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Biomedical subjects

J H Barker

Publications and source records attributed to J H Barker.

At least 73 records · Page 4Linked to original sources
PubMed1997

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↗
PubMed1997

Platelet-derived thromboxane A2 decreases microvascular perfusion after arterial repair.

Previous work suggests that cod liver oil helps to protect the microcirculation from the consequence of thromboembolic events. The possibility that altered synthesis of thromboxane A2 accounts for the protective effects seen with cod liver oil was investigated in the present study. This was done using the combined thromboxane A2 synthetase inhibitor and thromboxane A2-prostaglandin H2 receptor blocker R68070 (Ridogrel). A standardized microvascular injury was inflicted on the right iliac artery of the rat to generate emboli. The downstream cremaster muscle was used to visualize the passage of the ensuing emboli and to assess the effects of this arterial injury on capillary perfusion and arteriole diameters. The number of visible emboli was not changed by either cod liver oil diet or Ridogrel administration. However, capillary perfusion was preserved by using cod liver oil (n = 7) and was significantly increased by using Ridogrel (n = 7) in comparison with untreated controls (n = 7) in which capillary perfusion was decreased because of the emboli. The administration of Ridogrel to cod liver oil-treated animals (n = 7) provided no additive benefit. The percentage change in A-2 vessel diameters in cod liver oil-treated (n = 7) animals was no different from the control group (n = 7). Ridogrel (n = 7), on the other hand, produced a significant increase in A-3 vessel (n = 21) diameters, but its effects were comparatively less in the cod liver oil-treated animals (n = 7). The formation of platelet aggregates (emboli) appears relatively independent of thromboxane A2 in the rat. Ridogrel is very effective in protecting the microcirculation, and these effects appear to be mediated by A-3 vasodilatation, which, therefore, is at least partially thromboxane A2-dependent. The positive effects of cod liver oil may be mediated by a mechanism that reduces thromboxane A2 synthesis, but further studies are necessary.

Animals↗
PubMed1997

Effect of low dose aspirin on thrombus formation at arterial and venous microanastomoses and on the tissue microcirculation.

In free flap/replantation surgery, failure is usually associated with thrombotic occlusion of a microvascular anastomosis (risk zone I) or, on occasion, flow impairment in the microcirculation of the transferred or replanted tissue (risk zone II). The objective of this study is to describe the effect of low dose aspirin on blood flow at both risk zones in microvascular surgery. Risk zone I: In rat femoral arteries and veins, thrombus formation was measured at the anastomoses using transillumination and videomicroscopy. Forty male Wistar rats were assigned in equal numbers to four groups: either arterial or venous injury with either aspirin (5 mg/kg systemically) or saline treatment. We found that aspirin significantly reduces thrombus formation at the venous anastomosis (p = 0.001). Risk zone II: In the isolated rat cremaster muscle downstream from an arterial anastomosis, we measured capillary perfusion, arteriolar diameters, and the appearance of platelet emboli for 6 hours in the muscle microcirculation. Sixteen male Wistar rats in two equal groups received either aspirin (5 mg/kg systemically) or saline. We found that in aspirin-treated animals, capillary perfusion is significantly (p = 0.002) improved, whereas arteriolar diameters and emboli only slightly increased. In conclusion, low dose aspirin inhibits anastomotic venous thrombosis and improves microcirculatory perfusion in our rat model. These studies provide quantitative data confirming and clarifying the beneficial effects of low dose aspirin in microvascular surgery.

Anastomosis, Surgical↗
PubMed1997

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↗
PubMed1997

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↗
PubMed1997

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↗
PubMed1996

Thrombogenic properties of murine anti-cardiolipin antibodies induced by beta 2 glycoprotein 1 and human immunoglobulin G antiphospholipid antibodies.

BACKGROUND: Recurrent arterial thrombosis and venous thrombosis are frequent complications of the antiphospholipid syndrome (APS). Patients produce anti-cardiolipin antibodies, but the role of these antibodies in thrombus formation is uncertain. This study used a unique CD-1 mouse model of thrombosis to determine whether anti-cardiolipin and anti-beta 2 glycoprotein 1 (beta 2 GP1) antibodies induced immunologically in these animals are thrombogenic. METHODS AND RESULTS: The CD-1 mouse model enables measurement of the kinetics of a thrombus induced in the femoral vein of the animal. Animals are first anesthetized, then one femoral vein is exposed and subjected to a standardized, nonpenetrating "pinch" injury that induces a thrombus. The vein is trans-illuminated, and the growing thrombus is visualized on a television screen. The rate of formation and disappearance of the thrombus as well as its area can be measured by a computer attached to the television. Three groups of CD-1 mice (each group comprising seven animals) were studied. Group 1 mice were actively immunized with beta 2GP1, resulting in production of anti-beta 2GP1 and anti-cardiolipin antibodies. Group 2 mice were actively immunized with human immunoglobulin G (IgG) anti-cardiolipin antibodies and produced anti-human IgG as well as anti-cardiolipin antibodies (the latter by an idiotype-anti-idiotype reaction). These animals did not produce anti-beta 2GP1 antibodies. Group 3 mice were immunized with human serum albumin (HSA) and produced anti-HSA but not anti-cardiolipin antibodies. The kinetics of thrombus formation induced in the femoral veins of the experimental mice were compared. Results showed that the mean thrombus area as well as mean time during which thrombi persisted were significantly greater in group 1 and group 2 mice compared with group 3. There was no statistical difference between group 1 or group 2. CONCLUSIONS: Demonstration of a thrombogenic effect of murine anti-cardiolipin antibodies suggests that these antibodies may be pathogenic in humans with APS.

Animals↗
PubMed1996

Inhibition of wound contraction with colchicine and D-penicillamine.

The effects of locally injected combined colchicine and D-penicillamine on wound contraction were investigated in a murine model. Two full-thickness excisional wounds were made on either side of the back of hairless (hr/hr) mice. A volume of 0.15 ml of colchicine, D-penicillamine, or combined colchicine and D-penicillamine in normal saline vehicle were injected daily into the wound on one side of the animal and 0.15 ml of vehicle alone was injected into the wound on the other side for 5 or 10 days; thus, each animal served as its own control. The surface area of each wound was measured on Days 0, 5, and 10 to determine an index of the rate of wound contraction. At the end of the experimental period (Day 5 or 10), wounds were excised en bloc from euthanized animals for histological studies. The following histological parameters were determined: the thickness of the granulation tissue, the number of fibroblasts in granulation tissue per unit area, and the number of inflammatory cells (neutrophils, lymphocytes, macrophages, mast cells) in subjacent muscle per unit area. Our data showed that after 5 days of treatment, wound contraction was significantly inhibited only in wounds treated with combined colchicine and D-penicillamine. Wound contraction was significantly inhibited even after 10 days of treatment with the combination. Histological studies revealed that although the thickness of the granulation tissue and the number of inflammatory cells in subjacent muscle were decreased by D-penicillamine alone, only combined colchicine and D-penicillamine decreased the thickness of the granulation tissue, fibroblasts in granulation tissue, and inflammatory cells in subjacent muscle. Our data suggests that very low concentrations of colchicine and D-penicillamine when combined and injected locally may be potentially useful in controlling surface scar formation.

Animals↗
PubMed1996

Characterization of microvascular vasoconstriction following ischemia/reperfusion in skeletal muscle using videomicroscopy.

This study investigated the possible contribution of microvascular vasoconstriction to no-reflow following ischemia/reperfusion in a mouse skeletal muscle model. Using paired cremaster muscles, arterioles of diameter 10-100 microns were directly viewed and measured by the use of an in vivo videomicroscopy before and after a 6-hr period of complete ischemia at 27 degrees C. Following ischemia/reperfusion, feeder and arcading arterioles constricted significantly to 54.5 and 62% of pre-ischemic baseline diameters respectively (P < .05). While the calcium antagonist diltiazem and nitroprusside were both able to reverse arteriolar constriction, endothelium-dependent acetylcholine-induced dilatation was markedly impaired following reperfusion (P < 0.05). Superoxide dismutase did not attenuate the microvascular response, suggesting that the mechanism is likely to be at least partly free radical-independent.

Acetylcholine↗
PubMed1996

In vitro platelet aggregation studies in microvascular surgery research: a method in the rat model.

There is now a growing awareness of the central role of platelet function in microvascular thrombosis. Platelet aggregation studies remain one of the most useful ways of studying platelet function and response to different stimuli. This brief communication highlights some of the main variables that can affect platelet aggregation in rats and emphasizes the existence of important differences in these variables compared with human platelet aggregation.

Anastomosis, Surgical↗
PubMed1996

Anatomy of the feeding blood vessels of the cremaster muscle in the rat.

Since the early seventies over 300 studies have used the cremaster muscle as a flap model, yet little has been reported on the upstream feeding vessels of this muscle. The purpose of this study was to investigate the anatomy of the cranial feeding vessels of the left and right cremaster muscle in Sprague-Dawley rats. An additional aim was to compare these results with the anatomy of the feeding vessels of the cremaster muscle in another strain (Wistar). To permit identification of the cranial feeding vessels, the pedicle was dissected very carefully and thereafter perfused with green dye, which was administered through a cannula placed in the distal femoral artery. In Sprague-Dawley rats it was found that the cremaster muscle in only 30% of the animals received its total blood supply through the superior external pudendal artery. In Wistar rats the same was true in less than 45%. The cremaster muscle of the rest of the animals appeared to receive its blood either in part or in total from the hypogastric trunk. We suggest that the name pudic-epigastric trunk be abandoned.

Animals↗
PubMed1996

Ischemia increases the angiogenic potency of basic fibroblast growth factor (FGF-2).

The aim of this study was to investigate the angiogenic response to exogenously administered basic fibroblast growth factor (FGF-2) in normal and ischemic skin, using the hairless mouse ear microcirculatory model. The hairless mouse ear is a well-established model for in vivo studies of skin microcirculation. Using this model, angiogenesis- and angiogenesis-associated changes in the microcirculation can be directly and continuously viewed and quantified in a variety of different experimental settings. To create ischemia in the mouse ear, all but one of the three to four feeding vessels nourishing the ear were ligated 3 days prior to a local subdermal injection of FGF-2 (9.3 + 1-0.5 mm/mm2) or saline into the dorsum of the ears. Angiogenesis was quantified by direct observation, at high magnification, of the injection site where increases in total vessel length (TVL) were measured repeatedly over 18 days following injection. We found a significant (P < 0.01) increase in TVL in normal and ischemic ears injected with FGF-2. Saline injection also induced a significant increase in TVL in ischemic ears. However, the angiogenic response to FGF-2 in ischemic ears was significantly stronger than saline alone in ischemic ears or saline or FGF-2 in normal ears. This response could be used clinically to accelerate angiogenesis and thus increase perfusion in ischemic tissue.

Animals↗
PubMed1996

Prefabricated jejunal free-tissue transfer for tracheal reconstruction: an experimental study.

Reconstruction of long-segment tracheal defects is a problem for the reconstructive surgeon. Difficulties arise with the use of prosthetic materials because of their propensity for infection and extrusion. Autologous tissue is limited by poor structural characteristics and technical complexity. We propose a simple composite bioprosthesis that, through a process of prefabrication and subsequent neovascularization, may provide a functional tracheal analogue superior to existing forms of reconstruction. Ten rats had composite flaps constructed by combining an isolated, perfused, mucosectomized segment with an outer covering of a ring-reinforced woven Dacron vascular graft. This unit remained in the intraabdominal milieu for 20 days and was then inspected for viability, incorporation of jejunum and graft, flexibility, and tolerance to negative pressure. Seven experimental animals survived the initial phase. The jejunal bioprostheses in all cases tolerated negative pressures to -200 mmHg, rotation of 180 degrees, and flexion to 90 degrees without collapse of the graft segments. Vascular casts and standard histologic examination showed neovascularization of the Dacron graft and dense fibrovascular ingrowth into the interstices of the graft. We conclude that prefabrication utilizing autologous and prosthetic components to create a single axial flap for transfer is a feasible solution to long-segment tracheal reconstruction. Neovascularization permeates the full thickness of the prosthetic component and is accompanied by dense fibrous ingrowth during the delay period. This neotracheal analogue also possesses structural characteristics similar to those of the native trachea and a durable submucosal layer that can support ingrowth of epithelium.

Animals↗
PubMed1996

Evidence that barley 3-hydroxy-3-methylglutaryl-coenzyme a reductase kinase is a member of the sucrose nonfermenting-1-related protein kinase family.

A protein kinase was partially purified from barley (Hordeum vulgare L. cv Sundance) endosperm by ammonium sulfate fractionation, followed by ion-exchange, Reactive Blue, Mono-Q, and phosphocellulose chromatography. It was shown to phosphorylate Arabidopsis 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and a synthetic peptide that was shown previously to act as a substrate for HMG-CoA reductase kinase purified from cauliflower, confirming it to be barley HMG-CoA reductase kinase. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the partially purified preparation showed the presence of a polypeptide with an approximate relative molecular weight (M(r)) of 60,000, which is the size predicted for the barley sucrose nonfermenting-1 (SNF1)-related protein kinases BKIN2 and BKIN12. Antisera were raised to a rye (Secale cereale L.) SNF1-related protein kinase (RKIN1) expressed in Escherichia coli as a fusion with maltose-binding protein and to a synthetic peptide with a sequence that is conserved in, and specific to, plant members of the SNF1-related protein kinase family. The maltose-binding protein-RKIN1 fusion protein antiserum recognized a doublet of polypeptides with an approximate M(r), of 60,000 in crude endosperm extracts and a single polypeptide in root extracts, which co-migrated with the smaller polypeptide in the endosperm doublet. Both antisera recognized a polypeptide with an approximate M(r) of 60,000 in the partially purified protein kinase preparation, suggesting strongly that barley HMG-CoA reductase kinase is a member of the SNF1-related protein kinase family.

AMP-Activated Protein Kinases↗
PubMed1995

Can varying flow velocity across an arterial anastomosis prevent thromboembolic injury?

In this study, simulated "poor" repairs applied to transverse incisions in the iliac arteries of 40 rats were the basis for comparing the effect of variations in blood flow on thromboembolism. Using vital microscopy and digital image processing, we performed 2 experiments. In the first experiment (n = 20), the reduction of post-repair blood flow by approximately 50% resulted in an 83% reduction in the total number of emboli appearing in the microcirculation of the cremaster muscle distal to the repair. In the second experiment (n = 20), the same reduction in blood flow typically resulted in larger repair-site thrombi which required significantly more time to grow to their maximum size. We conclude that reducing pedicle artery blood flow to approximately half in our rat model during reperfusion can protect the downstream microcirculation from embolic injury without increasing the incidence of thrombotic occlusion.

Anastomosis, Surgical↗
PubMed1995

Microsurgery without a microscope: laboratory evaluation of a three-dimensional on-screen microsurgery system.

In microvascular surgery, procedures may be both technically and physically demanding. Precise movements sustained over long hours in addition to typically compromised surgeon and assistant positioning lead quickly to physical and mental fatigue. Many of the positioning problems encountered are related to the fact that the eyes of the surgeon must be continually fixed to the microscope eyepieces. This study explores a possible solution: a microscope system that eliminates the need to view the operative field through the microscope eyepieces. A Three-dimensional On-screen Microsurgical System (TOMS) was used and contrasted with conventional operative microvascular surgery in the laboratory setting. The surgeon's comfort, his ability to instruct microsurgical technique, pertinent technological performance, and the procedure itself were evaluated using a standardized questionnaire. Based on data collected in this study, we conclude that divorcing the surgeon's eyes from the microscope eyepieces using the TOMS may make prolonged microvascular procedures less physically demanding and may increase the comfort level of both the surgeon and his assistant, although refinements to the technology are required.

Anastomosis, Surgical↗