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Biomedical subjects

F G Spinale

Publications and source records attributed to F G Spinale.

186 records · Page 11Linked to original sources
PubMed1988

Comparison of bioimpedance and thermodilution methods for determining cardiac output: experimental and clinical studies.

The changes in electrical bioimpedance caused by the blood flow through a thoracic segment may be measured using a series of electrodes placed at opposing ends of this segment. Cardiac output (CO) is calculated by computer as the change in bioimpedance over time. This study was performed to determine the accuracy of bioimpedance CO (CObi) compared with standard thermodilution CO (COtd) in an animal model and in patients. COtd was determined using a thermodilution CO computer, and CObi was calculated with a bioimpedance computer in 10 dogs at baseline and at 5-minute intervals following the injection of 7 mEq of calcium chloride. A high correlation between COtd and CObi was observed (r = 0.91, p less than 0.001) over a range of 2.5 to 6 L/min. Thirty-three paired observations using the CObi and COtd methods were performed in 10 patients following elective coronary artery bypass surgery. A significant correlation between the two methods was determined with a CO range of 2.1 to 7.8 L/min (r = 0.77, p less than 0.001). CObi became inaccurate with severe tachycardia (pulse, 180/min), low CO, or frequent arrhythmias. These results indicate that this technique provides a continuous noninvasive method of determining CO that is comparable with thermodilution techniques. The technique of CObi holds promise for widespread use when continuous and noninvasive monitoring of CO is necessary.

Adult↗
PubMedDate not supplied

Left ventricular and myocyte structure and function following chronic ventricular tachycardia in rabbits.

Recent studies have shown that chronic pacing induced tachycardia in large animals such as dogs and pigs causes congestive heart failure accompanied by myocyte contractile abnormalities, neurohormonal activation, alterations in sarcolemmal receptor systems, and changes in myocardial structure. However, fundamental studies directed at identifying basic contributory mechanisms responsible for the development of this form of heart failure are problematic in these large animals. Accordingly, the present study examined the direct effects of pacing induced tachycardia upon LV and myocyte structure and function in the adult rabbit. Twelve adult rabbits (New Zealand White; 3.5-4.5 Kg) underwent 30 days of pacing induced ventricular tachycardia (VT; right ventricular paced, 400 bpm) and 12 additional age and weight matched rabbits served as controls. Echocardiography revealed increased LV end-diastolic dimension (1.92 +/- 0.04 vs 1.10 +/- 0.20 cm; p < 0.05) and decreased fractional shortening (41.5 +/- 3 vs 22.3 +/- 4%; p < 0.05) in the VT group compared to controls with no change in LV mass. Steady-state isolated myocyte contractile function was significantly reduced in the VT group compared to control. For example, isolated myocyte velocity of shortening was 41 +/- 2 microns/s in the VT group compared to 84 +/- 5 microns/s for controls (p < 0.05). In the presence of 8 mM extracellular Ca2+, myocyte velocity of shortening was 40% lower in the VT group compared to controls. Finally, myocyte contractile responsiveness with beta-adrenergic receptor stimulation was reduced by 52% in the VT group compared to controls. Isolated myocyte length significantly increased in the VT group compared to control (157 +/- 3 vs 128 +/- 2 microns; p < 0.05) with a concomitant decrease in cross-sectional area (274 +/- 6 vs 400 +/- 31 microns 2; p < 0.05). Myocyte myofibril volume fell by 27% in the VT group compared to control with no change in mitochondrial percent volume. In summary, this study demonstrated that chronic pacing induced tachycardia in rabbits caused: 1) LV dilation and dysfunction, 2) depressed isolated myocyte contractile function and inotropic responsiveness, and 3) alterations in myocyte structure and composition. The changes in LV and myocyte function and structure following chronic tachycardia in rabbits are similar to that reported previously with tachycardia induced heart failure in larger animals. These findings suggest that this rabbit model of chronic tachycardia may provide a useful and practical means by which to examine basic mechanisms responsible for the development of congestive heart failure.

Animals↗
PubMedDate not supplied

Alterations in the myocardial capillary vasculature accompany tachycardia-induced cardiomyopathy.

Changes in capillary structure and distribution within the left ventricle (LV) occur with pressure and volume overload hypertrophy. These changes may cause an impairment in myocardial blood flow (MBF) and oxygen delivery resulting in myocyte injury and LV dysfunction. However, it is unknown whether changes in the capillary vasculature accompany the development of LV dysfunction in dilated cardiomyopathies. Accordingly, this study examined the relation between LV function, MBF and capillary architecture after the development of dilated cardiomyopathy in pigs produced by chronic supraventricular tachycardia (SVT). LV function was examined by echo-catheterization, and capillary morphometrics were computed using lectin histochemistry in two groups of pigs: sham controls (n = 8); and after 3 weeks of pacing-induced SVT (n = 8). Chronic SVT resulted in significantly increased LV end-diastolic dimension and pressure with a 50% reduction in LV fractional shortening compared to CON (p less than 0.05). Although no significant change in capillary density (2180 +/- 164 vs 2402 +/- 147/mm2, p = 0.25) occurred in the SVT group compared to CON, a significant reduction in the volume fraction of capillaries (12.2 +/- 0.5 vs 9.9 +/- 0.7%, p less than 0.05) and increased capillary diffusion distance (8.4 +/- 0.5 vs 7.5 +/- 0.3 microns, p less than 0.05) was observed. Frequency distribution analysis revealed a higher percentage of smaller diameter capillaries with chronic SVT vs CON (p less than 0.05). Ultrastructural examination revealed an increased capillary-myocyte distance with chronic SVT (0.95 +/- 0.08 vs 1.95 +/- 0.12 microns, p less than 0.05). These changes were accompanied by ultrastructural evidence of significant subendocardial injury (p less than 0.05). MBF was measured using microspheres in five additional conscious pigs in each group. MBF was significantly reduced and coronary vascular resistance increased in the SVT group compared to CON (p less than 0.05). Chronic SVT caused significant remodeling of the capillary vasculature; these changes were associated with reduced MBF, myocyte injury, and LV dysfunction.

Animals↗
PubMedDate not supplied

Controlling myocardial matrix remodeling: implications for heart failure.

Progressive congestive heart failure (CHF) is often accompanied by a change in left ventricular geometry and myocardial architecture, commonly referred to as myocardial remodeling. It has been observed that important changes occur within the collagen matrix of the myocardium, potentially contributing to the remodeling process. The myocardial collagen matrix is influenced by 2 fundamental processes: collagen synthesis and collagen degradation. Matrix metalloproteinases are an endogenous family of zinc-dependent enzymes involved in matrix degradation and have been shown to be regulated by a class of proteins called the tissue inhibitors of metalloproteinases. Several studies have identified changes in myocardial matrix metalloproteinase and tissue inhibitors of metalloproteinase expression with the development of CHF. These observations have led to the hypothesis that increased metalloproteinase activity and decreased levels of tissue inhibitors of metalloproteinase result in collagen remodeling that disrupts myocyte alignment and facilitates the left ventricular remodeling process with CHF. Thus, the development of pharmacologic agents that will modulate the activity and expression of myocardial matrix metalloproteinases represents a new and potentially significant therapeutic target for developing CHF.

Animals↗
PubMedDate not supplied

Tranexamic acid reduces bleeding after cardiopulmonary bypass when compared to epsilon aminocaproic acid and placebo.

UNLABELLED: Perioperative bleeding following coronary artery bypass grafting (CABG) is associated with increased blood product usage. Although aprotonin is effective in reducing perioperative blood loss, excessive cost prohibits routine utilization. Epsilon aminocaproic acid (EACA) and tranexamic acid (TA) are inexpensive antifibrinolytic agents, which, when given prophylactically, may reduce blood loss. The present study was undertaken to compare the efficacy of TA and EACA in reducing perioperative blood loss. METHODS: The study population consisted of first-time CABG patients. Patients were allocated in a prospective double-blind fashion: (1) group EACA (loading dose 15 mg/kg, continuous infusion 10 mg/kg per hour for 6 hours, N = 20); (2) group TA (loading dose 15 mg/kg, continuous infusion 1 mg/kg per hour for 6 hours, N = 20); (3) control group (infusion of normal saline for 6 hours, N = 19). RESULTS: Treatment groups were similar preoperatively. No significant difference in intraoperative blood loss or perioperative use of blood products was noted. D-dimer concentration was elevated in the control group compared to the EACA and TA groups (p < 0.05). Group TA had less postoperative blood loss than the EACA and control groups at 6 and 12 hours postoperatively (p < 0.05). TA had reduced total blood loss (600 +/- 49 mL) postoperatively compared to EACA (961 +/- 148 mL) and control (1060 +/- 127 mL, p < 0.05). CONCLUSION: TA and EACA effectively inhibited fibrinolytic activity intraoperatively and throughout the first 24 hours postoperatively. TA was more effective in reducing blood loss postoperatively following CABG. This suggests that TA may be beneficial as an effective and inexpensive antifibrinolytic in first-time CABG patients.

Aminocaproic Acid↗