摘要:

ABSTRACTReopening of the ductus arteriosus after successful indomethacin-induced closure has become a major problem with indomethacin treatment. In full-term human newborns and lambs, the ductus behaves like ischemic tissue after its initial constriction. Its ability to continue to relax or contract depends on the amount of left-to-right shunt through the ductus lumen. To see if ductus constriction in preterm lambs would produce the same loss of ductus responsiveness, we delivered 42 lambs by cesarean section and ventilated them for 6.6 ± 0.5( ± SE) hr. We measured ductus arteriosus resistance and left-to-right shunt with the use of radionuclide-labeled microspheres. After the hemodynamic measurements were obtained, the ductus was studied in vitro. Immature lambs were more likely to have reactive ductus (after their initial ductus constriction) than were more mature lambs. This was due to a diminished degree of ductus constriction as well as persistence of ductus responsivenes in immature lambs when compared with more mature lambs. This persistence of ductus responsiveness in immature lambs after ductus constriction may account for the high reopening rate in preterm infants after successful indomethacin-induced closure.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

ABSTRACTMitral valve prolapse was observed in 26 of 92 animals in a harem breeding colony of rhesus monkeys (Macaca mulatta). The affected animals had a systolic murmur best auscultated over the mitral region with the animal in a sitting position. Mid-to-late systolic clicks were also heard. Phonocardiographic examination also demonstrated systolic murmurs and clicks in six of 16 animals. Twenty-three of the animals were studied by M mode and/or two-dimensional echocardiography. The diagnosis was confirmed in 12 animals that had a murmur during the examination. Electrocardiograms revealed T wave abnormalities in five animals and left or right ventricular hypertrophy in five. Four adult animals that died during the course of the study were confirmed at necropsy as having prolapse of the posterior and/or anterior mitral valve leaflets into the atrium. Analysis of the breeding records suggested that mitral valve prolapse was a dominant genetic trait with an approximate birth incidence of 16% to 20% in the colony. The existence of mitral valve prolapse in a nonhuman primate species provides a unique opportunity to study the disease in an experimental animal.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

ABSTRACTWe studied the hemodynamic effects of surgically induced regional cardiac tamponade in anesthetized dogs. Tamponade restricted to either the right or the left ventricle was compared with tamponade of either ventricle and both atria. Intrapericardial pressures were elevated to approximately 20 mm Hg. With tamponade of the right ventricle alone, aortic pressure rose from 161 ± 3.8 to 164 ± 3.4 mm Hg (p > .05) and cardiac output fell from 149.4 ± 16.1 to 134.9 ± 11.9 ml/kg/min (p > .05). However, tamponade of the right ventricle plus both atria decreased mean aortic pressure from 152.5 ± 3.6 to 115.9 ± 8.7 mm Hg (p < .01) and cardiac output fell from 1 18 ± 14.8 to 38.9 ± 4.8 ml/kg/min (p < .01). With tamponade of the left ventricle alone, aortic mean pressure changed significantly from 158.5 ± 6.1 (control) to 148.9 ± 5.0 mm Hg (tamponade) (p < .05) and cardiac output was 135.5 ± 28.3 (control) and 11l1 24.7 ml/kg/min (tamponade) (p > .05). However, when the atria were included, mean aortic pressure fell significantly more from 155.5 ± 5.4 to 105.5 ± 10.4 mm Hg (p < .01) and cardiac output fell from 142.2 ± 16 to 47.8 ± 6.4 ml/kg/min (p < .01). Atrial pressure rose when the atria were included, but not with tamponade of the left ventricle alone. Right but not left atrial pressure rose slightly with isolated right ventricular tamponade. We conclude that the principal hemodynamic effects of cardiac tamponade are not the result of compression of either the right or the left ventricle, but are the consequence of compression of the atria and/or the venae cavae and the pulmonary veins.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

ABSTRACTTo determine the better method of measuring pericardial constraint, pericardial pressure was recorded by a liquid-filled open-ended catheter and a liquid-containing flat balloon in six open-chest anesthetized dogs. Left ventricular pressure was measured by a micromanometer-tipped catheter and left ventricular anteroposterior diameter was measured by sonomicrometry. Left ventricular end-diastolic pressure was raised to 20 ± 1.7 (mean ± SD) mm Hg by intravenous saline. Left ventricular diastolic pressure-diameter loops were constructed (1) with incremental amounts of saline (0 to 50 ml) in the resealed pericardium, (2) with several small holes in the pericardium, and (3) with the pericardium widely open. Measured pericardial pressures were compared with what was assumed to be the correct pericardial pressure, i.e., the calculated difference between left ventricular diastolic pressure (at a given left ventricular diameter) before and after opening the pericardium. Pressure recorded by the flat balloon was similar to the calculated pericardial pressure at all pericardial liquid volumes. Pressure recorded by the open-ended catheter, however, was significantly lower (p < .05) than the calculated pressure unless there was at least 30 ml of liquid in the pericardium. After several holes had been made in the pericardium it still exerted a constraining effect, as shown by a marked rightward or downward shift of the left ventricular diastolic pressure-diameter relationships after completely opening the pericardium. After holes were made in the pericardium pressure recorded by the flat balloon was still similar to the calculated pericardial pressure. However, pressure recorded by the open-ended catheter was significantly (p < .02) lower than the calculated pressure. In four dogs the product of left ventricular anteroposterior and septum-to-free wall diameter was used as a volume parameter; comparison made between measured and calculated pericardial pressures confirmed the results obtained with use of anteroposterior diameter to assess left ventricular size. In conclusion, unless the pericardium is sealed and contains at least 30 ml of liquid, an open-ended catheter significantly underestimates pericardial constraint. However, a flat liquid-containing balloon correctly measures pericardial constraint regardless of the amount of pericardial liquid and also when the pericardium is not sealed.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

ABSTRACTUsing sonar microcrystals implanted in conscious dogs, we have characterized left ventricular segmental relaxation (LVSR) by measuring the mean rate to half end‐diastolic thinning (RHEDT) and the late diastolic thinning fraction (TF). In protocol 1 (five nonischemic dogs), RHEDT correlated with changes in left ventricular dP/dt (r = .87) and systemic arterial pressure (r = − .80) but not with alterations in heart rate. Only systemic arterial pressure importantly influenced TF (r = −.65). In protocol 2 (21 dogs), LVSR paralleled net systolic segmental wall thickness (NET) during both 2 and 4 hr of coronary occlusion followed by 1 month reperfusion. Both LVSR and NET remained depressed during 2 and 4 hr of coronary occlusion and through 24 hr of reperfusion, but both also gradually improved afterwards. In protocol 3, 31 dogs underwent 4 hr of coronary occlusion with 1 month of reperfusion. Among these animals, 11 dogs (group S4) received saline after 1 hr of occlusion, nine dogs (group P4) received propranolol, and 11 dogs (group D4) received diltiazem. Drug therapy was stopped at 2 hr of reperfusion. In segments with mildly and moderately depressed NET, LVSR was significantly increased in group D4 vs group S4 animals during the diltiazem infusion. Expressed as mean percentage of control value ± SEM, RHEDT of moderately dysfunctional segments in group D4 compared with group S4 measured 53 ± 10% vs 25 ± 5%, respectively, at 2 hr of occlusion of the left anterior descending coronary artery (p = .03), 76 ± 17% vs 28 8%, respectively, at 4 hr of occlusion (p = .01), and 74 ± 1 1% vs 33 ± 10%, respectively, at 1 hr of reperfusion (p < .05). The differences in TF at these same time points were 106 ± 10% vs 70 9% (p < .03), 105 ± 7% vs 65 ± 16% (p < .02), and 106 ± 11% vs 74 ± 13% (p < .05), respectively. The improvement in LVSR occurred independently of changes in NET. The values of LVSR in the diltiazem‐treated dogs fell to the levels of groups S4 and P4 within 24 hr of stopping the intervention. Propranolol did not significantly alter LVSR over the short or long term. The increase in LVSR during administration of diltiazem did not appear to be mediated by changes in contractility or regional myocardial blood flow, but were probably mediated in part by afterload reduction and possibly by a reduction in calcium entry into ischemic myocardium.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

ABSTRACTThe hypothesis that nitrates evoke prostacyclin production by vascular endothelium has been reevaluated on cultured umbilical vein endothelial cells and in vascular fragments, both obtained from humans. Endothelial cell monolayers (passages 1 and 2) were washed free of culture medium and exposed for 3 to 5 min to buffer or nitroglycerin (NTG), isosorbide dinitrate (ISDN), or isosorbide‐5‐mononitrate (ISMN) over a range of concentrations (10–9M to 10–6M) encompassing those usually attained in vivo, with or without 25 ±mUM sodium arachidonate. Basal prostacyclin production, measured by radioimmunoassay of the stable metabolite 6‐keto‐PGF±aL, depended on cell density in the endothelial monolayer (being higher in preconfluent cultures) and on incubation time. Basal prostacyclin, however, was not altered by incubation with NTG (3.3 ± 2.0 pg/1000 cells without drug vs 3.9 ± 3.8 pg/1000 cells with drug, mean ± SD), ISDN (3.1 ± 1.9 vs 3.1 ± 2.2), or ISMN (2.0 ± 0.9 vs 2.3 ± 1.5) at 10−7M (all differences NS). Also, long‐term incubation (2, 6, and 24 hr) with ISDN and ISMN did not alter prostacyclin production over control. Over a 30‐fold increase (p < .001) in prostacyclin production was obtained with arachidonate stimulation, but incubation with nitrates did not significantly modify the stimulated production. Saphenous vein. mesenteric artery, and atrial appendage fragments incubated at 370 C for 20 min in a shaking water bath with a control buffer procluced 27.8 ± 13.9, 189.7 ± 75.2, and 662.3 ± 390.6 pg 6‐keto‐PGF,±aL/mg tissue, respectively. Arachidonate (25 ±mUM) increased prostacyclin production by these tissues to 158.8 ± 120.6 (p < .001). 381.0 ± 48.2 (p < .01), and 885.6 ± 291.4 (NS). respectively. However no significant variation from control prostacyclin was obtained with 20 min exposure to NTG, ISDN, or ISMN in a range from 10−9M to 10–9M. No dose‐effect relationship for these drugs on prostacyclin production was found. These data suggest that nitrates do not increase endothelial prostacyclin production.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID