A tip for facilitating microsurgical anastomosis.
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Anastomosis, Surgical↗
Biomedical subjects
S M Carroll
Publications and source records attributed to S M Carroll.
Efficacy of a novel whey protein gel complex to increase the unsaturated fatty acid composition of bovine milk fat.
A novel whey protein emulsion gel (WPEG) complex was developed to protect dietary unsaturated fatty acids from rumen biohydrogenation with the goal of modifying the fatty acid composition of milk fat. Three experiments were conducted with WPEG complexes made from either whey protein concentrate containing 80% crude protein, whey protein isolate, or whey protein concentrate high-gel capacity. Each experiment lasted 3 wk. All cows received a basal total mixed ration (TMR). During wk 1 and 3, all cows received only the TMR. During wk 2, 3 control cows received 330 g/d of soybean oil added to the TMR, and the other 3 cows received 330 g/d of soybean oil in one of the WPEG complexes. During wk 2, C18:2 increased from 3.29 to 5.88 g/100 g of fat in Experiment 1, 2.91 to 7.42 g/100 g of fat in Experiment 2, and 3.57 to 6.56 g/100 g of fat in Experiment 3 for WPEG cows. Fatty acid C18:3 increased from 0.51 to 0.84, 0.52 to 1.15, and 0.51 to 0.97 g/100 g of fat for Experiments 1, 2, and 3, respectively, for WPEG cows. Higher proportions of C18:1 trans-9 in milk fat of control cows compared with WPEG cows were seen in all experiments. The proportion of C18:1 trans-11 was also higher in control cows in Experiments 1 and 2, but not in Experiment 3. The WPEG complexes successfully protected unsaturated fatty acids from rumen biohydrogenation and resulted in an increase in the unsaturated fatty acid composition of milk fat produced by Holstein cows without increasing the trans 18-carbon monoenes.
Animals↗
Noncommutative field theory and Lorentz violation.
The role of Lorentz symmetry in noncommutative field theory is considered. Any realistic noncommutative theory is found to be physically equivalent to a subset of a general Lorentz-violating standard-model extension involving ordinary fields. Some theoretical consequences are discussed. Existing experiments bound the scale of the noncommutativity parameter to (10 TeV)(-2).
Journal Article↗
Use of a mechanical leech in a reverse-flow radial forearm flap: case report.
The reverse-flow radial forearm flap provides excellent coverage for distal upper-limb defects. It is simply raised and does not require microsurgical skills. However, since its vascular pedicle is reversed, its venous outflow can be significantly diminished because of the venous valves. The authors present the case of a 16-year-old patient with a sagittal amputation of the radial aspect of the right thumb, who manifested at the time of surgery marked venous engorgement of a reverse-flow radial forearm flap. This was successfully relieved by the placement of a mechanical leech consisting of a Silastic rubber catheter--of the kind used to gain central vascular access in newborns--introduced in the lumen of the reversed vein at the extremity of the flap. This permitted intermittent evacuation of blood from the flap postoperatively, contributing to the success of this procedure. The technique used is detailed and pertinent literature is reviewed.
Adolescent↗
Vascular delay and administration of basic fibroblast growth factor augment latissimus dorsi muscle flap perfusion and function.
Ischemia of the distal latissimus dorsi muscle flap occurs when the entire muscle is acutely elevated. Although this level of ischemia may not be critical if the muscle is to be used as a conventional muscle flap, the ischemia causes decreased distal muscle function if it is used for dynamic muscle flap transfer. This experiment was designed to determine whether or not the administration of exogenous basic fibroblast growth factor (bFGF), combined with a sublethal ischemic insult (i.e., vascular delay), would further augment muscle perfusion and function. Both latissimus dorsi muscles of nine canines were subjected to a bipedicle vascular delay procedure immediately followed by thoracodorsal intraarterial injection of 100 microg of bFGF on one side and by intraarterial injection of vehicle on the other. Ten days later, both latissimus dorsi muscles were raised as thoracodorsally based island flaps, with perfusion determined by laser-Doppler fluximetry. The muscles were wrapped around silicone chambers, simulating cardiomyoplasty, and stimulating electrodes were placed around each thoracodorsal nerve. The muscles were then subjected to an experimental protocol to determine muscle contractile function. At the end of the experiment, latissimus dorsi muscle biopsies were obtained for measurement of bFGF expression. The results demonstrated that the administration of 100 microg of bFGF immediately after the vascular delay procedure increases expression of native bFGF. In the distal and middle muscle segments, it also significantly increased muscle perfusion by approximately 20 percent and fatigue resistance by approximately 300 percent. The administration of growth factors may serve as an important adjuvant to surgical procedures using dynamic muscle flap transfers.
Animals↗
Serotonergic 5-HT2A receptors important for the oestradiol-induced surge of luteinising hormone-releasing hormone in the rat.
Serotonin (5-HT) plays a role in mediating the oestradiol-induced surge of luteinising hormone (LH), but so far the 5-HT receptor subtype involved has not been identified. Our previous in-situ hybridization and pharmacological studies suggest that the action of 5-HT involves the 5-HT2A receptor. The aim of the present study was to investigate this possibility by the direct approach of determining whether 5-HT2A receptor antagonists block the oestradiol-induced surge of luteinising hormone releasing hormone (LHRH). Adult female Wistar rats, which had shown at least two consecutive 4-day oestrous cycles, were ovariectomised under halothane anaesthesia in the morning of dioestrus and injected with vehicle (arachis oil) alone or oestradiol benzoate (OB). At 12.00 h of the next day, presumptive pro-oestrus, the animals were injected intraperitoneally with one of three 5-HT2A antagonists, a selective 5-HT reuptake inhibitor (fluoxetine), or the appropriate vehicles; hypophysial portal blood was then collected under alphaxalone anaesthesia between 15.00 and 19.00 h. The amount of LHRH released into hypophysial portal blood during consecutive 30-min periods was determined by radioimmunoassay. As expected, oestradiol, but not oil, triggered a surge of LHRH in hypophysial portal blood with a peak at about 16.00 h of presumptive pro-oestrus. This oestradiol-induced surge of LHRH was blocked by ketanserin, ritanserin and the highly selective 5-HT2A receptor antagonist, RP62203, but not by fluoxetine. These results provide the first direct evidence that the 5-HT2A receptor plays an important role in the oestradiol-induced surge of LHRH.
Anesthesia↗
An animal model to study microcirculatory changes associated with vascular delay.
Vascular delay is a surgical procedure that renders a flap partially ischaemic several days prior to its transfer in order to increase its viability after its transfer. Though much debate exists regarding the actual mechanism of vascular delay, most theories agree that changes in the microcirculation play a key role. In this paper, we describe four experiments that establish the ear of the homozygous (hr/hr) hairless mouse as an effective model for directly viewing and measuring delay-induced changes in microcirculation. In our first experiment, we compared mouse ears that were delayed (n = 18) with ones that were not (control) (n = 13) and showed that vascular delay significantly (P < 0.05) reduced ear flap necrosis. In a second experiment, we delayed mouse ears for 2 (n = 9), 4 (n = 14), 6 (n = 10), 8 (n = 10), 10 (n = 10), 20 (n = 18), 40 (n = 10) and 80 (n = 11) days and found that the reduction in necrosis becomes statistically significant (P < 0.05) over non-delayed controls (n = 12) after a minimum delay period of 6 days. In a third experiment, we delayed mouse ears by ligating only the vein (n = 14), only the artery (n = 11), only the nerve (sympathectomy) (n = 14), and vein, artery and nerve (n = 14) of the main neurovascular pedicle and found significant (P < 0.05) reductions in flap necrosis in all groups compared to nondelayed controls (n = 12). Finally, in a fourth experiment, we measured vessel directionality changes in mouse ears that were delayed for 6 (n = 4), 10 (n = 4), 20 (n = 4), 40 (n = 4) and 80 (n = 4) days, and found that directionality changes became significant (P < 0.05) at 6 days of delay and remained so for all the days studied when compared with non-delayed controls (n = 4).
Animals↗
Quantification of the morphological features of a full microvascular network.
Investigations into the changes that occur in microvasculature following the surgical procedure called delay have brought about the need for a computer system capable of quantifying the morphological features of a full microvascular network in terms of average vessel length, diameter, and tortuosity. Both the formulaic conventions that have been developed to measure these quantities as well as their implementation in the form of a HP-9000/UNIX based computer software system that we developed specifically for this purpose are discussed. Reliability studies performed using the final system to measure the microcirculatory network of a mouse latissmus dorsi muscle (LDM) showed 95% confidence intervals within 5% of means and coefficients of variability within 7% of means for all quantities measured in large (150-300 microns), medium (50-150 microns), and small (< 50 microns) diameter vessels. These variations were significantly smaller than the changes that were observed in a preliminary study comparing these microvascular network parameters before and after delay in the hairless mouse LDM, showing the proposed quantification methods to be well suited to the study of the microvascular changes following delay. It is hoped that the formulaic conventions, implementation process and reliability data will provide a useful comparison for other researchers interested in measuring similar features of microcirculatory networks.
Animals↗
Augmentation of skeletal muscle flap survival using platelet derived growth factor.
Distal muscle flap ischemia and necrosis is a recognized complication of acute elevation of large skeletal muscle flaps. The aim of this study was to investigate whether the angiogenic properties of platelet derived growth factor (PDGF) could be used to augment skeletal muscle flap survival through the induction of new blood vessel formation before flap elevation. We compared this form of flap augmentation with that achieved by subjecting the muscle to a bipedicled vascular delay procedure. The animal model used was the latissimus dorsi muscle of the male homozygous (hr/hr) hairless mouse. Four groups of animals were investigated in this study (n = 10 per group). Group 1 was the control group in which the entire muscle was elevated as a thoracodorsally based island flap. In group 2, the muscle was subjected to a bipedicled vascular delay procedure. In group 3, the muscle was treated with 500 microg of recombinant human platelet derived growth factor BB. In group 4, the muscle was treated with placebo. Ten days later the entire latissimus dorsi muscle was elevated as a thoracodorsally based island flap in groups 2, 3, and 4. Percentage muscle flap survival was quantitated in all groups 5 days after elevation of the entire muscle. Angiogenesis was then quantitated by analyzing capillary to muscle fiber ratios after alkaline phosphatase staining of representative latissimus dorsi muscle samples from the proximal, middle, and distal flap segments. Percentage muscle flap survival was significantly better in PDGF treated muscles when compared with the vascularly delayed muscles (p < 0.001). Histologic analysis of latissimus dorsi muscle flaps demonstrated a significantly greater number of capillaries in the middle (p < 0.001) and distal (p < 0.001) flap segments of PDGF-treated flaps when compared with the vascularly delayed flaps. Treatment of skeletal muscle with PDGF before flap creation resulted in survival of the entire muscle flap. Our results suggest that this survival may be secondary to PDGF-induced angiogenesis.
Animals↗
Exercise training in swine promotes growth of arteriolar bed and capillary angiogenesis in heart.
Exercise training induces coronary vascular adaptations. The goal of this study was to contrast the effects of training on capillary and arteriolar growth. Minipigs were trained for 1, 3, 8, and 16 wk and compared with controls. Maximal O2 consumption increased continuously throughout the study. Capillary and arteriolar densities and diameters, and proliferation of vascular cells in these vessels, were determined in perfusion-fixed tissue. The arterioles were subdivided into five groups according to diameter: 10-19.9, 20-30, 31-40, 41-70, and 71-120 microgram. The total vascular bed cross-sectional area increased by 37% at 16 wk, mainly because of an increase in the number of the small arterioles and an increase in the diameter of the larger vessels. Capillary density increased at 3 wk and then returned to control levels by 16 wk; concomitantly, the number of arterioles (20-30 microgram) increased at 16 wk. We speculate that the "extra" capillaries observed at 3 wk were the source of the new arterioles.
Animals↗
Vascular delay of the latissimus dorsi muscle: an essential component of cardiomyoplasty.
BACKGROUND: Cardiomyoplasty (CMP) uses the latissimus dorsi muscle (LDM) to assist the heart in cases of cardiac failure. Distal ischemia and necrosis of the LDM is a recognized complication of CMP that can reduce distal muscle function and the mechanical effectiveness of CMP. METHODS: Canine (n = 9) LDMs were subjected to a 10-day period of vascular delay followed by a simulated CMP. Two weeks after simulated CMP (corresponding to the healing delay between CMP and the onset of LDM stimulation used in the clinical setting), LDM perfusion was measured in the distal, middle, and proximal segments of the muscle, and circumferential (distal and middle squeezing muscle function) and longitudinal (proximal pulling muscle function) force generation and fatigue rates were measured. The results were compared with the contralateral nondelayed simulated CMP. RESULTS: Muscle perfusion was significantly (p < 0.05) greater in the distal and middle segments of vascular-delayed LDMs. Circumferential muscle force generation and fatigue rates were significantly (p < 0.05) improved in the vascular-delayed LDMs. CONCLUSIONS: Vascular delay can significantly improve LDM perfusion and function in a model that closely reflects clinical CMP, and the use of vascular delay may improve clinical outcomes in CMP.
Animals↗
Regional perfusion and oxygenation in the pedicled latissimus dorsi muscle flap.
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Animals↗
Vascular delay improves latissimus dorsi muscle perfusion and muscle function for use in cardiomyoplasty.
Ischemia of the distal portion of the latissimus dorsi muscle occurs in muscle transfer for cardiomyoplasty and reduces distal muscle contractility and thus the mechanical effectiveness of cardiomyoplasty. We hypothesized that muscle function would be improved by a vascular delay procedure that increases distal muscle perfusion of the latissimus dorsi muscle. The latissimus dorsi muscles of 10 adult mongrel dogs were subjected to a vascular delay procedure on one side and a sham procedure on the other. Following 10 days of vascular delay, muscle perfusion was measured with a laser-Doppler perfusion imager before and after elevation of the muscles as flaps based only on their thoracodorsal neurovascular pedicles. The muscles were wrapped and sutured around silicone chambers (simulating cardiomyoplasty), a stimulating electrode was placed around each thoracodorsal nerve, and the muscles were stimulated to contract in both rhythmic and tetanic fashion. Circumferential (distal and middle latissimus dorsi muscle function) force generation and fatigue rates were measured independently. Circumferential muscle force, circumferential and longitudinal fatigue rate, and distal, middle, and overall perfusion were significantly (p < 0.05) improved in delayed muscle compared with nondelayed muscle. We found that a vascular delay procedure and a 10-day delay adaptation period significantly improve latissimus dorsi muscle flap perfusion and function, particularly in the distal and middle portions of the muscle. Delay should be considered as a means of improving the clinical outcome in cardiomyoplasty.
Adaptation, Physiological↗
Acute ischemic preconditioning of skeletal muscle prior to flap elevation augments muscle-flap survival.
Ischemic preconditioning of the myocardium with repeated brief periods of ischemia and reperfusion prior to prolonged ischemia significantly reduces subsequent myocardial infarction. Following ischemic preconditioning, two "windows of opportunity" (early and late) exist, during which time prolonged ischemia can occur with reduced infarction size. The early window occurs at approximately 4 hours and the late window at 24 hours following ischemic preconditioning of the myocardium. We investigated if ischemic preconditioning of skeletal muscle prior to flap creation improved subsequent flap survival and perfusion immediately or 24 hours following ischemic preconditioning. Currently, no data exist on the utilization of ischemic preconditioning in this fashion. The animal model used was the latissimus dorsi muscle of adult male Sprague-Dawley rats. Animals were assigned to three groups, and the right or left latissimus dorsi muscle was chosen randomly in each animal. Group 1 (n = 12) was the control group, in which the entire latissimus dorsi muscle was elevated acutely without ischemic preconditioning. Group 2 (n = 8) investigated the effects of ischemic preconditioning in the early window. In this group, the latissimus dorsi muscle was elevated immediately following preconditioning. Group 3 (n = 8) investigated the effects of ischemic preconditioning in the late window, with elevation of the latissimus dorsi muscle 24 hours following ischemic preconditioning. The preconditioning regimen used in groups 2 and 3 was two 30-minute episodes of normothermic global ischemia with intervening 10-minute episodes of reperfusion. Latissimus dorsi muscle ischemia was created by occlusion of the thoracodorsal artery and vein and the intercostal perforators, after isolation of the muscle on these vessels. Muscle perfusion was assessed by a laser-Doppler perfusion imager. One week after flap elevation, muscle necrosis was quantified in all groups by means of computer-assisted digital planimetry. Our results show that ischemic preconditioning resulted in a significant reduction (p < 0.05) in muscle-flap necrosis immediately and 24 hours following ischemic preconditioning. Perfusion changes after flap elevation were similar among the three groups. Ischemic preconditioning of skeletal muscle prior to flap creation significantly reduces subsequent muscle-flap necrosis caused by the ischemia of flap creation immediately and 24 hours following ischemic preconditioning. Further elaboration of the mechanisms of ischemic preconditioning may allow pharmacologic preconditioning to be used in the augmentation of skeletal muscle-flap survival in the clinical setting.
Animals↗
Vascular delay in skeletal muscle: a model for microcirculatory studies.
Dynamic myoplasty is a relatively new use for muscle flaps and has led us to revisit the mechanisms of vascular delay as a means of optimizing blood supply to muscle flaps. Despite the well-documented effectiveness of vascular delay in skin flaps, vascular delay in muscle flaps has not been widely reported. Regardless of the many mechanisms postulated in the literature as contributors to the delay effect in skin, the one element common to all these hypotheses is the importance placed on changes in the microcirculation. Based on this factor, in the present study we developed and validated an animal model in which delay-induced microvascular changes could be measured in skeletal muscle flaps. We used the hairless mouse latissimus dorsi muscle flap because its vascular distribution is similar to that of humans and its thin structure will enable us in future studies to directly view and measure its microvasculature using videomicroscopy. In 12 animals, we found that delay significantly (p < 0.01) reduced necrosis of the distal part of the muscle from 57 +/- 9 percent in nondelayed flaps (n = 7) to 22 +/- 3 percent in delayed (n = 5) flaps. In these studies, we also determined that the hairless mouse latissimus dorsi muscle flap will serve as an excellent model for defining microvascular changes throughout delay.
Animals↗
Gene expression in a swine model of right ventricular hypertrophy: intercellular adhesion molecule, vascular endothelial growth factor and plasminogen activators are upregulated during pressure overload.
We have investigated the molecular changes which occur during pressure overload hypertrophy of the RV in swine. Animals were banded on the pulmonary artery so that right ventricular pressure was increased two-fold. The heart was harvested at 3, 7, 24 and 72 h after surgery. Between 7 and 72 h there was evidence of muscle damage and inflammation. Northern blot experiments showed that pressure overload induced a transient increase in the expression of the immediate early genes and in the developmentally regulated atrial natriuretic factor and skeletal muscle alpha actin genes. Consistent with the histological observations of inflammation, increases in the expression of the gene for intercellular adhesion molecule, which encodes a protein involved in the binding of leukocytes by endothelial cells and myocytes, was observed between 3 and 24 h. In addition, the expression of vascular endothelial growth factor, a growth and permeability factor specific for endothelial cells was increased at 3 and 7 h of pressure overload. An increase in the expression of urokinase plasminogen activator and its inhibitors, plasminogen activator inhibitors I and II, was also observed between 3 and 24 h. This was associated with an increase in urokinase activity in the myocardial tissue. These results indicate that hypertrophy in a large mammal such as swine induces a program of gene expression similar to that previously described in rodents and suggests that up-regulation of a variety of other genes is an early response to pressure overload.
Animals↗
A 3-year epidemiological review of burn unit admissions in Dublin, Ireland: 1988-91.
A retrospective multifactorial epidemiological study of all patients admitted to the Burns Unit, St James's Hospital, Dublin during a 3-year period from January 1988 to December 1990 was undertaken. One hundred and twenty patients were admitted. All patients were aged over 14 years. The mean patient age was 48.2 years. Males accounted for 56 per cent of admissions. The mean percentage body surface area (%BSA) burned was 24.9 per cent. Flame was the cause of burns in 60 per cent of cases and produced the most extensive lesions. The home was the most common site of injury. Almost half the patients admitted from residential institutions sustained their burns in hot baths. Those aged over 60 years sustain smaller burns but are at increased risk from thermal injury. Twenty-one per cent of burns were caused by open fires used for heating the home. The mean time in hospital was 49.9 days. Twenty-three per cent of patients died as a result of their injuries. We have identified those living in residential institutions to be at increased risk from scald burns and suggest methods by which they may be protected.
Adolescent↗
Urokinase plasminogen activator activity is increased in the myocardium during coronary artery occlusion.
We have previously demonstrated that collateral development takes place in a swine model of coronary artery occlusion. In this report we have examined the effect of coronary artery occlusion on urokinase and tissue plasminogen activator activity in the myocardium. Urokinase activity was increased four-fold in the ischemic heart compared to sham and unoperated controls. In contrast, the level of tissue plasminogen activator activity remained relatively constant. The increase in urokinase activity was associated with an upregulation of urokinase RNA levels and of the RNAs corresponding to the plasminogen activator inhibitors, PAI I and II. Urokinase has been shown to be an important angiogenic protease both in vivo and in cultured cells. Its increase during collateral development suggests that urokinase may play a role in angiogenesis in the ischemic heart.
Animals↗