ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Cardiac hypertrophy is associated with a decrease in coronary reserve. However, factors which may modulate the interaction between myocardial growth and vascular proliferation, such as duration and severity of hypertrophy, have not been evaluated. We measured myocardial perfusion with microspheres in conscious, chronically instrumented Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats at 3, 7, and 15 months of age; and in SHR stroke-prone (SHR-SP) rats at 13–14 months of age. Myocardial perfusion was measured with microspheres in awake rats at rest and during maximal coronary dilation produced by dipyridamole infusion (2.0 mg/kg per min, iv). Arterial pressure was significantly elevated (P< 0.05) in all hypertensive groups (vs. age-matched WKY), both at rest and during dipyridamole infusion. Left ventricular mass in the SHR rats was increased significantly (P< 0.05) by 14%, 28%, and 29% at 3, 7, and 15 months, respectively. Left ventricular mass in the SHR-SP group was increased by 50% (P S 0.05) compared to the 15-month-old WKY. Left ventricular minimal coronary vascular resistance (per gram) was significantly greater (P< 0.05) in SHR at 7 months, and in the SHR-SP group (66% and 60%, respectively). Right ventricular minimal coronary vascular resistance was significantly greater (P< 0.05) in SHR at 7 and 15 months (50%), and in the SHR-SP group (122%), compared to 15-monthold WKY. The results indicate the following: (1) the increase in minimal coronary vascular resistance between SHR and WKY rats was greatest when left ventricular hypertrophy peaked (7 months) and was no longer present after left ventricular hypertrophy had stablized. (2) In 14-month-old SHR-SP rats, with more severe left ventricular hypertrophy and hypertension, minimal coronary vascular resistance was considerably higher than in SHR of approximately the same age. (3) Long-term arterial hypertension was associated with a higher right ventricular minimal coronary vascular resistance. Resistance appeared to change in proportion to the severity of hypertension, and the changes were independent of the presence of right ventricular hypertrophy.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The thoracic aorta of 21-, 28-, 35-, and 45-day-old spontaneously hypertensive (SH) and Wistar Kyoto (WK) rats was analyzed morphometrically to evaluate the cellular hypertrophy and proliferation of medial smooth muscle cells during the development of genetically determined hypertension. The absolute increase in volume of collagen and ground substance, and elastic tissue was also measured. In SH animals, cellular hypertrophy was found to be the dominant mechanism of muscle growth in the 21- to 28-day and 35- to 45-day intervals, resulting in an overall 68% enlargement of the mean cell volume from 21 to 45 days. The total number of smooth muscle cells increased only 21% (not statistically significant) and the tendency toward hyperplasia was restricted to the 28- to 35-day period. Normotensive controls showed cell proliferation mainly from 21 to 28 days and cellular hypertrophy from 35 to 45 days with an absolute 33% increase in the number of cells and a 26% larger volume of the mean smooth muscle cell at 45 days of age. From 21 to 45 days, the above changes in cell size and number provoked an overall 104% and 67% growth of the muscle mass in SH and WK rats, respectively. The initial response phase of spontaneous hypertension was also characterized by an increase of collagen and ground substance, 184%, which was slightly greater than that of the elastic component, 168%. Changes in mural concentration of fibrous proteins that were similar to but of less magnitude than those of controls, were seen. These results demonstrate that short-term spontaneous hypertension determines a simultaneous growth adaptation in every component structure of the media of the thoracic aorta leading to a disproportionate accumulation of scleroproteins that markedly exceeds that of the contractile component of the vessel wall. At a cellular level, smooth muscle cell hypertrophy is the prevailing process that underlies the tissue response of the aorta in early hypertension.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Lysophosphoglycerides including lysophosphatidyl choline (LPC), accumulate in ischemic myocardium, and in comparable concentrations induce electrophysiological alterations in vitro analogous to those seen in ischemic myocardium in vivo. The present study was performed to assess the amount of 14C-LPC incorporated into isolated tissue required to induce electrophysiological effects, to localize the sites of incorporation by electron microscopic autoradiography, and to assess the association between electrophysiological recovery and metabolism of incorporated LPC. “C-LPC (200 /J.M)” induced marked electrophysiological effects in Purkinje fibers when only 2.3% of cellular phospholipid was supplanted by exogenous LPC. Electrophysiological depression correlated with incorporation of LPC, and electrophysiological recovery correlated with metabolism of LPC to free fatty acid and phosphatidyl choline. Incubation of ventricular muscle strips with 14C-LPC (100;UM) resulted in incorporation of 0.42 nmol/mg protein of exogenous LPC at pH 7.4. Incorporation was similar at pH = 6.7 (0.36 nmol/mg protein), although electrophysiological derangements were markedly enhanced. Electron microscopic autoradiography showed that incorporated LPC was localized primarily to the sarcolemmal membrane. These findings indicate that incorporation of as little LPC as 1% of cellular phospholipid induces marked electrophysiological changes, that LPC rather than its major metabolites, fatty acid and phosphatidyl choline, are responsible for the electrophysiological alterations, and that reduction in pH enhances the membrane effects of LPC without increasing incorporation.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

A series of experiments was carried out to determine the effects of load variation on the character of stepwise shortening. We imposed afterloaded isotonic contractions on rat ventricular trabeculae, and measured the effect of load on pause duration, i.e., on the duration of the periods during which there was no sarcomere shortening. Sarcomere lengths were measured by optical diffraction. Increases of load brought about increases of pause duration; the relation was linear. The relation did not appear to depend on time during contraction, but did depend on sarcomere length: for a given load, pauses were longer at shorter sarcomere lengths. In a supplementary protocol in which we measured the dynamics of the central segment of the muscle during muscle isometric contraction, we found that the velocity of sarcomere shortening during the shortening step was approximately independent of load. These results provide a framework for interpretation of muscle force-velocity relations: diminished velocity at high loads may be the result of increased pause durations.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Autoregulatory responses to alterations in arterial or venous perfusion pressure were determined for individual arterioles within the rat cremaster muscle. The cremaster muscle of pentobarbital anesthetized rats (50 mg/kg, ip) was surgically exposed and maintained in a controlled tissue bath for visualization by in vivo television microscopy. Cremaster bath Poj was controlled at either a high (approximately 70 mm Hg) or low (approximately 18 mm Hg) level. Inside diameter and red blood cell velocity were measured for individual first (1A), second (2A), or third (3A) branching order arterioles, and instantaneous blood flows within each arteriole were calculated. To measure the autoregulatory responses, we decreased arterial perfusion pressure to the microvascular bed by gradually occluding the sacral aorta. Significant autoregulation was observed in all orders of vessels, but, in general, autoregulation was more pronounced at all vessel levels when bath Po-j was low, and the autoregulatory gain was greater for the smaller vessels compared to the larger vessels. Elevation of venous pressure within the vascular bed by gradual occlusion of the inferior vena cava led to a significant vasoconstriction of the smaller vessels, suggesting that a significant myogenic component was present. The vasoconstriction response to elevated venous pressure was more pronounced when bath P02 was high. Our data are not consistent with a purely myogenic or purely metabolic mechanism, but suggest that both mechanisms are simultaneously contributing to the local vascular regulation.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

We examined, in conscious dogs, the effects of β-adrenergic stimulation on measurements of left circumflex coronary arterial diameter and blood flow and on calculations of late diastolic coronary resistance (LDCR) and left circumflex coronary internal cross-sectional area (CSA). Isoproterenol (0.1 fig/kg) initially decreased mean arterial pressure by 25 % 2% (mean % SEM), and LDCR by 62 % 4%, and increased heart rate by 82 % 10%, left ventricular (LV) dP/dt by 79 % 12%, and mean coronary blood flow by 85 % 5%, while CSA rose slightly. The peak effects on CSA (24 % 2%) occurred later, along with decreases in mean arterial pressure (7.4 % 1.0%) and LDCR (25 % 5.3%) and increases in coronary blood flow (14 % 2%), LV dP/dt (12 % 3%), and heart rate (24 % 4%). Pirbuterol (1.0 jug/kg) induced changes that were qualitatively similar to those induced by isoproterenol. Prenalterol (20 /xg/kg), a cardioselective β1-adrenergic receptor agonist, did not affect mean arterial pressure, but increased heart rate by 40 % 5%, LV dP/dt by 72 % 10%, mean coronary blood flow by 34 % 11%, and CSA by 26 % 3%, and decreased LDCR by 29 % 5%. Isoproterenol and pirbuterol, but not prenalterol, increased coronary sinus Oj content and decreased A-V O > difference. After β1-adrenergic receptor blockade with atenolol (1 mg/kg), prenalterol no longer induced significant effects, whereas isoproterenol and pirbuterol decreased mean arterial pressure similarly to what was observed prior to blockade, but did not increase LV dP/dt, and induced attenuated increases in mean coronary blood flow, CSA, and decreases in LDCR. Thus, in the intact, conscious animal, large coronary arteries are regulated by β-adrenergic mechanisms. Surprisingly, a major fraction of large coronary arterial dilation appeared to be either directly or indirectly due to β-adrenergic receptor mechanisms, although β2-adrenergic effects were also significant.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The renal vascular effects of prostaglandin Ej (PGEj), 6-keto-PCE, and PGL were investigated in indomethacin-pretreated rats. These prostanoids were infused directly into the left renal artery at rates ranging from 0.01 to 1.0 /ig/min, while renal blood flow and mean arterial blood pressure were constantly monitored. PGE, 6-keto-PCEi, and PGIj produced reductions in mean arterial blood pressure with threshold doses of 1.0, 0.3, and 0.03;ig/min (P< 0.01), respectively, and maximal vasodepressor responses of 18.9 % 4.3, 37.0 % 7.8, and 58.7 % 8.2 mm Hg (P< 0.01), respectively. In addition, all three prostanoids caused a dose-related reduction in renal vascular resistance with a threshold dose of 0.01 /xg/min (P< 0.05). The maximal reductions in renal vascular resistance were 2.59 % 0.52, 4.41 % 1.20, and 5.29 % 1.06 mm Hg/(ml per min) for PGEj, 6-keto- PGEi, and PGI2 (P< 0.01), respectively. Whereas PGE2 and 6-keto-PGEi produced dose-dependent increases in renal blood flow (maximal increases of 1.5 % 0.3 and 1.0 % 0.3 ml/min, respectively (P< 0.01), PGI2 nonsignificantly increased renal blood flow at low doses and decreased renal blood flow at higher infusion rates (P< 0.01). These data indicate that the in vivo rat kidney, similar to the kidneys of other species, is vasodilated by low doses of PGE2, PGI2, and 6-keto-PGEi.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The influence of environmental heat stress on the arterial baroreflex control of heart rate (HR) was studied in eight conscious, chronically instrumented baboons. Inflations of balloon occluders around the inferior vena cava (IVC) and thoracic descending aorta (DA) were used to produce acute, graded changes in mean arterial blood pressure (MABP) in 5 mm Hg intervals ranging from ±5 to ±25 mm Hg. After determination of the HR responses to changes in MABP in the normothermic baboon (blood temperature ≤37.6°C), the animal was subjected to environmental heating to produce hyperthermia. When blood temperature reached approximately 39.5°C, HR responses to graded DA and IVC occlusions were again determined. During hyperthermia, the HR sensitivity (AHR/AMABP) to MABP changes was markedly diminished for reductions in MABP and significantly enhanced for increases in MABP. To determine whether these alterations in the HR response to changes in MABP were due to an alteration of the baroreflex control of HR, full, sigmoid-shaped HR-MABP curves for both the normothermic and hyperthermic states were constructed and characterized by total HR range, estimated slope of the steep portion of the curve, and MABP at the midpoint of the HR range (BP50). During hyperthermia (1) the whole HR-MABP curve shifted significantly upward by 35–40 beats/min, (2) total HR range, the estimated slope, and BP50did not change, and (3) the control point (pre-occlusion HR-MABP value) shifted upward along the steep portion of the HR-MABP curve. In six of the eight baboons, full HR-MABP curves were also constructed during either β-adrenergic blockade or cholinergic (Ch)-receptor blockade in the normothermic and hyperthermic state. Similar to that seen for the unblocked heart, the whole HRMABP curves were also shifted upward during hyperthermia in this group of baboons with no alteration in the total HR range, the estimated slope, or BP50. The upward shift in the HR-MABP curve during Ch-receptor blockade, unlike during β-receptor blockade, was much greater than that which could be attributed only to the local effect of blood temperature. Although the control point was also shifted upward along the steep portion of the curve during β- or Ch-receptor blockade, the upward shift observed during β-adrenergic blockade was similar to that observed in the unblocked state. Thus, a heat stress-induced hyperthermia produces a rise in HR without significantly altering the characteristics of the reflex control of HR by arterial baroreceptors. To rely solely on changes in HR sensitivity may lead to erroneous conclusions as to the effect of a particular stress on the baroreceptor reflex control of HR. Further, these results indicate that: (1) the upward shift in the HR-MABP curve is mediated by both the local effect of blood temperature on HR and cardiac sympathetic efferent neurons which are independent of the baroreceptor reflex, and (2) the upward shift in the control point is mediated predominantly by vagal withdrawal, probably as part of the compensatory response to a heat-induced hypotension.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Bradykinin stimulates afferent fibers arising in the heart and may be involved in the mediation of anginal pain and the pain associated with myocardial infarction. The sensation of pain requires that noxious information reach the brain. The purpose of the present study was to determine whether the spinothalamic tract is involved in transmitting noxious information from the heart to the brain. Bradykinin was injected (0.3–3.5 μg/kg) into the heart via a catheter in the left atrium while we recorded from single spinothalamic cells in the Cg to T5 spinal segments. Thirty-one of 41 cells responded to bradykinin. The responses of 12 cells were characterized by both an increase in discharge rate and entrairrment of cell activity with the cardiac cycle. Eighteen cells responded with only an increased rate, and one cell exhibited only entrainment of cell activity with the cardiac cycle. The mean onset of increased cell activity occurred 15 seconds following drug injection, and the average duration of the response was 54 seconds. Thirty cells increased their mean discharge rate from 11 % 2.5 to 29 % 4.4 spikes/second. Thus, some spinothalamic cells probably received input from both mechanosensitive and chemosensitive afferents. Tachyphylaxis to repeated doses of bradykinin was observed in 41% of cells. Cells responding to bradykinin had a spontaneous discharge rate that was significantly greater than that of nonresponding cells. Cells did not require input from C-fiber afferents to respond to bradykinin. No statistically significant relationships were found among anatomical locations (laminae and segments) and responses to bradykinin, although cells in lamina I seemed to be less responsive than more ventrally located cells. We conclude that the spinothalamic tract may be involved in the sensation of cardiac pain.

ISSN:0009-7330    

出版商:OVID    

年代:1982

数据来源: OVID