Biomedical subjects

I Palacios

Publications and source records attributed to I Palacios.

61 records · Page 4Linked to original sources

PubMed1981

Congenital extracardiac shunts with tetralogy of Fallot.

Congenital extracardiac shunts in tetralogy of Fallot may significantly alter the history and clinical findings and also have significant management implications. An unusual variant of severe tetralogy of Fallot in a 54-year-old man enabled long survival with minimal symptoms. The patient had pulmonary valvular and infundibular stenosis, a large ventricular septal defect, an overriding aorta, and large volume systemic-to-pulmonary artery shunting from his right internal mammary and accessory internal mammary arteries to his right pulmonary artery.

Coronary Circulation↗

PubMed1981

Right ventricular distension and left ventricular compliance.

The constraint of the right ventricle (RV) on the end-diastolic pressure-volume (PV) relationship of the nonischemic and ischemic left ventricle (LV) was studied. The model used was the isovolumic beating LV, with separately perfused ejecting RV with controlled RV distension. The effect of augmented RV distension on the nonischemic LV PV relationship was examined. A change from mild [right ventricular end-diastolic pressure (RVEDP) = 1.5 mm Hg] to severe (RVEDP = 16 mmHg) RV distension resulted in a significant leftward shift of the LV PV relationship. Ischemia was produced for 90 min by reducing flow in the cannulated left main coronary artery and the effect of two levels of stable RV distension on the PV relationship of the ischemic LV was examined. Mild RV distension and moderate (RVEDP = 6 mmHg) RV distension were used. In both groups, there was a progressive leftward shift in the LV PV relationship that was significant by 60 min of ischemia. No change was seen in nonischemic controls. Ventricular relaxation, as described by the time constant of isovolumic relaxation, T, was impaired throughout ischemia but was not sufficiently prolonged to explain the above changes. Thus, the time course of change in the LV PV relationship during ischemia differs from that previously reported after pacing-induced ischemia in humans. Neither the external constraint of the RV nor incomplete relaxation explains this difference.

Animals↗

PubMed1981

Pulmonary capillary wedge pressure, as inferred from lung areas in gated blood-pool scintigrams: concise communication.

To determine whether the apex-to-base distribution of pulmonary blood volume, as obtained from gated cardiac blood-pool scans, could be used as a noninvasive method to estimate mean pulmonary capillary wedge pressure (PCWP), gated blood-pool scans were analyzed in 77 patients who also had PCWP measurements at cardiac catheterization. Ten of these patients had gated cardiac blood-pool scans and PCWP measurements both at rest and during exercise. The apex-to-base distribution of pulmonary blood volume was determined from the end-systolic frame of the left anterior oblique view by placing equal-sized regions of interest over the apex and base of the right lung. The ratio of apex counts over base counts (A/B ratio) was considered abnormal if greater than unity. The mean A/B ratio was 1.15 +/- 0.27 (1 s.d.) for the 32 studies associated with an abnormal mean PCWP (greater than 12 mm Hg). The mean A/B ratio was 0.85 +/- 0.23 for the 55 studies associated with a normal mean PCWP (p less than 0.01 comparing normal group with abnormal). The sensitivity of the A/B ratio for a mean PCWP greater than 12 mm Hg was 81%R (26/32). The specificity of the A/B ratio for a mean PCWP greater than or equal to 12 mm Hg was 89% (49/55). Thus, noninvasive determination of the pulmonary apex-to-base ratio from gated cardiac blood-pool scans appears to differentiate subjects with normal and abnormal mean pulmonary capillary wedge pressures.

Adult↗

PubMed1979

Effect of hypoxia on mechanical properties of hyperthyroid cat papillary muscle.

It has been previously established that hyperthyroid myocardium exhibits increased performance under well-oxygenated conditions. To date, it is not known whether hyperthyroid cardiac muscle can maintain this increased performance during hypoxia. The responses of isolated right ventricular papillary muscles from hyperthyroid and euthyroid kittens to hypoxia were compared under isometric conditions at 31 degrees C. Under well-oxygenated conditions, the hyperthyroid cardiac muscle exhibited both an increased contractility and an accelerated rate of relaxation. A similar degree of acute hypoxic stress for 15 min resulted in a greater decrease in contractility in the hyperthyroid compared with the euthyroid papillary muscle as indicated by a greater fall in both peak tension development (2.2 +/- 0.25 from 4.2 +/- 0.2 vs. 0.9 +/- 0.15 from 3.2 +/- 0.4 g/mm2, P less than 0.01) and +dT/dt (12.9 +/- 2.3 from 25 +/- 3 vs. 4.0 +/- 0.6 from 14 +/- 1 g-s-1-mm-2, P less than 0.01). In addition, compared with the euthyroid data, hypoxia resulted in impaired myocardial relaxation in the hyperthyroid cardiac muscle. Thus, the hyperthyroid compared with the euthyroid papillary muscle exhibits both a greater decrease in contractility and an impairment of myocardial relaxation during hypoxia, indicating a greater susceptibility to a given hypoxic stress.

Animals↗

PubMed1978

Effects of acute global ischemia on diastolic relaxation in canine hearts.

It is not known whether ventricular relaxation can be altered by ischemia independent of associated hemodynamic changes. The effect of acute myocardial ischemia on diastolic relaxation was studied under controlled hemodynamic conditions in 16 anesthetized dogs on right-heart bypass. In nine dogs, left ventricular end-diastolic pressure was maintained constant throughout the experiments. Ischemia produced a significant prolongation of the isovolumetric relaxation period (IVRP) from 29 +/- 3 (SE) to 88 +/- 7 ms (P less than 0.01). Ischemia, per se, the associated decrease in contractility, or the fall in peak left ventricular pressure (LVP) may have contributed to the increase in IVRP. The latter was not the only mechanism involved, because in seven dogs studied with constant peak LVP, IVRP again was prolonged from 64 +/- 8 to 95 +/- 8 ms (P less than 0.01). Moreover, in five nonischemic hearts in which peak LVP was maintained constant, contractility was decreased by sodium pentobarbital to the same extent as with ischemia; IVRP did not change. Thus, the additional prolongation of the IVRP in the ischemia experiments is secondary to a direct effect of ischemia on the relaxation process of the myocardium.

Animals↗

PubMed1978

Effect of hypoxia on myocardial relaxation in isometric cat papillary muscle.

Myocardial relaxation is an important energy-dependent process. Hypoxia, unlike ischemia, has not been shown to impair myocardial relaxation. This difference may be because (a) the traditional index to assess isometric muscle relaxation (half time to relaxation or RT((1/2))) reflects both changes in developed tension as well as relaxation and (b) the relaxation process is highly sensitive to temperature and previous papillary muscle studies have been conducted under hypothermic conditions. The present study examines the effect of hypoxia on the relaxation process of 31 isometrically contracting kitten papillary muscles at hypothermic (29 degrees C) and euthermic (38 degrees C) conditions using RT((1/2)), the peak rate of tension fall (-dT/dt) and -dT/dt normalized for tension ([peak -dT/dt]/T and max [-dT/dt per T]). Hypoxia at 29 degrees C resulted in a fall in RT((1/2)) from 278+/-11 (SEM) to 230+/-17 ms (P < 0.01) and no change in (peak -dT/dt)/T and max (-dT/dt per T). However, at 38 degrees C, hypoxia impaired relaxation as reflected in a prolongation of RT((1/2)) from 101+/-6 to 126+/-8 ms (P < 0.01) in spite of a substantial fall in peak tension. Moreover, (peak -dT/dt)/T decreased from -15.4+/-0.7 to -11.0+/-0.8/s (P < 0.01) and max (-dT/dt per T) decreased from -25.1+/-1.8 to -13.8+/-0.9/s (P < 0.01). In conclusion, the present study demonstrates that hypoxia impairs the relaxation process of cardiac muscle.

Animals↗

PubMed1976

Left ventricular end-diastolic pressure volume relationships with experimental acute global ischemia.

The mechanism of elevation of left ventricular end-diastolic pressure during acute global ischemia was evaluated by examiniation of the relative contributions of a decrease in contractility and an alteration of the pressure-volume relationship. The external circumference (mercury-in-silastic gauge) pressure relationship, as an index of the pressure-volume relationship, was studied in beta adrenergic and ganglionic blocked, open chest dogs on right heart bypass at constant heart rate ane aortic pressure. Ischemia of one and two hours' duration was produced by reducing total coronary blood flow in cannulated left and right coronary arteries until left ventricular end-diastolic pressure rose significantly. At a constant stroke work, left ventricular end-diastolic pressure rose from 5.0 +/- 0.5 to 15.0 +/- 0.5 cm H2O in the experiments of one hour of ischemia, and from 7.0 +/- 1.0 to 17.0 +/- 1.0 cm H2O in experiments of two hours of ischemia. Ischemia was followed by one hour of restoration of coronary blood flow. Ischemia produced a marked depression of ventricular function: stroke work, considered at a left ventricular end-diastolic pressure of 15 cm H2O, decreased from 21.0 +/- 3.0 to 3.5 +/- 0.5 gm-m, and from 15.0 +/- 2.0 to 2.5 +/- 0.5 gm-m, in the experiments of one and two hours, respectively. Neither ischemia nor reflow changed the pressure-volume relationship. Thus, the elevation of left ventricular end-diastolic pressure during ischemia in an otherwise normal canine myocardium is due to a decrease in systolic performance of the heart rather than to an alteration of the pressure-volume relationship.

Acute Disease↗