasons: first, the change in muscle metabolism from anaerobic to aerobic may have rendered the muscle fibers more susceptible to ischemia. Second, because of the larger diameter of the distal fibers in normal and stimulated latissimus dorsi muscle, the diffusion distance for oxygen to the center of the distal fibers is increased, making fiber survival more difficult. Third, even though angiogenesis was significantly increased in the flap, cutting all but the single vascular pedicle resulted in the newly formed capillaries not receiving enough blood to provide nourishment to the distal latissimus dorsi muscle. The authors' findings indicate that chronic electrical stimulation as tested in these experiments could not be used to prevent distal latissimus dorsi muscle flap ischemia and necrosis in cardiomyoplasty.
  Plastic &amp Reconstructive Surgery 02/2003; 111(1):178-88. · 3.38 Impact Factor
• Article: Cold (0°C) ischaemic tolerance of latissimus dorsi free flaps in rats: A macroscopic and morphological study

  Ph.D. Paul M. N. Werker M.D, Moshe Kon, Colin J. Green, Patricia R. Fryer, Ralph J. P. M. Franken, Max L. E. Overgoor, Paul M. N. Werker
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  ABSTRACT: The purpose of this study was to define the cold (0°C) ischaemic tolerance (CIT) of the latissimus dorsi free flap in inbred rats. Flaps were isolated, stored at 0°C for periods of time ranging from 0 to 120 hr and then revascularised and reperfused for 14 days. Thereafter the CIT was assessed macroscopically, and by light microscopy. Electron microscopy was performed in flaps after 0 and 24 hr of reperfusion following a cold ischaemic interval ranging from 0 to 120 hr. From this preliminary study, it was concluded that the CIT was 48-72 hr.
  Microsurgery 12/1993; 15(3):187 - 192. · 1.61 Impact Factor