摘要:

Controversy persists over the relative tolerance of the immature myocardium to global ischemia. Thus, we evaluated the physiologic effects of 30, 60, and 180 minutes of global ischemia in an isolated, isovolumic rabbit heart model, at 3 different ages: newborns (less than 1 week of age) (n = 36), juveniles (4 to 6 weeks old) (n = 36), and adults (5 to 7 months old) (n = 36). Following 30 and 60 minutes of ischemia, respectively, adults recovered 87 ± 4% (mean ± SEM) and 90 ± 7% of baseline systolic function, and juveniles recovered 91 ± 10% and 85 ± 8%. In contrast, newborns recovered only 27 ± 6% and 28 ± 4% of baseline systolic function (p<0.05 compared to adults and juveniles). During ischemia, newborn hearts became stiff more rapidly, reaching 361 ± 46% of baseline stiffness by 60 minutes, whereas adults and juveniles were at 122 ± 33% and 92 ± 18% of baseline stiffness (p<0.05 newborns compared to adults and juveniles). With reperfusion after 60 minutes of ischemia, the work efficiency of the newborn heart deteriorated to 39 ± 7% of baseline, compared with 95 ± 7% and 91 ± 7% of baseline efficiency in the adult and juvenile hearts (p<0.05, newborns compared to adults and juveniles). The ratio of tissue wet-to-dry weights were similar in all age groups after ischemia. However, tissue pH was significantly higher in newborns during ischemia (6.54 ± 0.06, 6.69 ± 0.07, and 6.85 ± 0.09 in adults, juveniles, and newborns, after 60 minutes of ischemia) (p<0.05 newborns versus adults). We conclude that the newborn rabbit hearts are more susceptible to ischemic injury than the juvenile and adult hearts. (Circulation Research 1987;61:609-615)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

This study was undertaken to determine what changes occur in the intestinal microvasculature during the rapid growth associated with juvenile maturation. A technique was developed that permitted the comparison of the same microvessels in exactly the same intestinal region at two time periods of an animal's life. A region of the terminal ileum of 5-week-old rats was exposed and marked, and photographs and video recordings were made of the microvessels. Four weeks later, the marked intestinal region was located, and photography and videography of the microvessels were repeated. Comparison of indexes for body, intestinal, and microvascular growth for the treated rats and age- and colony-matched controls revealed no significant differences. The number and branching pattern of arterioles observed in the marked region remained remarkably constant during the 4 weeks between observation periods, even though body and bowel mass of the treated animals increased approximately 2.5 times. The lengths of the arterioles were increased (18%) by almost the same proportion as the axis of bowel (22%) in which they were oriented. The average distance between capillaries in the radial intestinal muscle layer was also increased by about the same percentage (24%) as that of tissue elongation (22%). The overall data are consistent with the hypothesis that during the growth spurt of juvenile life, the arterioles present at the weanling stage are elongated and new branches do not develop. The net effect of tissue growth with a minimal change in numbers of arterioles is a decreased ratio of number of arterioles to tissue mass as a normal consequence of maturation. (Circulation Research 1987;61:616-624)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Receptor-stimulated phosphatidylinositol turnover has been studied in isolated, perfused, [3H]inositol-labelled rat hearts by measuring accumulation of inositol phosphates in the presence of lithium chloride. Inositol phosphate accumulation was stimulated by norepinephrine (3±10-5M) and carbachol (10-3M), the increases averaging from 931 ± 59 (n = 6, mean ± SEM, cpm/g heart) to 4,165 ± 609 (n = 6, p<0.01) for norepinephrine and to 1,853 ± 354 (n = 6, p<0.05) for carbachol. The norepinephrine stimulation was antagonized by prazosin (10-7M) but not by propranolol (10-7M), indicating mediation via α1-adrenoceptors. The carbachol stimulation was antagonized by atropine (10-7M). The stimulation by norepinephrine was significantly higher in right atria (837 ± 151 to 6,614 ± 1,210, n = 6, cpm/g tissue) than in other regions of the heart. Both norepinephrine and carbachol stimulated the formation of inositol monophosphate, inositol bisphosphate, and inositol trisphosphate with norepinephrine stimulation being detected as early as 15 seconds. Furthermore, the inositol trisphosphate was identified as the -1,4,5 isomer by anlon exchange high-performance liquid chromatography. These data are consistent with the hydrolysis of phosphatidylinositol-(4,5)-bisphosphate yielding inositol-(l,4,5)-trisphosphate. Inositol-(l,3,4)-trisphosphate was not detected in heart preparations, suggesting unusual metabolism of inositol-(l,4,5)-trisphosphate in heart tissue. (Circulation Research 1987;61:625-631)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The goal of the present study was to determine if voltage-sensitive calcium channels are present in bovine aortic endothelial cell plasmalemma and if they contribute to the rise in cytosolic calcium produced by bradykinin. After bradykinin (100 nM) exposure, endothelial cell associated fura-2 fluorescence peaked within 10-20 seconds and then declined to a steady level 2- to 3-fold above resting values. Pretreatment with lanthanum (20 μM) abolished the steady level produced by bradykinin but had little effect on the initial, transient rise in cytosolic calcium. Chelation of extracellular calcium with EGTA before addition of bradykinin resulted in a substantial decrease in the fura-2 transient and elimination of the long-lasting component. Nimodipine (3 μM) and nitrendipine (1 μM) were without effect on either phase of the bradykinin-induced response. Moreover, elevation of extracellular potassium failed to produce a rise in intracellular calcium. With the use of the tight seal technique to voltage clamp the cells, inwardly rectifying and calcium-activated potassium currents were found to exist in the endothelial cells. Addition of bradykinin (100 nM) elicited a calcium-activated potassium current that was eliminated in the absence of intracellular potassium. No voltage-sensitive calcium currents were activated when the cells were exposed to 10 mM or 110 mM calcium chloride in the presence or absence of bradykinin. The binding of [3H]( + )PN200-110 to endothelial cell membrane preparations was 1-3 orders of magnitude lower than that observed in PC-12, GH3, or BC3H1 cell membranes. Together, these results suggest that cloned bovine aortic endothelial cells lack voltage-sensitive calcium channels. Therefore, the changes in cytosolic calcium stimulated by bradykinin that are dependent on extracellular calcium must occur via some other calcium influx pathway. (Circulation Research 1987;61:632-640)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Female Sprague-Dawley rats were made hypertensive by the two kidney/one clip Goldblatt procedure, while control animals were sham-operated. One week later, half of the animals were subjected to a moderate swimming exercise and the other half remained sedentary. Thus, four experimental groups, each consisting of 14 rats, were formed: control animals that were exercised or kept sedentary and corresponding renal hypertensive animals either exercised or sedentary. In hypertensive rats, a significantly increased left ventricular weight and reduced coronary reserve were found. Cardiac hypertrophy in hypertensive rats was characterized by a lower number of capillaries on a tissue cross-section, larger heterogeneity of the capillary net, and a less uniform orientation of capillaries in space. Total length of capillaries in the hypertrophic hearts increased significantly, but less than the increase in cardiac weight, resulting in reduced capillary length density. Chronic swimming for 2 hr/day for a period of 6 weeks, subsequent to a 4-week acclimation period, did not significantly influence any of the investigated indexes of capillaries from hypertrophic hearts. In the normotensive rats, chronic swimming resulted only in a moderate increase in total capillary length associated with a small increase in the left ventricular weight of similar degree. Thus, chronic exercise in normotensive rats induced a moderate increase in total capillary length per left ventricle, while it did not alleviate impaired capillarization of hypertrophic hearts from hypertensive rats. (Clrculation Research 1987;61:641-647)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The purpose of this study was to contrast the effects of static and pulsatile pressure on carotid baroreceptor activity over a wide range of mean arterial pressure. Static and pulsatile pressure were applied to the isolated carotid sinus of dogs anesthetized with chloralose. Recordings were obtained from single baroreceptor units as well as from the whole sinus nerve or a large strand of the nerve. Three observations are reported. First, in single units the pulsatile pressure threshold, which averaged 48 ± 8 (SEM) mm Hg, was far below the static pressure threshold, which averaged 79 ± 8 mm Hg (p<0.05, n=15). Thus, pulsatility decreased the threshold by an average of 31 mm Hg in contrast to the minimal or lack of decrease in threshold reported by others in aortic baroreceptors. Second, at moderate arterial pressures a shift from static to pulsatile pressure caused a decrease in single and multiple unit activities. In single units, the decrease approximated 15% (from 42.0 ± 2.1 to 35.5 ± 1.9 spikes/sec, p<0.05, n = 25). In all units, there was no diastolic nerve activity (“silence”) when diastolic pressure was 1 to 10 mm Hg above static pressure threshold; 80% of the units exhibited "diastolic silence" when diastolic pressure was 20-30 mm Hg above threshold and 40% of the units showed silence at-diastolic pressures 40-50 mm Hg above threshold. In whole nerve recordings, pulsatility increased activity from 57 ± 15 to 142 ± 29 spikes/sec (p<0.05) at low mean arterial pressures (50 and 75 mm Hg), as expected from the reduction in pressure threshold noted in single units, and decreased activity approximately 15% (from 373 ± 69 to 320 ± 55 spikes/sec, p<0.05, n = 9) at mean arterial pressures of 125 and 150 mm Hg. This decrease in activity with a shift from static to pulsatile pressure at moderate arterial pressures has not been reported previously. Third, the static pressure-activity curve was sigmoid, and its gain peaked sharply at 75-100 mm Hg; in contrast, the pulsatile pressure-activity curve was linear between 25 and 150 mm Hg, and its maximum gain was half the maximum gain during static pressure. These differences between the static pressure-activity curve and the pulsatile pressure-activity curve were noted during both increases and decreases in carotid sinus pressure; both curves exhibited some hysteresis during the decreases in pressure. (Circulation Research 1987:61:648-658)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

We investigated the physiologic effects of normal saline versus 5% albuminated saline fluid resuscitation on 10-12-day-old piglets infected with group B streptococci for four hours. After intravenously receiving 1 ± 1010bacteria/kg over 45 minutes, one group was untreated while the two fluid-treated groups received enough intravenous fluid to maintain the baseline cardiac output. An increase in the resistance to venous blood return was the major limitation to cardiac output. The resistance nearly quadrupled in the untreated piglets as shown by a 50% decrease in cardiac output with a nearly doubling of the driving pressure for venous return (mean circulatory pressure was normal and atrial pressures decreased by 70%). In both fluid-treated groups, resistance doubled as shown by an unchanged cardiac output with a doubling of the driving pressure (mean circulatory pressure increased by 50%) and atrial pressures remained at baseline). Blood volume was 9% below control in the untreated group and 13% above control in both fluid-treated groups. Much more crystalloid (155 ml/kg) than colloid (58 ml/kg) was necessary to maintain baseline cardiac output; this resulted in a 36% decrease in the plasma protein oncotic pressure of the former group and a 15% increase in the oncotic pressure of the latter group. Organ edema formation (ileum, pancreas, kidney, adrenal gland, lung) occurred only in the saline-treated animals. We conclude that increased resistance to venous return was the primary cause of shock in our model and that this can be effectively treated by giving enough intravenous fluid to elevate the mean circulatory pressure. However, if the plasma protein oncotic pressure is also lowered (saline group), organ edema results. (Circulation Research 1987;61:659-669)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

We investigated the effect of converting enzyme inhibition (CEI) on the relationship between renal perfusion pressure (RPP) and steady-state plasma renin activity (PRA) in uninephrectomized conscious dogs on normal-salt (80 meq Na+/day) and low-salt (10 meq Na+/day) diets. Stimulus-response curves for the renal baroreceptor were determined by measuring the steady-state PRA while the RPP was lowered and then held constant by an inflatable cuff placed around the renal artery. On each diet the control stimulus-response curve can be described by two lines intersecting at a threshold pressure; in the higher pressure range PRA is relatively insensitive to changes in RPP, while in the lower pressure range PRA is very responsive to changes in RPP. On the normal-salt diet CEI significantly increases the sensitivity of PRA to RPP in the responsive range without affecting the threshold pressure itself or the values of PRA at pressures greater than the threshold pressure. On the low-salt diet CEI also increases the sensitivity of PRA to RPP significantly in the responsive range; we were unable to determine the effect of CEI on PRA at RPPs greater than the threshold pressure in the low-salt state because CEI causes a significant drop in blood pressure under these circumstances. The effect of CEI was significantly greater in the dogs on the low-salt diet than in the dogs on the normal-salt diet. Thus, CEI and salt depletion interact synergistically to increase the sensitivity of the renal baroreceptor only in the responsive range of the stimulus-response curve, i.e., at renal perfusion pressures below the threshold pressure. (Circulation Research 1987;61:670-677)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The effects of unloading the carotid sinus baroreceptors before and during the development of perinephritic hypertension were studied in conscious dogs instrumented with aortic catheters to measure arterial pressure and heart rate, and electromagnetic flow probes to measure cardiac output and calculate total peripheral resistance. Prior to hypertension, bilateral carotid occlusion (BCO) increased mean arterial pressure by 38 ± 2 from 101 ± 2 mm Hg and total peripheral resistance by 19 ± 2 from 46 ± 3 mm Hg/l/min, while cardiac output and heart rate did not change from 2,299 ± 128 ml/min and 84 ± 4 beats/min, respectively. At 2 weeks after renal wrapping, there were significant increases in baseline mean arterial pressure, cardiac output, and total peripheral resistance and decreases in heart rate; BCO increased mean arterial pressure by 59 ± 5 from 130 ± 4 mm Hg, heart rate by 36 ± 5 beats/min from 69 ± 3 beats/min, and cardiac output by 458 ± 103 from 2,711 ± 239 ml/min. By 4 weeks after renal wrapping, heart rate and mean arterial pressure responses to BCO were approaching baseline levels. After β-adrenergic receptor blockade, responses to BCO of mean arterial pressure, cardiac output, and heart rate were no longer significantly enhanced during the development of hypertension. Thus, in conscious dogs, reflex pressor responses to baroreceptor unloading via BCO were enhanced during the development of hypertension but no longer present 3 weeks later. The augmented mean arterial pressor responses to BCO were mediated by increases in cardiac output and heart rate, which in turn, appeared to be controlled by β-adrenergic receptor mechanisms. (Circulation Research 1987;61:678-686)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The fundamental natural frequency of the closed cusps of porcine bioprosthetic valves, fabricated from the normal leaflets of pig aortic valves, was estimated using a finite element model. Both normal and stiffened leaflets were considered in the vibrational analysis. The effects of conditions that simulated degeneration, such as stiffening, central perforation, a tear, calcium deposits in the commissural attachments, and combinations of these were determined. The primary frequency of vibration of the normal leaflets was within the range of the dominant frequency of the heart sounds determined clinically by spectral analysis of the recorded phonocardiogram. If only one leaflet was stiffened or calcified, there was only a marginal change of frequency. With stiffening and calcification of the commissures of all 3 leaflets, the frequency of vibration increased. Introduction of a tear in a single leaflet of a stiffened and calcified valve markedly reduced the fundamental frequency. In view of the relation between the frequency content of heart sounds and the frequency of valve vibration, this mathematical simulation establishes a possible basis for the observation of a varying dominant frequency of heart sounds in patients with bioprosthetic valves that are in the process of degenerating. (Circulation Research 1987;61:687-694)

ISSN:0009-7330    

出版商:OVID    

年代:1987

数据来源: OVID