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Biomedical subjects

F G Spinale

Publications and source records attributed to F G Spinale.

At least 181 records · Page 10Linked to original sources

Ventricular failure and cellular remodeling with chronic supraventricular tachycardia.

Chronic supraventricular tachycardia has been associated with ventricular dysfunction in human beings and in animals. The changes in ventricular size and shape and the myocyte remodeling that may occur with chronic supraventricular tachycardia are unknown. Left and right ventricular remodeling and myocyte changes were examined in 12 pigs after 3 weeks of atrial pacing (supraventricular tachycardia at 240 beats/min and in 10 control pigs (105 +/- 3 beats/min). Chronic supraventricular tachycardia resulted in decreased left ventricular and right ventricular ejection fractions compared with control values (left ventricle, 26% +/- 4% versus 60% +/- 1%; right ventricle, 19% +/- 3% versus 53% +/- 3%; p less than 0.05 for both), decreased wall thickness (left ventricle, 8.3 +/- 0.1 mm versus 10.5 +/- 0.2 mm; right ventricle, 2.8 +/- 0.3 mm versus 4.2 +/- 0.2 mm; p less than 0.05 for both), and increased end-diastolic volumes (left ventricle, 66 +/- 10 ml versus 54 +/- 4 ml; right ventricle, 78 +/- 8 ml versus 56 +/- 4 ml; p less than 0.05 for both). Myocardial water content was significantly higher with supraventricular tachycardia than in control pigs (left ventricle, 82% +/- 4% versus 76% +/- 4%; right ventricle, 83% +/- 4% versus 78% +/- 2%; p less than 0.05 for both). According to computer-aided stereological studies, the percent volume of myocytes in the subendocardial layer of the hearts that underwent supraventricular tachycardia was smaller than that of the control hearts (left ventricle, 62% +/- 2% versus 79% +/- 1%; right ventricle, 55% +/- 4% versus 77% +/- 1%; p less than 0.05 for both) and myocyte diameter was reduced (left ventricle, 16 +/- 1 microns versus 23 +/- 2 microns; right ventricle, 13 +/- 1 microns versus 22 +/- 2 microns; p less than 0.05 for both). Further, myocytes isolated from the left ventricles of the group with supraventricular tachycardia were significantly longer than were control myocytes (190 +/- 25 microns versus 145 +/- 30 microns, p less than 0.05 for both). In summary, chronic supraventricular tachycardia caused significant right and left ventricular failure, with a reduction in wall thickness and chamber dilatation. This was accompanied by a reduction in the percent volume of myocytes occupying the subendocardial layer, with reduced myocyte diameter and increased myocyte length and water content. These changes are likely to be important in understanding supraventricular tachycardia-induced ventricular dysfunction.

Animals↗

Immunocytochemical and enzyme histochemical localization of Na+,K(+)-ATPase in normal and ischemic porcine myocardium.

Na+,K(+)-ATPase is involved in generating transmembrane ion gradients and the associated potential difference necessary for contraction of cardiac myocytes. It is possible that changes in the activity or membrane content of this enzyme may occur under ischemic conditions. To investigate this question, right ventricular (RV) ischemia was produced in closed chest pigs and the RV ejection fraction was measured using a fast response thermistor in the pulmonary artery. Sections of RV collected at 15, 30, 45, and 60 min of ischemia were assayed for changes in sarcolemmal Na+,K(+)-ATPase activity using an enzyme coupled histochemical reaction as well as a biochemical assay. Similar sections were examined for changes in the distribution and content of Na+,K(+)-ATPase using an immunocytochemical procedure. The RV ejection fraction fell significantly from baseline after 15 min of ischemia (62 +/- 3% vs 39 +/- 3% respectively, P less than 0.05, n = 10). A decrease in sarcolemmal Na+,K(+)-ATPase activity was first detected after 30 min of occlusion and a significant reduction in enzyme activity was present at 45 min of ischemia. In contrast no changes were detected in the distribution or content of immunoreactive Na+,K(+)-ATPase in the sarcolemma at any time point. In addition, the amount of Na+,K(+)-ATPase in tissue homogenates showed no significant changes after 45 min of ischemia. These findings show that acute ischemia results in the disruption of sarcolemmal Na+,K(+)-ATPase activity and suggests that the decrease in enzyme activity is not due to the loss or redistribution of sarcolemmal Na+,K(+)-ATPase.

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Bioimpedance: a novel method for the determination of extravascular lung water.

Extravascular lung water (EVLW) can be measured using the double indicator dilution technique (DD). However, because this method is highly invasive and complicated, its clinical used has been limited. In theory, changes in thoracic conductivity, or bioimpedance (BI), can reflect changes in EVLW. However, past studies were unable to directly quantitate changes in EVLW since the contribution of dynamic variables such as ventricular volumes, hematocrit (HCT), and EVLW to this impedance signal could not be discerned. Recent studies have shown that a thermodilution pulmonary artery catheter mounted with a fast response thermistor accurately measures right ventricular end-diastolic volume (RVEDV). With changes in the RVEDV and HCT known, the contribution of EVLW to the bioimpedance signal may be isolated and used to more directly measure changes in EVLW. This hypothesis was tested by creating acute sepsis in seven pigs by infusion of Pseudomonas aeruginosa. Changes in EVLW from baseline were measured using DD at 30 min and at 1, 2, and 4 hr and compared with the change in EVLW computed from a mathematical model comprising the measured changes in BI, RVEDV, and HCT at the same time points. Changes in EVLW using DD and BI were significantly correlated over the length of the study (r = 0.85, P less than 0.01). In early sepsis (30 min), BI overestimated EVLW when compared with DD (P less than 0.05). However, at 1, 2, and 4 hr there was no significant difference between the two methods. In conclusion, the use of bioimpedance and a volumetric catheter may provide a relatively simple and reliable method for continuously monitoring changes in EVLW in the intensive care setting.

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Relationship between bioimpedance, thermodilution, and ventriculographic measurements in experimental congestive heart failure.

PURPOSE OF INVESTIGATION - Bioimpedance cardiography has been suggested as a non-invasive means to monitor cardiac function but has not been tested in cases of severe ventricular dysfunction. This study compared thermodilution stroke volume, ventriculographic left ventricular ejection fraction, bioimpedance stroke volume, and the maximum first derivative of the bioimpedance signal dZ/dtmax, during the development of experimental congestive heart failure. DESIGN - Simultaneous thermodilution stroke volume, ventriculography, and bioimpedance measurements were serially measured in pigs following acute pacing, and after 1, 2, and 3 weeks of tachycardia. Thermodilution stroke volume measurements were obtained by positioning a thermistor tipped catheter into the pulmonary artery and integrating the thermodilution curve with respect to heart rate. Left ventricular stroke volume and ejection fractions were measured from single plane ventriculograms using the area-length method. Using a series of electrodes positioned on the thoracic segment and a low level current (2.5 ma), the bioimpedance waveform was recorded and stroke volume and dZ/dtmax computed. SUBJECTS - The subjects were eight pigs (23-30 kg) with developing ventricular dysfunction due to chronic rapid atrial pacing (240 beats.min-1) and four controls. MEASUREMENTS AND MAIN RESULTS - Left ventricular ejection fraction decreased significantly from acutely paced values following 7 d tachycardia [60(SEM 1)% v 41(3)% respectively, p less than 0.01] and continued to decline with longer durations of tachycardia. A significant correlation was observed between ejection fraction and dZ/dtmax (r = 0.74, n = 32). Thermodilution and bioimpedance stroke volumes fell significantly from acutely paced values after week 2 of tachycardia [thermodilution: 13.8(0.9) v 8.5(1.4) ml; bioimpedance: 13.6(1.1) v 11.2(1.5) ml respectively, p less than 0.05] and were highly correlated throughout the study period (r = 0.90, n = 32). However, bioimpedance overestimated thermodilution values at week 2 (p less than 0.05) and at week 3 of tachycardia [thermodilution: 8.4(0.8) ml v bioimpedance: 9.6(1.0) ml, NS]. CONCLUSION - In a tachycardia induced model of heart failure, bioimpedance was significantly correlated with thermodilution stroke volume. The peak first derivative of the bioimpedance signal dZ/dtmax may provide a non-invasive index of ventricular pump performance. While these results are promising, further studies are required to evaluate the diagnostic value of bioimpedance cardiography in the clinical setting.

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Relationship of bioimpedance to thermodilution and echocardiographic measurements of cardiac function.

Bioimpedance cardiography has been suggested as a noninvasive means to monitor cardiac function. However, this method has not been compared to more conventional techniques such as echocardiography. This study compared simultaneously obtained thermodilution cardiac output and right ventricular ejection fraction (RVEF), and echocardiographic left ventricular fractional shortening (LVFS), to bioimpedance cardiac output and the maximum first derivative of the bioimpedance signal (dZ/dtmax) during positive inotropic stimulation and preload reduction. Eight pigs were instrumented with a rapid response thermistor (positioned in the pulmonary artery) and bioimpedance electrodes. Simultaneous thermodilution, echocardiographic, and bioimpedance measurements were performed at baseline and after 5, 10, and 15 min of isoproterenol infusion (0.5 microgram/kg.min). In six pigs, measurements were also performed after balloon occlusion of the inferior vena cava. A significant correlation was observed between LVFS and dZ/dtmax (r = .88, n = 35) over all time points. Thermodilution and bioimpedance cardiac output were in close agreement (r = .92, n = 35). However, bioimpedance overestimated cardiac output in the very low and high output states. The mean difference between thermodilution and bioimpedance cardiac outputs was -0.02 +/- 0.37 L/min. There was a positive relationship between RVEF and dZ/dtmax (r = .54, n = 35). In summary, bioimpedance was significantly correlated with thermodilution cardiac output over a wide hemodynamic range. The peak first derivative of the bioimpedance signal dZ/dtmax may provide a noninvasive index of ventricular pump performance. Further studies are required to evaluate the diagnostic value of bioimpedance cardiography in the clinical setting.

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Wavefront myocyte injury and relationship to function in right ventricular ischemia.

Past studies of acute canine right ventricular (RV) ischemia have failed to demonstrate early irreversible injury or decreased function. However, the dog frequently has an extensive collateral circulation not found in all humans. The aim of this study was to measure RV global and regional function after right coronary occlusion in 32 closed-chest pigs. RV function was assessed by biplane ventriculography, and myocardial injury was examined by immunohistochemical localization of creatine kinase (CK) and by electron microscopy. Global RV ejection fraction and apical and midventricular regional function declined significantly after 10 min of occlusion. Injury to the myocardium progressed from the endocardium to the epicardium. Significant injury was observed in myocytes of the endocardium, midmyocardium, and epicardium at 10, 30, and 60 min of occlusion, respectively. Regional RV function and the extent of myocardial injury showed a high correlation (r = 0.96, P less than 0.01). The strong CK immunostaining seen in control hearts was diminished in myocytes along the endocardium at 15 min of occlusion. Depletion of immunoreactive CK in myocytes progressed toward the epicardium with longer ischemic times. These findings demonstrate that RV ischemic injury progresses in a wavefront fashion in the pig, which has similar coronary anatomy to humans, and irreversible myocardial injury occurred after 15-30 min of ischemia.

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Chronic supraventricular tachycardia causes ventricular dysfunction and subendocardial injury in swine.

Chronic supraventricular tachycardia has been associated with ventricular dysfunction in humans and animals. However, this ventricular failure is poorly characterized, and the ultrastructural consequences of supraventricular tachycardia are unknown. We serially examined right and left ventricular function, endomyocardial ultrastructure, and creatine kinase activity in eight pigs at base line and again at 1, 2, and 3 wk following rapid atrial pacing. Left and right ventricular ejection fractions fell significantly from base line after 1 wk of chronic tachycardia. Three weeks of chronic pacing resulted in further deterioration in ejection fractions. Significant biventricular chamber dilatation developed and was associated with a reduction in end-diastolic wall thickness after 2 wk of tachycardia. Mitochondrial injury and diminished mitochondrial cytochrome oxidase staining of subendocardial myocytes were observed after 2 wk of tachycardia. Endomyocardial creatine kinase activity fell from control levels following 2 wk of pacing. Postmortem examination revealed a reduction in left ventricular wall thickness compared with 14 control animals. Fibrosis occurred along the subendocardial layer in paced animals, and glycogen content was also reduced. In summary, chronic supraventricular tachycardia resulted in severe biventricular pump dysfunction and chamber dilatation that were associated with ultrastructural alterations and reduced enzyme activity of the subendocardial myocytes. These ultrastructural and metabolic changes may be potential mechanisms responsible for the ventricular dysfunction and dilatation observed in this model.

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Right ventricular function and three-dimensional modeling using computer-aided design.

Right ventricular (RV) volumetric and morphological analysis is complicated by the trabeculations and geometric configuration of the RV chamber. To improve RV analysis, custom computer-aided design programs were employed to obtain RV volumes and three-dimensional models from biplane ventriculograms. Biplane RV ventriculograms were analyzed from 14 anesthetized dogs and 22 RV casts. Computed volumes were highly correlated with reference RV volumes (r = 0.98, n = 36, P less than 0.01) with a range of 5-73 ml. Three-dimensional wire-frame and solid models constructed from the ventriculographic images provided excellent detail and a new perspective in chamber shape. This modeling technique was then used to examine RV volumes, geometric conformation, and regional shortening in 10 pigs during inotropic stimulation and preload reduction. Changes in RV volumes, ejection fraction, and regional motion were detected as well as alterations in chamber conformation. In summary 1) computer-aided design offers an accurate and simplified means to compute RV volumes using basic microcomputer equipment, and 2) three-dimensional reconstruction provided a unique view of RV geometry and a means to examine regional RV function.

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Thermodilution right ventricular ejection fraction. Catheter positioning effects.

Right ventricular (RV) ejection fractions have been difficult to estimate clinically. It has been demonstrated recently that RV ejection fractions can be calculated by thermodilution techniques using a rapid response thermistor and computer. This method critically depends on adequate mixing of the thermal bolus and sensing of the rapid response thermistor. This study examined the effects of the thermistor position within the pulmonary artery and injectate site within the right atrium on RV thermodilution ejection fraction measurements. Ten pigs were instrumented with a RV thermodilution catheter in the pulmonary artery, an injectate catheter in the right atrium, an atrial-pacing electrode, and a systemic arterial catheter. The RV ejection fractions were determined using thermodilution in two ways: (1) with incremental increases in pulmonic valve to thermistor distance, and (2) with incremental increases in injectate port to tricuspid valve. These measurements were obtained at a paced rate of 107 +/- 1 beats per minute (bpm) and then repeated with pacing-induced tachycardia (140 bpm). The highest RV ejection fraction with the lowest coefficient of variation was with the thermistor 2 cm from the pulmonic valve (50 +/- 2 percent), with a significant decline from this value at 10 cm (42 +/- 4 percent, p less than 0.05). This reduction in RV ejection fraction values with increased pulmonic valve to thermistor distance became more pronounced with tachycardia where a significant decline in RV ejection fraction occurred at 4 cm from the valve when compared with 0 cm (38 +/- 6 percent vs 47 +/- 3 percent, respectively, p less than 0.05). There was no significant change in RV ejection fraction at any injectate port to tricuspid valve distance at the lower heart rate. With tachycardia, however, a significant decline in RV ejection fraction occurred with the injectate port located 7 cm from the tricuspid valve (p less than 0.05). These results demonstrate that RV ejection fractions can be reliably obtained using thermodilution. Positioning of the thermodilution catheter is an important consideration for obtaining optimal RV ejection fraction measurements. Care should be taken to position the catheter with the thermistor a minimal distance from the pulmonic valve and the injectate port within the central body of the right atrium.

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Cardiac function and morphology of Hanford miniature swine and Yucatan miniature and micro swine.

The use of miniature swine in biomedical research is increasing; however, a comparison of cardiac function and morphology between strains has yet to be characterized. The purpose of this project was to examine comprehensive hemodynamics and cardiac morphology of three groups of ten normal, 4 months old, age-matched Yucatan miniature (MINI) pigs, Yucatan micropigs (MICRO) and Hanford (HAN) miniature pigs, 5 males and five females per group. Closed chest cardiac catheterization under equivalent conditions was performed followed by post mortem cardiac morphometry. Mean arterial pressure was significantly greater in the Hanford group when compared to both the minipig and micropig pigs (HAN: 89 +/- 4; MINI: 48 +/- 3; MICRO: 53 +/- 2 mmHg). Pulmonary vascular resistance was significantly different between the three groups (HAN: 9 +/- 1; MINI: 60 +/- 12; MICRO: 111 +/- 29 dyne x sec/cm x m2). The Hanford strain had a significantly smaller heart weight to body weight ratio than the other two groups (HAN: 4.6 +/- 1.0; MINI: 5.7 +/- 0.1; MICRO: 5.5 +/- 1.0). Variations in cardiovascular parameters occur among these strains and should be considered when constructing experimental designs.

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Heritable ventricular septal defect in Yucatan miniature swine.

A heritable ventricular septal defect (VSD) was found in a strain of Yucatan miniature swine. The defect was determined to be a high membranous VSD analogous in anatomic location to the most common from of VSD in humans. Eighteen animals were studied clinically, hemodynamically and at necropsy to characterize the defect. Three mature animals developed pulmonary hypertension. Three animals were found to have a patent foramen ovale (PFO) in addition to the VSD. VSD is heritable probably due to polygenic factors. VSD in Yucatan miniature swine may be a suitable model of the human disease syndrome.

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The pig as a model of tachycardia and dilated cardiomyopathy.

Chronic Supraventricular Tachycardia (SVT) can produce a dilated cardiomyopathy which has a poorly understood association with ventricular dysfunction in humans and animals. The purpose of this study was to produce a model of chronic SVT and dilated cardiomyopathy using swine, which have a cardiac anatomy similar to man. Eight pigs were implanted with chronic atrial catheters and a pacemaker, with four additional sham-operated pigs serving as controls. We examined ventricular function and morphology at baseline (120 +/- 3 bpm), pacing baseline (240 bpm), and at 1, 2 and 3 weeks of rapid atrial pacing (240 bpm). Ventricular ejection fractions fell significantly from baseline following 1 week (left: 38 +/- 3% vs baseline 61 +/- 1%; right: 31 +/- 5% vs baseline 56 +/- 1%; p less than 0.05) and deteriorated further by 3 weeks of SVT (left: 26 +/- 4%, right: 19 +/- 3%; p less than 0.05). Significant biventricular chamber dilation developed by 2 weeks of SVT (left: 50 +/- 5 cc vs paced baseline 27 +/- 2 cc; right: 67 +/- 6 cc vs paced baseline 28 +/- 3 cc; p less than 0.05) and continued to increase by week 3 of SVT (left: 66 +/- 11 cc; right: 78 +/- 8 cc; p less than 0.05). Five additional paced pigs, without chronic atrial catheters, were followed using echocardiography.(ABSTRACT TRUNCATED AT 250 WORDS)

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Right ventricular function computed by thermodilution and ventriculography. A comparison of methods.

Right ventricular ejection fractions have been difficult to estimate clinically. It has been recently suggested that right ventricular ejection fractions can be calculated by thermodilution techniques with a fast-response thermistor and computer. These studies were performed to compare right ventricular ejection fractions obtained from thermodilution and biplane ventriculography. Ten pigs were instrumented with a right ventricular angiographic, thermodilution, and systemic arterial catheter. Right ventricular ejection fractions were determined by thermodilution and ventriculography at four times: (1) baseline, (2) infusion of isoporterenol (5 micrograms/min), (3) 50% of baseline mean arterial pressure produced by hemorrhage, and (4) reinfusion of isoproterenol during hypovolemia. A significant correlation existed between thermodilution and ventriculographic ejection fractions (r = 0.74, p = 0.004). However, during hypovolemia, thermodilution measurements of right ventricular ejection fraction were significantly lower than ventriculographic measurements (p less than 0.05). To determine if the position of the thermistor had a significant effect on thermodilution computations, right ventricular ejection fractions were computed by thermodilution in 10 additional pigs by means of a jugular and femoral insertion, as well as by ventriculography in each pig. Femoral insertion resulted in a greater distance from pulmonic valve to thermistor as compared with jugular placement (p = 0.005). Right ventricular ejection fractions obtained from femoral placement were significantly less than those obtained by jugular insertion (p = 0.008) and ventriculography (p = 0.006). There was no significant difference between jugular and ventriculographic ejection fractions (p = 0.35). Results from these studies demonstrates that thermodilution right ventricular ejection fraction measurements are strongly correlated to ventriculographic methods over a wide hemodynamic range and that improved accuracy is obtained when the pulmonic valve to thermistor distance is minimized. Thus thermodilution may provide a simple and repeatable means to monitor right ventricular function in the critical care setting.

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Noninvasive estimation of extravascular lung water using bioimpedance.

Currently, accurate measurements of extravascular lung water (EVLW) are obtained using the double dye dilution technique (DD). However, this method is invasive and complicated and has limited its clinical use. The purpose of this study was to develop a noninvasive method for determining changes in EVLW using bioimpedance (BI) and compare these measurements with DD in a model of acute pulmonary injury. Nine adult dogs were anesthetized and instrumented with a pulmonary artery and an EVLW arterial catheter with EVLW-DD and cardiac output calculated from the dye and thermal dilution curves. Eight external electrodes were placed on the thorax and impedance changes were measured by computer. Changes in EVLW-BI were computed as a function of the thoracic volume and impedance. Cardiac output (CO) from BI was obtained by electronically differentiating the bioimpedance signal. EVLW and CO were measured using DD and BI at 0, 15, 30, and 60 min following injection of oleic acid (0.1 cc/kg). Changes in EVLW were correlated over all time periods using DD and BI (r = 0.70, P less than 0.05); however, several impedance EVLW estimates varied greatly from double dilution methods. There was no difference in computed EVLW using DD and BI at 15, 30, and 60 min following oleic acid infusion (P greater than 0.35). CO was significantly correlated using DD and BI (r = 0.81, P less than 0.05). In summary, bioimpedance may hold promise as a noninvasive and continuous means for estimation of EVLW in the critical care setting.

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Conventional versus high frequency jet ventilation with a bronchopleural fistula.

A bronchopleural fistula (BPF) is an aberrant pathway through which inspired gas exits the lungs. A BPF may cause significant respiratory compromise, which in turn may result in the need of mechanical ventilation. The purpose of this study was to compare the efficacy of conventional positive pressure ventilation (CV) with high frequency jet ventilation (HFJV) using increasing increments of positive end expiratory pressure (PEEP) in the management of an induced BPF. A reproducible model of a BPF was surgically created in 10 mongrel dogs. Measurements of blood pressure (BP), cardiac output (CO), mean airway pressure (Maw), peak airway pressure (Paw), and fistula flow (FF) were carried out with the chest closed. Selective occlusion of the BPF allowed for blood gas stabilization at increased values of PEEP. Paired observations were performed at 0, 5, 10, 15, and 20 cm H2O of PEEP, while maintaining PaCO2 between 30 and 50 Torr. There was no difference in BP or CO between ventilation methods even though significantly lower Maw and Paw pressures were obtained using HFJV. While FF increased significantly with each increment of PEEP, there was no improvement in flows obtained using HFJV. This acute model of a BPF demonstrated that increasing PEEP dramatically increases FF irrespective of the method of ventilation.

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Supernormal ejection performance is isolated to the ipsilateral congenitally pressure-overloaded ventricle.

Congenital left ventricular pressure overload is associated with "excessive" hypertrophy that leads to subnormal afterload (wall stress), permitting enhanced ventricular ejection performance. Whether congenital right ventricular pressure overload is associated with a similar phenomenon is uncertain. It is also unknown whether supranormal ejection performance affects only the overloaded ventricle or is a general process affecting both ventricles. Conflicting data exist about whether the hypertrophic process associated with pressure overload is induced primarily by local loading conditions or by neuroendocrine influences. If the former postulate is true, the hypertrophic response should be confined to the overloaded ventricle; if the latter is true, one might predict that both ventricles would be affected by a less specific response to circulating catecholamines. To help resolve these issues, both right and left ventricular performance was examined in seven patients with isolated congenital pulmonary stenosis (average pulmonary pressure gradient 78 +/- 13 mm Hg), six patients with isolated congenital aortic stenosis (average gradient 80 +/- 10 mm Hg) and six normal subjects. Right ventricular ejection fraction was increased in patients with pulmonary stenosis (61 +/- 2%) compared with the value in normal subjects (53 +/- 2%, p less than 0.01) and in patients with aortic stenosis (50 +/- 3%, p = 0.007). Left ventricular ejection fraction was increased in patients with congenital aortic stenosis (84 +/- 4%) compared with the value in normal subjects (70 +/- 4%, p less than 0.01) and in patients with congenital pulmonary stenosis (65 +/- 2%, p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Stenosis↗

Technical aspects of cardiac catheterization of swine.

Long-term cardiovascular studies requiring repeated cardiac catheterizations often pose technical problems for investigator using swine. The purpose of this paper is to describe two reliable methods of cardiac catheterization that are used in swine to acquire complete hemodynamic data. Due to the depth of the vessels, vascular cut-downs are usually required. Hemodynamic, angiographic, and interventional cardiac catheters are introduced into either the femoral vessels or the external jugular vein and internal carotid artery. An alternative technique that obviates the need for multiple surgeries involves implantation of silastic catheters into both atria. This allows the passage of catheters directly into the heart chambers. A disadvantage of repeated vascular cut-downs is that a reduction of vascular access occurs. Chronic lines require careful attention to prevent infection and maintain patency.

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Demonstration of early ischemic injury in porcine right ventricular myocardium.

Past studies of acute canine right ventricular (RV) ischemia have failed to demonstrate early irreversible injury or decreased function; however, the dog has extensive collateral circulation that may attenuate RV myocardial injury. The aim of this study was to measure RV function using contrast ventriculography and assess myocardial injury by immunohistochemical evaluation of creatine kinase (CK), lactate dehydrogenase (LDH), and tropomyosin (TROP) as well as by electron microscopy after right coronary occlusion in 14 closed-chest pigs. Significant depression in RV ejection fraction and stroke volume index after 10 minutes and was observed (P less than 0.05). CK, LDH, and TROP were positive in control tissue with a diminution of CK and LDH staining along the subendocardium after 15 minutes of ischemia. Irreversible ultrastructural injury in conjunction with large losses of CK and LDH became evident after 30 minutes. Thus, in the pig, which has a coronary anatomy similar to humans, significant RV dysfunction and irreversible myocardial injury can be demonstrated after 15 to 30 minutes of ischemia.

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