ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

We studied steady state transvascular fluid and protein exchange after uneven obstruction of the pulmonary arteries. In anesthetized sheep, ventilated by positive pressure, we measured pulmonary artery and left atrial pressures, cardiac output, lung lymph flow, and lymph/plasma protein ratios. We calculated pulmonary vascular resistance. In 16 sheep we obstructed the pulmonary arteries with various microemboli or balloons in lobar arteries until pulmonary vascular resistance was 2-3 times baseline. In every experiment, lung lymph flow increased as pulmonary vascular resistance increased. The lymph/plasma protein ratio did not change. In four sheep, we increased left atrial pressure by balloon obstruction of the mitral orifice. Pulmonary artery pressure increased as much as in the embolization experiments and lymph flow increased but the lymph/plasma protein ratio decreased, meaning that the increased fluid and protein flux after embolization cannot be due to high pulmonary artery or pulmonary venous outflow pressures alone. In four sheep we compared obstruction of the lower lobe pulmonary arteries by balloons with that of upper lobe pulmonary arteries. Lower lobe arterial obstruction caused the lymph flow which drains predominantly from the lower lobes to decrease whereas upper lobe artery obstruction increased lymph flow. This means that the increased fluid and protein flux occurred mainly in the open, perfused portion of the microvascular bed. The mechanism of the increased fluid filtration and protein permeability may be related to high vascular pressure and high linear blood flow velocity through a markedly restricted microvascular bed, although release of substances that affect endothelial permeability is not ruled out.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Because creatine kinase (CK) appears in cardiac lymph after myocardial infarction, this study was undertaken to determine whether lymph inactivates CK in vitro and whether interruption of cardiac lymph flow influences estimation of infarct size based on plasma CK changes in conscious dogs. After the effects of incubation of canine myocardial CK in native, deproteinized, or sulfhydrylfortified lymph and dialysates had been characterized; effects of interruption of cardiac lymph flow on plasma CK time-activity curves after coronary occlusion were assessed in 13 conscious dogs, seven of which had exteriorized occlusive snares around cardiac lymphatics as well as the left anterior descending coronary artery. Native and deproteinized lymph as well as lymph dialysate markedly inactivated CK in vitro with associated nonenzymatically mediated proteolysis detectable on SDS gels. CK released into blood after coronary occlusion compared to myocardial CK depletion was 50% less in dogs with lymphatic occlusion (P<0.01) although CK loss in the centers of infarcts (73% and 69%) and overall CK depletion (18% and 20%) were similar in the two groups. Based on comparison of observed to projected plasma CK values prior to lymphatic occlusion, significantly less CK appeared in blood when coronary occlusion was followed by lymphatic occlusion (P<0.01), although the rate of disappearance of CK from the systemic circulation was not altered. Thus, lymph inactivates CK in vitro, and plasma CK time-activity curves after coronary occlusion are influenced considerably by interruption of cardiac lymph flow, a factor that should be incorporated to refine enzymatic estimates of infarct size.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

We studied the control of arterial pressure by the carotid sinus baroreceptors in 35 hypertensive humans, using a variable pressure neck chamber to alter carotid sinus transmural pressure in a graded fashion. The results were compared with those obtained from 11 normotensives. As in normotensives, reduction in carotid transmural pressure caused a linearly related pressor response and vice versa. However, whereas in normotensives the pressure response was greater than the depressor, the reverse was the case in hypertensives. Furthermore, the pressor response decreased and the depressor response increased progressively with an increase in severity of the hypertension. Thus while in normotensives the carotid baroreflex is more effective in protecting against hypotension, in hypertensives the antihypertensive function of the reflex is favored. Similar differences between hypertensives and normotensives were found with respect to the carotid baroreceptor control of heart rate. In eight hypertensives, reflex changes in heart rate also were studied by injection of phenylephrine and trinitroglycerine to vary not only carotid baroreceptor activity, but also activity of extracarotid baroreceptors. The results were compared with results of similar studies on eight normotensives. These comparisons suggest that, whereas the carotid baroreceptor reflex remains active in hypertension, reflexes stemming from extracarotid baroreceptor areas are much diminished.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Recent studies of cardiac and skeletal muscle suggest that the sites at which Mn2+uncouples excitation and contraction are restricted to a space functionally equivalent to the interstitium. We sought to corroborate this hypothesis by using the ferrocyanide anion, Fe(CN)6−4. This anion is relatively innocuous to myocardial tissue, is compatible with solutions containing alkaline and alkaline earth cations, but immediately precipitates when combined with cations of the transitionelement series, particularly Mn2+. The finding of interest is that heart tissue pretreated with 20 nut Na4Fe(CN)6is “protected” from the normal action of Mn2+, the uncoupling of excitation and contraction. This finding would be expected if Fe(CN)64∼could precipitate Mn2+influx in one or several compartments. Protection was not a function of the duration of the pretreatment as long as an interval of several minutes was allowed. However, protection markedly declined as a function of the interval following the cessation of Fe(CN)64∼treatment and preceding the addition of Mn2+. Quantified in this way using thin-diameter papillary and trabecular muscles from rabbits, protection was found to be approximately monoexponential and most likely confined to a single, rapidly effluxing compartment, the interstitium. Studies were conducted using the perfused rabbit septum to divulge the washout kinetics of 54Mn2+and [14C]Na4Fe(CN)6. Analyses of these washouts suggest that Mn2Fe(CN)6precipitated in the interstitium not because this was the only compartment reached by both agents but because this was the space in which Mn2+ exerted its uncoupling action.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Previous studies showed that pyruvate with Tris buffer improves mechanical and metabolic functions of globally ischemic swine hearts. The purpose of the present study was to evaluate their effects during short periods of moderate regional ischemia. Studies were conducted on 21 swine hearts during maintenance of control flow to the anterior descending (LAD) and circumflex (LCf) coronary arteries and through 15 minutes of LAD ischemia (flow reduced from 47.1-19.0 ml/min). Pyruvate at control coronary flows increased systolic and total shortening at the apex (0.24-0.36 mm,P<0.01, and 0.34-0.47 mm,P<0.025, respectively) and increased oxygen extraction (O2EXT) and consumption (MVO2) across both beds (LAD: O2EXT 36.5-48.6%, P<0.005; MVO2 106.1-130.7 /imol/min, P<0.05; LCf: O2EXT 31.6-43.8%,P<0.005; MVO2125.3-159.3 /imol/min, P<0.025). Pyruvate during LAD ischemia, as compared with untreated myocardium, increased diastolic and total shortening at the apex (0.21-0.25 mm,P<0.05, and 0.18-0.31 mm,P<0.05, respectively) and increased global contractility (left ventricular max dp/dt from 2726-3220 mm Hg/sec, P<0.05). O2EXT and MVO2were not further increased in the LAD bed, but glucose utilization, as estimated from the release of 3H2O from glucose[2-3H] infusions, was accelerated (3.93-6.05 /imol/min,P<0.01). O2EXT and MVO2in the LCf circuit during LAD ischemia were significantly increased (42.4-52.7%,P<0.05, and 169.4-189.7 /imol/min,P<0.05, respectively). The increases in mechanical function persisted in treated hearts during the immediate postischemic period at 1 and 5 minutes of reflow. Thus, buffered pyruvate effected significant improvements in regional motion both at control and ischemic coronary flows in working swine hearts and was associated with increases both in aerobic and anaerobic metabolism.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

The interaction of carotid chemoreceptor and pulmonary inflation reflex control of vascular responses in the mesenteric, renal, and iliac beds was examined in conscious dogs by comparing responses to chemoreceptor stimulation (intracarotid injection of nicotine or cyanide) during spontaneous and controlled respiration. A biphasic response was evoked which was characterized by an initial bradycardia, an increase in mean arterial pressure, and a marked increase in resistance in the iliac [102 ± 17% (mean ± SE)] as compared with the mesenteric (16 ± 3%) and renal (9 ± 2%) beds. After the chemoreceptor-induced increases in ventilation, there was a later phase characterized by tachycardia, a decrease in mean arterial pressure, and a striking decrease in resistance in the iliac (—51 ± 2%) as compared with the mesenteric (—3 ± 4%) and renal (-11 ± 3%) beds. Alphablockade with phentolamine nearly abolished the early vasoconstriction and later vasodilation. When the chemoreceptor induced increase in respiration was prevented, or after bilateral vagotomy, there was significantly more (P<0.01) vasoconstriction in all three beds and no later vasodilation. After mechanical hyperinflation of the lungs, a striking decrease in resistance was observed in the iliac (—56 ± 3%) as compared with the mesenteric (—17 ± 5%) and renal (—6 ± 6%) beds; these responses were not observed after alpha blockade or after vagotomy. Responses to carotid chemoreceptor stimulation were not observed after carotid sinus nerve section. Thus, carotid chemoreceptor stimulation in conscious dogs with spontaneous respiration results in a biphasic vascular response. Pulmonary inflation reflexes attenuate the initial vasoconstrictor response to carotid chemoreceptor stimulation and are responsible for the later period of vasodilation.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

We used the estrogen-treated cockerel as a model to study the regulation of very low density lipoproteins (VLDL) at the molecular level. A single injection of estrogen induced marked elevation of plasma VLDL in the cockerel. Messenger RNA (mRNA) activity for a major VLDL apoprotein (apoVLDLII) in hepatic polyribosomes was assayed in vitro, and increased at the same rate as plasma VLDL levels. Simultaneous determinations of mRNA activities for albumin and apoA-I (a major HDL apoprotein) showed that these were unchanged. Specific estrogen-binding sites were measured in the liver cell nuclei and a single class of sites with a Kd of 2 × 10−9M was observed. The number of such sites increased after estrogen treatment prior to any detectable increase in plasma VLDL. Simultaneously, RNA polymerase I and II activities were markedly stimulated by the hormone. ApoVLDLIImRNA was purified to apparent homogeneity by (1) total nucleic acid extraction, (2) zonal ultracentrifugation, (3) Sepharose 4B chromatography in EDTA, (4) Sepharose 6B chromatography, (5) Sepharose 4B chromatography in MgCU, and (6) sucrose gradient centrifugation. The in vitro translation product of apoVLDLIImRNA was about 12 amino acids larger than apoVLDLn isolated from the blood. The identification of such a product (designated pre-apoVLDLn) is compatible with Blobel's hypothesis that, like other secretory proteins, VLDLIIis synthesized initially as a larger protein and the JV-terminal sequence is cleaved prior to completion of synthesis and secretion of the VLDL particle.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

In isolated rat atria, endogenous neurotransmitters were released by electrical pulses that were below threshold for activation of the myocardial cells. A brief train of pulses was delivered at a specified time after each atrial activation to determine the relationship between the time of stimulus delivery during an atrial cycle (P-St interval) and the subsequent cardiac cycle length (P-P interval). These stimuli caused a change in P-P interval from a mean control level of 291 msec to a mean maximum P-P interval of 592 msec. This change was attributed to the release of neurotransmitters from sympathetic and parasympathetic fibers, but the effects from the parasympathetic nerve terminals predominated. Increasing the number of pulses per burst increased the atrial slowing. The extent of slowing was dependent on the time of stimulus delivery in an atrial cycle. The region of minimal effectiveness (mean P-P interval of 412 msec during stimulation) was obtained with P-St intervals that were only slightly greater (about 10 msec) than those that were maximally effective. Stimuli delivered at times in the cardiac cycle that fell between the P-St intervals that elicited maximum and minimum changes in heart rate occasionally caused profound irregularities in heart rate. These changes in cycle length do not appear to be due to pacemaker shifts, but are probably the result of the interaction between acetylcholine and the sinoatrial nodal cell membrane. The responsiveness of this membrane to acetylcholine changes with time during the cardiac cycle.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

In isolated rat spleen perfused with Tyrode's solution, prostaglandin (PG) E1and E2, 0.2-2.5 ng/ml, reduced the vasoconstrictor responses to sympathetic nerve stimulation by 38-89% and 35-73% and to injected norepinephrine by 18-53% and 18-34%, respectively. In contrast, PGF2αand thromboxane B2 (TXB2) produced vasoconstriction and potentiated the vascular responses to both adrenergic stimuli, whereas PGD2 had variable effects. Stimulation of adrenergic nerves or an injection of norepinephrine enhanced the efflux of a PGE-like substance from the rat spleen. Administration of a PG synthetase inhibitor, indomethacin, 100 ng/ml, abolished the efflux of PGE evoked by adrenergic stimuli and potentiated the vasoconstrictor responses to nerve stimulation and to injected norepinephrine. The facilitatory effect of indomethacin on the vasoconstrictor responses to both adrenergic stimuli was abolished by the infusion of PGE2.A PG precursor, arachidonic acid, inhibited the vasoconstrictor responses to nerve stimulation and to injected norepinephrine. Because the inhibitory effect of arachidonic acid was abolished by the administration of indomethacin, it appears to be mediated, at least in part, through the conversion of the acid to a PG(s). These observations and the effect of exogenous PGE compounds suggest that PGs of the E series participate in the modulation of the vascular responses of the rat spleen to adrenergic stimuli. However, the modulatory effect of PGE compounds varies in different vascular beds of rat, viz, facilitatory in renal and mesenteric vasculature and inhibitory in the splenic vasculature. This study also indicates that other products of arachidonic acid metabolism, including PGF2O and TxB2, also may contribute to the modulation of vascular responses to adrenergic stimuli and affect the actions of PGE2at the adrenergic neuroeffector junction in the rat spleen.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID