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V E Hjortdal

Publications and source records attributed to V E Hjortdal.

At least 37 records · Page 2Linked to original sources
PubMed1999

Evaluation of stimulation parameters on aortomyoplasty, using Latissimus Dorsi muscle in a goat model: an acute study.

OBJECTIVE: Dynamic aortomyoplasty using Latissimus Dorsi muscle (LDM) has been shown to improve myocardial function. However, systematic examination of the effects of stimulation parameters on aortic wrap function has not been done. Thus, the present study measures the direct effect of stimulation voltage, pulse train duration, frequency of the pulses, and the duration of the stimulation delay from R wave on the aortic wrap function. METHODS: In eight female goats, the left LDM was wrapped around the descending aorta. The muscle was then subjected to electrical stimulation, altering frequency of stimulation pulses (16.6, 20, 25, 33 and 50 Hz), amplitude (2, 4, 6, 8 and 10 V), and number of pulses (2, 4, 6, 8 and 10 pulses) in a train stimulation. Left ventricular, aortic pressure, and pressure generated by LDM on aorta (wrap pressure) was measured. The changes in hemodynamic parameters mentioned above were calculated and compared for different stimulation parameters during unassisted and assisted cardiac cycles. RESULTS: Aortomyoplasty counterpulsation using LDM provided significant improvement in wrap pressure (78 mmHg +/- 2), aortic diastolic pressure, and changes in aortic diastolic pressure from 2 to 4 V (P < 0.05). Further increase in amplitude did not make any significant improvements of the above mentioned parameters. Significant augmentation of wrap pressure (82 mmHg +/- 2), aortic diastolic pressure (79 mmHg +/- 3) and changes in aortic diastolic pressure (12 mmHg +/- 1) occurred at 6 pulses (P < 0.05). Other changes in number of pulses did not show any significant improvements. Significant improvement of wrap pressure (80 mmHg +/- 2), aortic diastolic pressure (73 mmHg +/- 3) and changes in aortic diastolic pressure (12 mmHg +/- 1) was observed with a frequency of 33 Hz. To examine a wide range of delays from the onset of the QRS complex to LDM stimulation, stimulation was delivered randomly. The exact delay was determined from the ECG signal and superimposed LDM stimulation pulses. CONCLUSIONS: In this study we present a new measurement, wrap pressure. We also present that in aortomyoplasty using LDM, the most significant improvement in wrap pressure, aortic diastolic pressure and changes in aortic diastolic pressure occurs when the stimulation consists of an amplitude of 4 V, a frequency of 33 Hz and a train stimulation of 6 pulses.

Animals↗
PubMed1999

Aprotinin attenuates platelet accumulation in ischaemia-reperfusion-injured porcine skeletal muscle.

This purpose of this study was to evaluate the effect of aprotinin, a serine protease inhibitor, in ischaemia- and reperfusion-injured myocutaneous flaps and skin flaps. Flap survival, microcirculatory platelet accumulation, and regional blood flow were investigated in seventeen pigs which had been subjected to 8 h of ischaemia and 18 h of reperfusion. The pigs were randomly assigned to aprotinin treatment (n = 9) or saline (n = 8). In-vitro studies were performed to investigate the influence of aprotinin on the activated partial thromboplastin time. The survival of skeletal muscle correlated positively with the concentration of aprotinin (P = 0.02) and could not be explained by regional changes in blood flow. Platelet accumulation was decreased in aprotinin-treated muscle (P = 0.04). In-vitro (n = 10), 100 kallikrein inactivator units/ml aprotinin prolonged the activated partial thromboplastin time both in plasma (P = 0.001) and in blood (P = 0.002), suggesting an anticoagulant rather than a procoagulant effect. In conclusion, aprotinin at high concentrations may be beneficial for the survival of skeletal muscle and provides protection from platelet accumulation in the microcirculation of skeletal muscle exposed to ischaemia and reperfusion injury.

Animals↗
PubMed1999

Intravenous acetylsalicylic acid, magnesium and their combination in experimental arterial thrombosis in rats.

Intravenous acetylsalicylic acid (ASA) and magnesium (Mg) both possess antiplatelet properties and are thus potential inhibitors of the formation of arterial thrombi. Their effect on the dynamic aspects of arterial thrombus formation was investigated following intravenous administration of both substances alone and in combination. A blinded, placebo-controlled, in-vivo study was performed in 71 rats. Thrombus formation was induced by a standardized arteriotomy in the right femoral artery with inversion of the vessel wall during subsequent closure. Thrombus formation was recorded on video tapes and analysed off-line for 30 min. Animals were randomly assigned to one of four groups: 20 mg bolus of ASA followed by 0.3 mmol/h Mg (ASA/Mg group); NaCl followed by 0.3 mmol/h Mg (Mg group); 20 mg bolus of ASA followed by NaCl (ASA group); or NaCl throughout the experiment (control group). In the ASA-treated groups, serum levels of thromboxane B2 were reduced significantly, and the Mg-treated groups reached a serum level of Mg just above 2.0 mmol/l. No significant differences were observed in initial or maximum thrombus area or in mean thrombus area during the study period. In the ASA/Mg group, a trend towards reduced thrombus formation was observed (P = 0.06). In the same group, seven of 22 animals developed an occlusive thrombus (P < 0.01), an unexpected adverse event possibly related to the combined administration of ASA and Mg.

Animals↗
PubMed1999

Pulmonary and caval flow dynamics after total cavopulmonary connection.

OBJECTIVE: To assess flow dynamics after total cavopulmonary connection (TCPC). DESIGN: Cross-sectional study. SETTING: Aarhus University Hospital. PATIENTS: Seven patients (mean age 9 (4-18) years) who had previously undergone a lateral tunnel TCPC mean 2 (0. 3-5) years earlier. INTERVENTIONS: Pressure recordings (cardiac catheterisation), flow volume, and temporal changes of flow in the lateral tunnel, superior vena cava, and right and left pulmonary arteries (magnetic resonance velocity mapping). RESULTS: Superior vena cava flow was similar to lateral tunnel flow (1.7 (0.6-1.9) v 1. 3 (0.9-2.4) l/min*m2) (NS), and right pulmonary artery flow was higher than left pulmonary artery flow (1.7 (0.6-4.3) v 1.1 (0.8-2. 5) l/min*m2, p < 0.05). The flow pulsatility index was highest in the lateral tunnel (2.0 (1.1-8.5)), lowest in the superior vena cava (0.8 (0.5-2.4)), and intermediate in the left and right pulmonary arteries (1.6 (0.9-2.0) and 1.2 (0.4-1.9), respectively). Flow and pressure waveforms were biphasic with maxima in atrial systole and late ventricular systole. CONCLUSIONS: Following a standard lateral tunnel TCPC, flow returning via the superior vena cava is not lower than flow returning via the inferior vena cava as otherwise seen in healthy subjects; flow distribution to the pulmonary arteries is optimal; and some pulsatility is preserved primarily in the lateral tunnel and the corresponding pulmonary artery. This study provides in vivo data for future in vitro and computer model studies.

Adolescent↗
PubMed1999

Inhibition of nitric oxide synthesis improves left ventricular contractility in neonatal pigs late after cardiopulmonary bypass.

BACKGROUND: Following neonatal open heart surgery a nadir occurs in left ventricular function six to 12 hours after cardiopulmonary bypass. Although initiated by intraoperative events, little is known about the mechanisms involved. OBJECTIVE: To evaluate the involvement of nitric oxide in this late phase dysfunction in piglets. DESIGN: Piglets aged 2 to 3 weeks (4-5 kg) underwent cardiopulmonary bypass (1 h) and cardioplegic arrest (0.5 h) and then remained ventilated with inotropic support. Twelve hours after bypass, while receiving dobutamine (5 microg/kg/min), the left ventricular response to non-selective nitric oxide synthase inhibition (l-N(G)-monomethylarginine (l-NMMA)) was evaluated using load dependent and load independent indices (E(es), the slope of the end systolic pressure-volume relation; M(w), the slope of the stroke work-end diastolic volume relation; [dP/dt(max)](edv), the slope of the dP/dt(max)-end diastolic volume relation), derived from left ventricular pressure-volume loops generated by conductance and microtip pressure catheters. RESULTS: 10 pigs received 7.5 mg l-NMMA intravenously and six of these received two additional doses (37.5 mg and 75 mg). E(es) (mean (SD)) increased with all three doses, from 54.9 (40.1) mm Hg/ml (control) to 86.3 (69.5) at 7.5 mg, 117.9 (65.1) at 37.5 mg, and 119 (80.4) at 75 mg (p < 0.05). At the two highest doses, [dP/dt(max)](edv) increased from 260.8 (209.3) (control) to 470.5 (22.8) at 37.5 mg and 474.1 (296.6) at 75 mg (p < 0.05); and end diastolic pressure decreased from 16.5 (5.6) mm Hg (control) to 11.3 (5.0) at 37.5 mg and 11.4 (4.9) at 75 mg (p < 0. 05). CONCLUSIONS: In neonatal pigs 12 hours after cardiopulmonary bypass with ischaemic arrest, low dose l-NMMA improved left ventricular function, implying that there is a net deleterious cardiac action of nitric oxide at this time.

Animals↗
PubMed1999

Intravenous magnesium reduces infarct size after ischemia/reperfusion injury combined with a thrombogenic lesion in the left anterior descending artery.

Experimental studies have demonstrated that intravenous magnesium (Mg) can protect the ischemic myocardium and has an antithrombotic effect. In patients with myocardial infarction, the reperfusion injury is complicated by the presence of a thrombogenic area in the affected coronary artery that may cause repetitive thrombus formation and embolization. We investigated the effect of Mg on infarct size in a randomized study in pigs. Myocardial infarction was induced by a 50-minute mechanical occlusion of the left anterior descending artery combined with an arterial injury, which stimulated a dynamic thrombus formation with emboli shedding on reperfusion. Magnesium sulfate (6 mmol/20 min plus 3 mmol/h) or saline was started at 30 minutes after coronary occlusion. Real-time ventricular pressure-volume loops were generated from the left ventricle by using a microtip pressure manometer and a conductance catheter. Platelet accumulation in the myocardium was evaluated by using 111In-labeled platelets. After 4 hours of reperfusion, the infarct size/area at risk ratio in the placebo group was 46+/-0.06% (n=8) compared with 22+/-0.07% (n=6) in the Mg-treated animals (P=0. 03). Ejection fraction decreased significantly in the control group but not in the Mg-treated animals (P=0.03). Platelet accumulation in the myocardium did not change significantly between the Mg- and placebo-treated animals (placebo group, 191+/-19%; Mg group, 177+/-29%; NS). The present study demonstrates that intravenous Mg infusion is able to reduce infarct size by >50% and preserve the ejection fraction in this model where ischemia/reperfusion injury was evaluated in the presence of a thrombogenic area in the nutrient artery.

Animals↗
PubMed1998

The effect of changing excitation frequency on parallel conductance in different sized hearts.

OBJECTIVE: An important component of the ventricular volume measured using the conductance catheter technique is due to parallel conductance (Vc), which results from the extension of the electric field beyond the ventricular blood pool. Parallel conductance volume is normally estimated using the saline dilution method (Vc(saline dilution)), in which the conductivity of blood in the ventricle is transiently increased by injection of hypertonic saline. A simpler alternative has been reported by Gawne et al. [12]. Vc(dual frequency) is estimated from the difference in total conductance measured at two exciting frequencies and the method is based on the assumption that parallel conductance is mainly capacitive and hence is negligible at low frequency. The objective of this study was to determine whether the dual frequency technique could be used to substitute the saline dilution method to estimate Vc in different sized hearts. METHODS: The accuracy and linearity of a custom-built conductance catheter (CC) system was initially assessed in vitro. Subsequently, a CC and micromanometer were inserted into the left ventricle of seven 5 kg pigs (group 1) and six 50 kg pigs (group 2). Cardiac output was determined using thermodilution (group 1) and an ultrasonic flow probe (group 2) from which the slope coefficient (alpha) was determined. Steady state measurements and Vc estimated using saline dilution were performed at frequencies in the range of 5-40 kHz. All measurements were made at end-expiration. Finally, Vc was estimated from the change in end-systolic conductance between 5 kHz and 40 kHz using the dual frequency technique of Gawne et al. [12]. RESULTS: There was no change in measured volume of a simple insulated cylindrical model when the stimulating frequency was varied from 5-40 kHz. Vc(saline dilution) varied significantly with frequency in group 1 (8.63 +/- 2.74 ml at 5 kHz; 11.51 +/- 2.65 ml at 40 kHz) (p = 0.01). Similar results were obtained in group 2 (69.43 +/- 27.76 ml at 5 kHz; 101.24 +/- 15.21 ml at 40 kHz) (p < 0.001). However, the data indicate that the resistive component of the parallel conductance is substantial (Vc at 0 Hz estimated as 8.01 ml in group 1 and 62.3 ml in group 2). There was an increase in alpha with frequency in both groups but this did not reach significance. The correspondence between Vc(dual frequency) and Vc(saline dilution) methods was poor (group 1 R2 = 0.69; group 2 R2 = 0.22). CONCLUSION: At a lower excitation frequency of 5 kHz a smaller percentage of the electric current extends beyond the blood pool so parallel conductance is reduced. While parallel conductance is frequency dependent, it has a substantial resistive component. The dual frequency method is based on the assumption that parallel conductance is negligible at low frequencies and this is clearly not the case. The results of this study confirm that the dual frequency technique cannot be used to substitute the saline dilution technique.

Animals↗
PubMed1998

Gentacoll hampers epithelialisation and neovascularisation in excisional wounds in hairless mice.

Our aim was to analyse the effect of Gentacoll on the rate of epithelialisation and neovascularisation in wound healing. Standardised circular full thickness dermal wounds 2.25 mm in diameter were created on the dorsum of each ear on 24 hairless homozygous mice (n = 48). The cartilaginous layer was left intact. The wounds were treated in a randomised blinded fashion with bovine collagen implants with gentamicin (Gentacoll) (n = 17); bovine collagen implants without gentamicin (n = 15); and Silicone film (n = 16). Epithelialisation and neovascularisation were measured directly by intravital video-microscopy and computerised planimetry immediately after the wounds had been made and every third day until the wounds closed. Only five of the wounds treated with Gentacoll (n = 17) epithelialised completely; and their mean (SEM) epithelialisation time was 22.8 (1.6) days, significantly longer than controls without gentamicin (n = 15) for which the corresponding figures were 14.5 (0.6) days. In nine wounds treated with Gentacoll the ear cartilage in the wound bed perforated and two wounds developed severe inflammation, which was followed by self-mutilation. Neovascularisation was incomplete in all of the wounds in the Gentacoll group, whereas it was completed by 25.3 (0.7) days in the control group treated with implants without gentamicin. In the silicone treated group (n = 16), epithelialisation was completed by 12.7 (0.7) days and neovascularisation by 25.1 (0.5) days. None of wounds treated with collagen or silicone alone showed reactions similar to the Gentacoll-treated ears. Gentacoll hampers epithelialisation and neovascularisation, and might damage exposed cartilage.

Animals↗
PubMed1998

Microvascular damage secondary to thromboembologenic arterial injury--a new experimental model.

BACKGROUND AND AIMS: The isolated rat cremaster model is used extensively for evaluating the microcirculation secondary to arterial injury. Current techniques, however, do not allow for assessment of injury and effect within the same animal. The purpose of this study was to develop a model incorporating the following points: visualization of the upstream arterial injury and the downstream microvascular damage in the same animal, analysis of capillary density by randomization of measuring windows throughout the cremaster muscle, and simplification of the arterial injury. MATERIALS AND METHODS: Thirteen male Wistar rats were randomized into two groups. In group I, the entire isolation of the cremaster muscle was performed, without arterial damage. In group II, arterial damage consisting of a standardized pinch was applied to the feeding vessel. RESULTS AND CONCLUSIONS: It was possible to produce a simplified arterial injury and visualize the resulting downstream microvascular damage in the same animal, in a quantitative and randomized fashion. In group I, no thrombus formation was seen. In group II, all animals produced an embolizing arterial thrombus, which was dynamic within the first hour of observation. Capillary density was reduced from 6.5 to 3.5 capillaries/measuring window within the first hour after arterial thromboembolism.

Animals↗
PubMed1997

[Total and partial cavo-pulmonary anastomosis for univentricular hearts].

Between January 1990 and January 1995, 37 children and young adults with univentricular hearts were evaluated for total cavo-pulmonary connection (TCPC) or partial cavo-pulmonary connection (PCPC). Nineteen patients had tricuspid atresia, ten double-inlet left ventricle, five mitral atresia, and three had other complex univentricular lesions. Twenty-eight patients had previously been palliated by a systemic-pulmonary artery shunt or by pulmonary artery banding. All patients underwent physical examination, two-dimensional echo-cardiography, and cardiac catheterization. Suitability for TCPC was decided according to the modified Choussat criteria. Nine patients (24%), were judged unsuitable for any type of cava-pulmonary connection. Seventeen patients aged 5 (2-20) years underwent TCPC, and two patients awaited TCPC at follow-up (October 1995) Nine patients aged 10 (1-40) years had borderline morphology or haemodynamics and therefore underwent PCPC. One of these had, however, to be taken down immediately due to development of superior vena cava syndrome. The postoperative follow-up time was 20 (0.3 5.4) years. The 30-day, 1-, and 5-year survival rates (Kaplan-Meier) were 82%, 76%, and 76% after TCPC and 100%, 100%, and 100% after PCPC. All deaths were due to ventricular failure. At latest follow-up, all hospital survivors were in NYHA class I or II. All PCPC, and 85% of the TCPC patients were in sinus rhythm. All patients had good ventricular function. TCPC and PCPC can be performed in selected patients with univentricular hearts with an acceptable mortality and morbidity and result in significant functional improvement.

Adolescent↗
PubMed1997

Secondary ischemia caused by venous or arterial occlusion shows differential effects on myocutaneous island flap survival and muscle ATP levels.

Ischemia-reperfusion injury is one of the major problems in reconstructive microsurgery. The ischemic insult may be due to an occlusion of either the artery or the vein. Clinical observations have suggested that flap survival is more sensitive to venous stasis than to arterial ischemia. The current study evaluated the viability of the myocutaneous rectus abdominis flap following secondary arterial or venous occlusion and its possible dependency on tissue metabolites and length of the preceding reperfusion period. Forty-eight bilateral 5 X 10 cm myocutaneous rectus abdominis flaps were elevated in 24 pigs and exposed to consecutive periods of primary ischemia (2 hours), reperfusion (1, 4, 8, and 12 hours), and secondary pedicle occlusion (6, 8, 10, 12, 14, or 16 hours) of arterial or venous origin. Muscle adenosine triphosphate (ATP) and glucose-6-phosphate (G6P) were assessed immediately after flap elevation, at the end of primary ischemia, after reperfusion, and at the end of secondary ischemia. Flap viability was assessed 5 days after the operation. Secondary venous occlusion resulted in reduced survival rates as compared with arterial occlusion (9 of 24 versus 20 of 24; p < 0.01), although the average ATP content was higher in flaps subjected to venous stasis [median (25 to 75) percentiles, 3.7 (1.7 to 7.1) micromol/gm protein] than in those subjected to arterial ischemia 1.2 (0.8 to 1.8 micromol/gm protein) (p < 0.01). During reperfusion, muscle ATP decreased from 28.5 (17.9 to 36.6) micromol/gm protein to 15.4 (7.4 to 24.9) micromol/gm protein (p < 0.01) and glucose-6-phosphate from 7.6 (4.1 to 11.6) micromol/gm protein to 1.0 (0.5 to 4.1) micromol/gm protein (p < 0.01). Still, flap survival following secondary arterial ischemia was improved by increasing the reperfusion time from 1 to 8 hours (p < 0.05). No effect of reperfusion time was seen on viability after venous stasis. In conclusion, despite poorer flap survival, venous stasis was less detrimental to tissue ATP level, suggesting that the continued inflow may have supplied substrates for glycolysis. Furthermore, the larger blood volume may have accumulated the glycolytic waste products. After reperfusion, the recovery of aerobic metabolism was far from complete, and cellular glycolytic substrates were nearly exhausted. However, prolongation of the reperfusion time preceding secondary arterial ischemia improved flap survival.

Adenosine Triphosphate↗
PubMed1997

Early administration of intravenous magnesium inhibits arterial thrombus formation.

An antiplatelet effect of magnesium has been demonstrated in vitro and ex vivo, and this effect may be advantageous in patients with acute myocardial infarction to inhibit reocclusion after coronary angioplasty or thrombolysis. We investigated the antithrombotic in vivo effect of intravenous magnesium in a placebo-controlled, blinded study in 46 male Wistar rats. Thrombus formation was induced by standardized arteriotomy of the femoral artery and partial inversion of the vessel wall to produce a thrombogenic area. The vessel was transilluminated and visualized dynamically by in vivo microscopy. Thrombus area was measured every minute for 30 minutes after removal of the vessel clamp by image analysis techniques, and the number of visible emboli was registered. Animals were randomized into three groups: groups 1 and 2 received saline (control group, n = 15) or MgSO4 (Mg-early group, n = 15), respectively, during the entire infusion period. In group 3 intravenous saline was given during preparation of the arteriotomy followed by infusion of MgSO4 (Mg-late group, n = 16) from 10 minutes after removal of the vessel clamp. Thrombus area was significantly reduced by 75% in the Mg-early group (P < .005) but not in the Mg-late group compared with the control group. Mean number of emboli was reduced during magnesium infusion. The serum magnesium level increased to 2.2 (2.1 to 2.5) and 3.5 (3.0 to 4.2) mmol/L after infusion in the Mg-late and the Mg-early group, respectively. In the present study, intravenous infusion of MgSO4 significantly reduced thrombus formation in vivo but only when it was given before reperfusion. The antithrombotic effect of magnesium may be utilized in patients with acute myocardial infarction to reduce the rate of reocclusion. Magnesium infusion may also be of value in elective arterial angioplasty, but this option has not been investigated in clinical trials. However, correct timing of magnesium administration is critical to obtain an efficient antithrombotic effect.

Animals↗
PubMed1997

Sedimentation of formed elements in distally ischaemic flaps.

Our aim was to find out whether thrombosis has a key role in distally ischaemic flaps and whether heparin improves flap survival in distally ischaemic myocutaneous and pure skin flaps in pigs. In experiment 1 we measured the concentration of coagulation factors in the venous effluent from both viable flaps and distally ischaemic flaps. In experiment 2 radioactively labelled blood components (red cells, platelets and fibrinogen) were injected intravenously and the distribution of each tracer was measured. In experiment 3 either heparin or saline was given as a local, continuous direct intra-arterial infusion. Fluorescein was used in all experiments to estimate the eventual flap survival. Our results indicate that thrombosis is not an important factor in distal ischaemia, and that heparin did not improve survival. Instead, there seems to be selective pooling of formed elements in the ischaemic portion of the flap.

Animals↗
PubMed1997

Endogenous TGF-beta 1 and TGF-beta 2 are not essential for epithelialization and neovascularization in the hairless mouse ear wound model.

BACKGROUND AND AIMS: TGF-beta stimulates neovascularization and epithelialization in healing wounds, yet relatively little is known about the mechanisms involved. Using the hairless mouse ear wound model, we studied the effects endogenous TGF-beta 1 and TGF-beta 2 have on epithelialization and neovascularization following the application of neutralizing antibodies. MATERIAL AND METHODS: Forty-three adult male hairless mice had an excisional wound made on the dorsum of each ear. Using vital microscopy, epithelialization and neovascularization were measured every third day until completion. TGF-beta 1 and TGF-beta 2 antibody, control-IgG, or phosphate buffered saline (PBS) were applied to the wounds. RESULTS AND CONCLUSIONS: Excisional wounds treated with anti-TGF-beta 1 and anti-TGF-beta 2, IgGcontrol IgG, and PBS epithelialized in 11.2 +/- 0.5 days (N = 22), 10.9 +/- 0.6 days (N = 17), and 10.6 +/- 0.6 days (N = 15), respectively and neovascularized in 27.9 +/- 0.5 days (N = 17), 27.1 +/- 0.8 days (N = 14), and 26.1 +/- 0.8 days (N = 10), respectively (mean +/- SEM). There were no significant differences in time to epithelialization and neovascularization between the three groups. Furthermore, there were no differences in the average time course of epithelialization and neovascularization between the three groups throughout the healing process. We conclude that endogenous TGF-beta 1 and TGF-beta 2 are not essential for epithelialization and neovascularization in the hairless mouse ear wound model.

Animals↗
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↗
PubMed1994

Differential release of endothelin in myocutaneous island flaps in response to gradually insetting venous stasis or arterial ischemia.

Endothelin (ET) provokes strong and sustained contraction in preparations of isolated vascular smooth muscle, and the production of ET is thought to increase secondary to increased wall shear stress and hypoxia. The release of ET and blood flow distribution between arteriovenous shunts and capillaries were studied in autoperfused myocutaneous pig island flaps during graded arterial or venous blood flow reduction (N = 12). A group comprising four flaps was not exposed to blood flow reduction and served as controls. Total flap blood flow (venous outflow [VO]) was reduced in 1-hour periods to 50%, 25%, and 0%. Downregulation of VO caused a lower capillary blood flow (CBF) at 25% (P < .05) and at 50% (P < .05) in flaps exposed to venous stasis as compared with flaps with arterial ischemia. The reduction in blood flow was paralleled by decreasing oxygen consumption, although flaps with venous stasis had lower oxygen consumption than flaps exposed to arterial ischemia (P < .05). ET was found to be released from these island flaps before blood flow was reduced. Gradual arterial clamping caused a statistically significant (P < .05) decrease in the release of ET from 8.7 +/- 1.3 fmol/min before ischemia to 4.1 +/- 1.7 at 50% blood flow and 4.1 +/- 1.0 at 25% blood flow. In contrast, the release of ET with venous stasis remained unchanged at a level of 7.5 +/- 1.6 fmol/min before blood flow reduction, 7.3 +/- 0.7 at 50% blood flow, and 8.5 +/- 1.6 at 25% blood flow. These data suggest a relationship between CBF, intravascular pressure, and ET production.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Venous ischemia in skin flaps: microcirculatory intravascular thrombosis.

Although endothelial cell injury and microcirculatory intravascular clotting have been implicated in the pathophysiology of skin-flap failure and various hematologically active drugs have been used to improve flap survival, the basic underlying pathophysiology has not been documented previously. In this study of venous ischemia in pig flaps, we focus on the accumulation and distribution of platelets and fibrinogen in the flap, on the morphologic changes in the flap microcirculation, and on changes in various coagulation factors in the venous effluent from the flap. Bilateral buttock skin flaps and latissimus dorsi myocutaneous flaps were designed and elevated on 12 pigs. All flaps had a primary ischemic insult (clamp application to the vascular pedicle) of 2 hours, followed by 2 hours of reperfusion, and then one side was subjected to a 6-hour period of secondary venous ischemia (clamp application to the dominant flap vein). In six animals, radioactively labeled autologous platelets and human fibrinogen were injected intravenously half an hour before termination of secondary venous ischemia. Flaps were weighed and counted for radioactivity. Flap biopsies and the buffy coat of venous effluent were processed for electron microscopy. In the other six animals, venous effluent was collected before secondary ischemia, upon immediate reperfusion, and at 4 and 8 hours after termination of secondary ischemia. Venous plasma levels of fibrinogen, von Willebrand factor, and antithrombin III were measured. Platelet and fibrinogen accumulation was increased in flaps with venous stasis when compared with control flaps at both time intervals studied; a twofold increase was seen prior to reperfusion, and a threefold increase was seen following 4 hours of reperfusion. Venous effluent could not be collected from buttock skin flaps because of slow reflow and clotting in the collecting system. In comparing the venous effluent of control flaps with that of venous ischemic latissimus dorsi flaps, hematocrit was significantly elevated. Blood samples collected for analysis of fibrinogen, antithrombin III, and von Willebrand factor could not be analyzed because of postcollection clotting. Electron microscopy showed extravasation of red blood cells and activated platelets, fibrin, and red blood cells in distended and partly disrupted capillaries. The venous ischemia reperfusion injury is associated with thrombosis in the microcirculation and alterations in consumption of coagulation factors. This study gives physiologic support for potential beneficial effects of treatment modalities that aim at counteracting the different components of thrombus formation.

Animals↗