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Ann Thorac Surg 1995;59:632-637
© 1995 The Society of Thoracic Surgeons

Influence of a Delay on Latissimus Dorsi Muscle Flap Blood Flow

First Department of Surgery, Yokohama City University, School of Medicine, Yokohama, Japan

Accepted for publication November 2, 1994.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
The regional and total blood flow of canine latissimus dorsi muscle flaps (LDMFs) were examined to study the effect of a delay procedure, ligation of the perforators, before complete flap elevation. The regional blood flow of the middle and distal regions of the nondelayed LDMFs was poor and significantly lower than the proximal region at rest. The regional blood flow during the exercise test was improved and significantly higher in the middle (62% increase) and distal regions (187% increase) of the delayed LDMFs as compared with the nondelayed LDMFs. The mean total blood flow of the delayed LDMFs was 14 mL • min^-1 • 100^-1 g at rest, increased to 30 mL • min^-1 • 100^-1 g during exercise tests with intermittent burst electrical stimulation, and was maximal at 40 mL • min^-1 • 100^-1 g immediately after the exercise. The phasic arterial blood flow of the delayed LDMFs was inhibited during contraction at 9 mL • min^-1 • 100^-1 g, whereas it was 44 mL • min^-1 • 100^-1 g during relaxation. In contrast, the phasic venous blood flow was accentuated during contraction to 32 mL • min^-1 • 100^-1 g compared with 16 mL • min^-1 • 100^-1 g during relaxation.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
See also page 638.

Latissimus dorsi muscle flaps (LDMFs) are used for cardiac assist in two principal areas: cardiomyoplasty [1–4] and skeletal muscle ventricles [5, 6]. Cardiomyoplasty consists of wrapping the failing heart with the LDMF, which is electrically stimulated in synchrony with the heart. This procedure has been performed clinically in more than 500 patients. A skeletal muscle ventricle is a circulatory assist device constructed from a LDMF and has demonstrated promising efficacy in animal research.

The latissimus dorsi muscle (LDM) is perfused principally by the thoracodorsal artery and by perforators from intercostal and lumbar arteries [7]. To mobilize the LDMF for use in circulatory assist, the perforators must be ligated. This ligation of the perforators reduces the perfusion of the middle and distal regions of the muscle. Atrophy of muscle fibers and fibrosis were observed in the distal region of electrically conditioned LDMFs that were elevated without a delay [8, 9]. Our hypothesis is that ischemia of the middle and distal LDMF after elevation without delay might contribute to muscle degeneration, fibrotic change and regional necrosis of the muscle. A delay procedure in which the perforators are ligated before the complete elevation of the LDMF might reduce the risk of muscle degeneration due to ischemia.

This study was designed to evaluate (1) the regional blood flow of canine LDMFs after perforator ligation, (2) the effect of a 1-month delay on regional perfusion of LDMFs, (3) the total blood flow of delayed LDMFs, and (4) the effect of electrically induced muscle contraction on phasic arterial and venous blood flow of delayed LDMFs.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Seventeen mongrel dogs weighing from 6 kg to 10.5 kg were studied. All operations were performed in accordance with the ``Guide for the Care and Use of Laboratory Animals'' (NIH publication 85-23, revised 1985). Anesthesia for all animals was induced and maintained with pentobarbital (first dose, 25 mg/kg), and ventilation was maintained with a tidal volume of 15 mL/kg. The femoral arterial pressure was monitored and the systolic peak pressures were maintained between 100 and 120 mm Hg. After the terminal experiments, all animals were euthanized with an intravenous potassium chloride injection (5 mEq/kg) under deep anesthesia and the LDMFs were excised and weighed. Left LDMs were used for the study in all animals.

The animals were divided into two groups. Group 1 (n = 5) consisted of nondelayed LDMFs and regional blood flow was measured immediately after ligation of the perforators and elevation of the LDMs. In group 2 (n = 12) the LDMFs were delayed. The perforators of the LDMs in group 2 were ligated at an initial operation. After a 1-month delay the LDMFs then were elevated. The regional blood flow was measured in 6 of the group 2 animals, and the total blood flow was measured in the remaining 6.

LDMF Preparation
A left mid-axillary incision was made and the anterolateral border of the LDM was incised. All perforators between the LDM and the chest wall were ligated. In group 2 the anterolateral muscular border and the skin incision were closed. Immediately after the ligation of the perforators in group 1 and after a 1-month delay in group 2, all of the attachments of LDM were detached except the humeral insertion and the neurovascular pedicle.

After elevation of the LDMF, bipolar stainless electrodes were placed around the thoracodorsal nerve to electrically induce exercise of the LDMF without load. The electrical stimulation was produced by an extracorporeal electric stimulator (SEN 3201, S-201J; Nihon Koden Co Ltd, Tokyo, Japan) for 5 minutes set at a 33 Hz frequency intermittent burst, 400 ms duty cycle on, 600 ms cycle off, 1.0 ms pulse width, and 5.0 V amplitude (supramaximal stimulation). The muscles were kept at normal body temperature with a heating blanket. All of the LDMs were unconditioned, fatigue-prone muscles.

Regional Blood Flow Measurement
In 6 of the group 2 animals, the costal surface of a LDMF was exposed after elevation. The regional blood flow was measured in 7 regions: proximal (cranial, regions 1, 2, and 3), middle (regions 4 and 5) and distal (caudal, regions 6 and 7) (Fig 1). For the measurements at rest, three measurements were performed in each region: the ventral, middle, and dorsal sides of the LDMF. Regional mean blood flow was measured using a He-Ne laser blood flowmeter (ALF 2100; Advance Co Ltd, Tokyo, Japan) and a needle-type probe (modified N type; Advance Co) with a 45-degree ground angle at the tip of the needle (4 mm long and 1 mm wide). The 21 measurement points were marked with 4-0 silk suture, and regional mean blood flow at rest was measured consecutively. The value for the region at rest was expressed as the mean value of the three points in the same region. Regional mean blood flow in the exercise test was measured at three points consecutively: proximal (region 2), middle (region 4) and distal (region 6) at rest and 15 to 30 seconds after the completion of exercise. Thirty minutes after the first exercise test, another exercise test was performed, and the measurements were done consecutively in the reverse order. The value for the region during the exercise test was the mean value of the first and the second measurements.

View larger version (15K): [in this window] [in a new window]   Fig 1. . Measurement regions of the latissimus dorsi muscle flap. The entire flap was divided into three parts, proximal (regions 1, 2, and 3), middle (regions 4 and 5), and distal (regions 6 and 7).

Analysis
The differences in the data between groups 1 and 2, between the regions in the same group, and those between rest and exercise in the same region were tested by two-way analyses of variance. The results of the phasic blood flows in group 2 during the contraction and relaxation were tested by the Student's t test. Differences in the mean flows were considered significant when the p value was less than 0.05. All data were expressed as the mean ± standard error of the mean.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Surgical Gross Findings
After ligation of the perforators of the LDMs, the distal region of LDMFs demonstrated marked cyanosis, and the middle region appeared slightly cyanotic in all animals. At the second operation, after a 1-month delay, the total LDMFs of all animals in group 2 showed neither cyanosis nor a fibrotic appearance.

Regional Blood Flow
The mean regional blood flow at rest in groups 1 (nondelayed) and 2 (delayed) is shown in Figure 2. In group 1, the flows to the middle and distal regions were significantly lower than those in the proximal regions. In group 2, all of the regions demonstrated significantly higher flows than in group 1, with the exception of region 2. There was a flow increase of 55%, 37% and 44% in proximal regions 1, 2, and 3, respectively, an increase of 106% and 86% in middle regions 4 and 5, respectively, and an increase of 113% and 83% in distal regions 6 and 7, respectively. The flows in the distal regions of the LDMFs in group 2 were significantly lower than those in the proximal regions in group 2.

View larger version (24K): [in this window] [in a new window]   Fig 2. . Mean regional blood flow of the latissimus dorsi muscle flaps of group 1 (Non-Delay) and group 2 (Delay) at rest. Values are given as mean ± standard error of the mean.

View larger version (27K): [in this window] [in a new window]   Fig 3. . Mean regional blood flow of the latissimus dorsi muscle flaps of group 1 (Non-Delay) and group 2 (Delay) at exercise (Ex) test. Values are given as mean ± standard error of the mean.

View larger version (23K): [in this window] [in a new window]   Fig 4. . Mean blood flow of the total latissimus dorsi muscle flaps of group 3 (Delay) at exercise test for 5 minutes. Values are given as mean ± standard error of the mean.

View larger version (19K): [in this window] [in a new window]   Fig 5. . Phasic blood flow of the thoracodorsal artery and vein during contraction or relaxation period 4 minutes into the exercise test. Values are given as mean ± standard error of the mean.

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

Delay Technique
The plastic surgical ``delay technique'' was developed to improve the survival of flaps used for various reconstructive procedures [7]. This delay procedure is accomplished by partially interrupting the LDM blood supply by ligating the perforators on the costal side of the muscle before elevation. The ischemia caused by the procedure results in a dilatation of existing vessels with maximal effect in the zone of the ``choke vessels'', connecting a dominant pedicle to adjacent secondary segmental pedicles [14]. The delay also causes a reorientation of the vessels along the axis of the flap, and enhances the flap's blood supply and increases its tolerance to ischemia [7]. Ligation of the perforators initially causes relative ischemia of the middle and distal regions of the LDMF and stimulates the development of improved perfusion in these areas. We term the delay before elevation of the LDM a ``classic delay'' to distinguish it from the vascular recovery period extending from the elevation of the LDMF until the institution of electrical stimulation. This ``alternate delay'' or ``vascular delay'' is used routinely in the process of performing cardiomyoplasty or constructing a skeletal muscle ventricle [1–6]. Two-stage cardiomyoplasty applying a classic delay before the elevation of the LDMF has been performed in a few institutions [2]. Elevation of LDMFs without a classic delay may cause greater ischemia than the elevation with a classic delay that can be perfused retrograde from lumbar arteries [15] and possibly by cutaneous blood vessels.

This experiment demonstrates that the regional perfusion in the middle and distal regions of the LDMFs elevated after a classic delay is significantly better than in the LDMFs elevated without the classic delay. We believe that classic delay will result in better blood perfusion of the LDMFs during the postoperative phase, better preservation of the muscle tissue during electrical conditioning, better overall performance of the LDMFs, and an improved postoperative course. Excluding patients with the most critically severe forms of congestive heart failure, there should be sufficient time to perform a delay procedure before the actual cardiomyoplasty.

Classic Delay and LDMF Survival
There is the potential for serious ischemic damage to the distal portion of the LDMFs after elevation without a classic delay [7–9]. The mechanism of this damage might include the effects of electrical conditioning, mechanical compression, and stretch, in addition to ischemia. The significantly lower blood flow in the middle and distal regions of the nondelayed LDMF compared with the proximal regions in our study also underscore the potential risk of ischemic damage to the muscle.

Previously, Mannion and associates [16] studied the effects of collateral ligation on the blood flow of the canine LDMF. They demonstrated decreased perfusion of the nondelayed LDMFs after collateral ligation as compared with the contralateral control of in situ LDMs. They also measured a tendency toward improved proximal and distal perfusion in the LDMFs that had undergone a 3-week delay compared with those that did not. Mannion and colleagues separated their LDMFs into two regions for blood flow measurements; however, the small animal numbers in their groups made statistical assessment difficult. We divided our LDMFs into seven regions for the measurements at rest and into 3 regions during the exercise test. Our findings confirmed Mannion and colleagues' in that there was a statistically significant greater blood flow to the middle and distal regions when delayed versus nondelayed LDMFs were compared. Mannion and colleagues also demonstrated the absence of an increase in the perfusion of the distal portion of the nondelayed canine LDMF during the exercise test. Our study confirmed their findings in the distal region. These results suggest that the capacity of the vascular bed in the distal region is fully utilized at rest and that the increased metabolic demands during the exercise test are not met by an augmentation in blood flow.

The recommended delay interval for skin flaps ranges from 10 days to 3 to 4 weeks, and experimental data indicate that blood flow peaks 1 week after a delay procedure [7]. Mannion and colleagues [16] demonstrated the partial recovery of blood flow of LDMFs after a 3-week classic delay. Our study, using alternate methodology that is available in the operating room for the patients, confirmed their findings and demonstrated improvement of the middle and distal regional perfusion at rest and during exercise after a 1-month classic delay. A remarkable finding in our study was the threefold increase in distal regional perfusion with exercise after a 1-month classic delay. The flow increase in the middle region was 62% and 30% in the proximal region. It seems that the 1-month delay procedure promoted marked improvement in the perfusion of the middle and distal regions of the LDMFs. The improvement in the augmentation of perfusion with exercise in the distal region of the delayed LDMFs suggests that vascular capacity of this region should be sufficient to tolerate electrical stimulation.

Alternate Delay and Electrical Conditioning
Mannion and colleagues [16] applied electrical conditioning with 2 or 10 Hz to the LDM after a 3-week classical delay and demonstrated no evidence of ischemic necrosis, decrease in muscle fiber size and interfiber connective tissue. They also applied electrical conditioning with 2 Hz to LDMF skeletal muscle ventricles after a 3-week alternate delay, and documented preserved muscle architecture and an increase in interfiber and intermuscular connective tissue [13]. In contrast, Kratz and co-workers [8] applied electrical conditioning with 25 Hz to LDMFs elevated without a classic or an alternate delay, and observed severe muscular atrophy and fibrosis, particularly in the distal region of the flap. Therefore, electrical conditioning of a relatively ischemic area of a LDMF can cause muscular damage.

On the other hand, electrical conditioning of skeletal muscle does seem to exert favorable effects upon blood perfusion. Mannion and colleagues [16] have demonstrated an improvement in perfusion to the distal portion of nondelayed LDMFs by electrical conditioning in situ. Electrical conditioning also stimulates an increase in muscular capillary density. The muscular twitching induced by electrical conditioning should require more perfusion than is required in the resting state. Electrical conditioning should, therefore, cause relative ischemia in critically underperfused regions. This, in turn, could promote recovery of perfusion during a delay period [7]. Therefore, the effect of electrical conditioning on relatively poorly perfused regions of a LDMF can lead to two opposing outcomes, depending upon the exact conditions of the muscle perfusion and electrical stimulation. Electrical conditioning could, on the one hand, accentuate regional ischemia or, on the other hand, enhance muscular perfusion.

Blood Supply and Muscle Performance
Because electrical burst stimulation used to stimulate the LDMF to perform cardiac assist produces higher oxygen demand than does electrical conditioning, the improvement of regional blood flow after a successful classic or alternate delay should enhance the performance of the LDMF. In our previous study, the canine 1-month delayed LDMFs demonstrated a 30% improvement in fractional shortening, a 42% improvement in total work capacity, and a 68% improvement in external work capacity as compared with the nondelayed contralateral LDMFs [17]. Furthermore, Pochettino and associates [18] reported that skeletal muscle ventricles, after an 18-week alternate delay, demonstrated better performance than those after a 4-week alternate delay. Even though the adaptation to the new muscle length and the remodeling of the muscle might affect the performance, a longer delay seems to enhance the LDM function as a cardiac assist device, and the delay process may continue for more than 1 month. Actually, 9 to 11 weeks, including a 3-week alternate delay and a 6- to 8-week preconditioning period, are allowed for the vascular healing process or delay process before using the LDMFs as skeletal muscle ventricles for cardiac assist [5, 6]. Similarly, 8 weeks, including a 2-week alternative delay and 6 weeks of progressive electrical conditioning, are allotted to the LDMFs before they are subjected to tetanic stimulation for cardiomyoplasty [4]. A classic delay before elevation of the LDMF in cardiomyoplasty might be useful to promote better preservation of the muscle. Further study, including morphologic analysis, is needed.

Blood Flow Capacity of the LDMF
Electrically conditioned skeletal muscle that is used for circulatory assist as a cardiomyoplasty procedure or a skeletal muscle ventricle is more dependent on aerobic metabolism for its energy source than it is under normal conditions [11–13]. Therefore, the blood flow capacity of the LDMF is the essential limiting factor determining LDMF performance. Mannion and colleagues [16] reported the blood flow to a 6-week electrically conditioned LDMF after a 3-week alternative delay as 40 to 60 mL • min^-1 • 100^-1 g during exercise. In comparison, the perfusion of the left ventricle was 120 to 130 mL • min^-1 • 100^-1 g and that of the right ventricle was 70 to 80 mL • min^-1 • 100^-1 g [5]. The total blood flow of the 1-month delayed unconditioned LDMFs was 30 to 40 mL • min^-1 • 100^-1 g during and after exercise in this study. The maximal regional blood flow of untreated human skeletal muscle is reported to rise as high as 150 mL • 100^-1 g • min^-1 [19]. The disparity among these values might be accounted for by muscle fiber composition in different species, the effect of electrical conditioning, an incomplete delay process, limitation of blood flow through the thoracodorsal artery, the effects of anesthesia, incomplete loading during the exercise test, and differences in methodology. The total blood flow of the 1-month delayed, unconditioned LDMFs seems to be approximately one-third to two-thirds of the normal canine myocardial blood flow expressed as milliliters per 100 grams of muscle weight. Assuming the energy production of the LDMF is dependent on its blood flow capacity, one might predict that the work capacity of these delayed unconditioned LDMFs would, therefore, be less than that of normal myocardium.

Blood Flow Pattern
Previously, Gealow and colleagues [20], using similar methodology, mentioned the reduction of phasic arterial blood flow during contraction of skeletal muscle ventricles; however, the magnitude of this reduction was not specified and venous flows were not studied. In this study, during the period of induced contraction, the phasic arterial blood flow of the delayed LDMFs was reduced to one-fifth of the blood flow during relaxation. The immediate increase in blood flow from 30 to 40 mL • min^-1 • 100^-1 g after exercise termination to a similar level as that found during the period of relaxation (44 mL • 100^-1 g • min^-1) supports the inference that the flow was truly reduced during the period of induced contraction. This reduction in phasic blood flow could be caused by high intramuscular pressure due to muscle contraction or due to vasoconstriction caused by local sympathetic discharge. This study suggests that a longer duty cycle might decrease the blood flow to the LDMFs during a state of maximal vasodilation. The influence of the duty cycle length on the mean blood flow might depend on several factors, including the state of vasodilation, electrical conditioning, the intensity of the electrical stimulation, and the form of exercise. The increase in venous flow during the period of induced contraction was probably due to the ``pumping effect'' of the muscular contraction upon the venous bed.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
This study was supported by a Grant-in-Aid (C-04670833, C-05671127) for Scientific Research from the Ministry of Education, Science, and Culture, Japan.

We are grateful to Dr Larry W. Stephenson for his advice and critical review of this article.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Address reprints requests to Dr Isoda, First Department of Surgery, Yokohama City University, School of Medicine, 3-9, Fukuura, Kanazawaku, Yokohama 236, Japan.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Henry L. Walters, III Jiro Kondo Akihiko Matsumoto Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Isoda, S. Articles by Matsumoto, A. Search for Related Content PubMed PubMed Citation Articles by Isoda, S. Articles by Matsumoto, A. Related Collections Related Article