Relationships between voltage and tension in sheep cardiac Purkinje fibers

The two-microelectrode technique of voltage clamping sheep cardiac Purkinje fibers was used to examine the changes in contraction which occur during trains of voltage clamps. (A "train" is defined as a series of voltage clamps delivered at a particular rate, beginning after a rest long enough that the effects of previous stimulation have died away.) Contractions showed striking staircases, or progressive changes in peak isometric tension, during trains. Short clamps, clamps to voltages more negative than --20 or --30 mV, or holding potentials less negative than the resting potential favored negative staircases, while long clamps, clamps to positive voltages, and holding potentials near the resting potential each favored positive staircases. The staircase behavior appeared to be due to changes in the initial rate of recovery of the ability to contract. The changes in staircase behavior as a function of clamp voltage suggested that the relationship between peak tension and clamp voltage should depend on the experimental design. When the steady-state contraction was plotted as a function of clamp voltage, voltage-tension relations like those recently reported for working ventricle were obtained, with a threshold between --30 and - -40 mV and a steep relation between tension and voltage. When the first contraction after a rest was plotted, the threshold voltage was more negative, the curve was flatter, and the peak tensions at inside positive voltages were reduced.     

Relationship between oxygen tension, coronary vasodilation and prostaglandin biosynthesis in the isolated rabbit heart

In isolated perfused rabbit hearts, coronary vasodilation, produced by reduced oxygen tension seems to be independent of myocardial prostaglandin biosynthesis. a) Anoxia (N₂: CO₂ 95: 5%) produced coronary vasodilation without causing prostaglandin-like substance (PLS) biosynthesis and release; b) the decrease in coronary resistance during hypoxia (N₂:O₂:CO₂ — 80:15:5 %) was sustained during myocardial perfusion with the low oxygen media despite the transitory nature of its PLS release; and c) indomethacin, which abolished basal or ADP stimulated myocardial PLS release, did not abolish the coronary vasodilation produced by ischemia, hypoxia, or anoxia.     

Neuropeptide Y modulates the action of vasodilator agents in guinea-pig epicardial coronary arteries

Recently, we have demonstrated that guinea-pig epicardial coronary arteries are supplied by numerous nerve fibres containing neuropeptide Y (NPY) immunoreactivity. However, examination of vasomotor responses revealed that NPY did not elicit a contractile response in these arteries. In contrast, acetylcholine (ACh), calcitonin gene-related peptide (CGRP), substance P and vasoactive intestinal polypeptide (VIP) all relaxed precontracted arteries. In the present study, we have used histochemical, immunohistochemical and in vitro pharmacological techniques, in order to further investigate the possible role of NPY in guinea-pig epicardial coronary arteries. A double-immunofluorescence staining technique revealed that CGRP and substance P were co-localized in nerve fibres distinct from those displaying NPY immunoreactivity. Furthermore, using a method combining immunofluorescence and histochemical techniques, we observed that putative cholinergic nerve fibres (identified by their acetylcholinesterase content) and NPY-immunoreactive nerve fibres are two different nerve populations. An in vitro pharmacological method demonstrated that NPY markedly inhibited the relaxant responses mediated by ACh, VIP, substance P and isoprenaline but had no effect on CGRP. These results suggest that NPY-containing nerves associated with guinea-pig epicardial coronary arteries may be predominantly involved in modulating the action of vasodilator agents.     

Relationships between embolism,stem water tension,and diameter changes

A model for embolism in the sapflow process was developed, in which embolism is described as a physical process linked to real physical properties of the conduits and the thermodynamic state of water. Different mechanisms leading to embolism and their effect on water relations and especially diurnal diameter changes in a tree were examined. The mechanisms of heterogeneous nucleation, air-seeding, and bubble growth have been considered. The significance of embolism has been revealed here by examining diameter changes, which is an easily measurable quantity under field conditions. The most fundamental effects of embolism on sapflow are decrease in permeability and release of water from embolizing conduits to the transpiration stream. These can be indirectly detected by observing diameter changes. If possible changes in elasticity are not accounted for, embolism generally tends to enhance the amplitude of the diurnal diameter changes due to reduced permeability and increased tensions. In the case of reduced elasticity, embolism gives rise to smaller amplitudes of diameter changes.     

短时间高温处理下桃树活性氧代谢与桃芽自然休眠解除的关系

以6年生曙光油桃为试验材料,研究40 ℃、45 ℃、50 ℃ 3个梯度高温短时间处理对桃树花芽和叶芽存活率、萌芽级数、活性氧含量及其相关酶活性的影响,探讨短时间高温处理对桃芽自然休眠解除的调控效应.结果表明：随着短时间高温处理时期的延后以及处理温度的升高和处理持续时间的延长,高温处理对桃芽自然休眠的解除作用增强.11月30日处理中,40 ℃处理对桃芽自然休眠的解除具有负调控效应,其萌芽级数、·OH和 O₂^-.产生速率、H₂O₂含量、过氧化物酶（POD）和过氧化氢酶（CAT）活性均低于对照,而超氧化物歧化酶（SOD）活性高于对照;45 ℃和50 ℃处理对桃芽自然休眠的解除呈正调控效应,其萌芽级数、·OH和 O₂^-·产生速率、H₂O₂含量及POD、CAT活性与对照相比明显升高,而SOD活性显著降低.12月10日处理中,40 ℃处理对桃芽自然休眠解除的调控效应不明显,45 ℃和50 ℃处理与11月30日处理相同,但前者对桃芽自然休眠的调控效果优于后者.相关分析表明,活性氧的迅速增加可能是高温解除桃芽自然休眠的原因.     

Relationships between burn size,immunosuppression, and macrophage hyperactivity in a murine model of thermal injury

Burn injury induces immune dysfunction and alters numerous physiological parameters. While clinical studies indicate that burn injury size profoundly impacts patient immune status, only limited experimental studies have systematically addressed its impact on immune functional parameters. In the present study, mice were subjected to burn injuries of varying sizes and splenic immune cells (splenocytes and macrophages) were isolated 7 days thereafter. Burn injury suppressed splenic T-cell proliferation in an injury size-dependent manner that correlated with the release of the immunosuppressive mediators PGE(2) and nitric oxide. In addition, a shift towards an immunosuppressive Th-2 cytokine profile and a hyperactive macrophage phenotype (increased release of inflammatory mediators) was observed post-injury, however, this effect was in part independent of burn size. Thus, unlike patient survival data, burn injury-induced changes in immune function do not necessarily correlate with the size of the injury.     

The autoregulation of intracellular oxygen tension and the modification of cellular radiosensitivity. The development of an adaptation hypothesis

A hypothesis is reported postulating that the range within which the intracellular oxygen content varies with changes in the external oxygenation conditions is responsible for the oxygen-dependent radiosensitivity modification that may be controlled by the diffusion resistance of a cytoplasmic membrane. The adaptation mechanism of intracellular Po2 autoregulation is involved when drastic changes in the oxygen content of the environment occur. As the oxygen content decreases this mechanism provides maximal values of the intracellular Po2 required for optimizing cell viability; the increased oxygen content prevents cells from oxygen intoxication.     

Relationship between cytosolic calcium and oxygen consumption in isolated rat hearts.

Maximum oxygen consumption was attained in isolated perfused rat hearts using high perfusate calcium and/or isoproterenol, or phenylephrine. The amplitude of calcium transients was directly related to oxygen consumption until oxygen consumed per beat reached maximum. At saturating oxygen consumption the amplitude of [Ca2+]i transients continued to increase, indicative of a calcium overload. In all cases +dP/dt correlated proportionately with +dCa2+/dt. Augmented developed pressure, related to isoproterenol-induced increase in cytosolic cAMP, cannot be attributed totally to elevated levels of [Ca2+]i transients. Adenosine (10(-5) M) added to the medium containing isoproterenol (10(-6) M) negated the isoproterenol-induced increase in cAMP and returned cardiac performance, oxygen consumption, and amplitude of [Ca2+]i transients to control state.     

Metabolic consequences of positive inotropy in rat and guinea-pig hearts

The metabolic and physiological responses of hearts from male rats and guinea-pigs to isoprenaline and SK&F 94120 (a phosphodiesterase III inhibitor), have been studied. Doses which gave similar chronotropic stimulation gave different inotropic responses. In both species, isoprenaline generated a greater increase in developed tension than SK&F 94120. With both drugs the inotropic response in the rat was less than than in the guinea-pig. 31P-NMR investigation of high-energy phosphate levels showed reduction in PCr concentration and an accompanying acidosis in the isoprenaline-perfused rat heart only. In both species, lactate production was stimulated by SK&F 94120 but not by isoprenaline. These results are discussed with reference to G-protein activation of ion channels and differences in Ca2+ handling by the two species.     

Relationships between regional myocardial wall stress and bioenergetics in hearts with left ventricular hypertrophy

This study utilized porcine models of postinfarction left ventricular (LV) remodeling [myocardial infarction (MI); n = 8] and concentric LV hypertrophy secondary to aortic banding (AoB; n = 8) to examine the relationships between regional myocardial contractile function (tagged MRI), wall stress (MRI and LV pressure), and bioenergetics ((31)P-magnetic resonance spectroscopy). Physiological assessments were conducted at a 4-wk time point after MI or AoB surgery. Comparisons were made with size-matched normal animals (normal; n = 8). Both MI and AoB instigated significant LV hypertrophy. Ejection fraction was not significantly altered in the AoB group, but significantly decreased in the MI group (P < 0.01 vs. normal and AoB). Systolic and diastolic wall stresses were approximately two times greater than normal in the infarct region and border zone. Wall stress in the AoB group was not significantly different from that in normal hearts. The infarct border zone demonstrated profound bioenergetic abnormalities, especially in the subendocardium, where the ratio of PCr/ATP decreased from 1.98 +/- 0.16 (normal) to 1.06 +/- 0.30 (MI; P < 0.01). The systolic radial thickening fraction and the circumferential shortening fraction in the anterior wall were severely reduced (MI, P < 0.01 vs. normal). The radial thickening fraction and circumferential shortening fraction in the AoB group were not significantly different from normal. The severely elevated wall stress in the infarct border zone was associated with a significant increase in chemical energy demand and abnormal myocardial energy metabolism. Such severe metabolic perturbations cannot support normal cardiac function, which may explain the observed regional contractile abnormalities in the infarct border zone.     

Relationships among pressure, tension, and shape of the diaphragm

The shape of the diaphragm dome was calculated from transdiaphragmatic pressure and tension in the diaphragm. It was assumed that the muscle acts as a free membrane, attached at its edges to the inside of a vertical rib cage circular in cross section, that the attachments are inferior to the point at which the dome makes contract with the rib cage, and that the abdomen is filled with fluid with a hydrostatic gradient in pressure. The shape is different from a section of a sphere, with a radius of curvature substantially greater at the apex of the dome than at the sides. Observed shapes of human hemidiaphragm domes at functional residual capacity are not spherical but closely match the calculated shapes. Best-fitting shapes correspond to transdiaphragmatic pressures of about 3 cmH2O transdiaphragmatic pressure, suggesting that such a pressure and corresponding tension are present in the human diaphragm when it is at rest in an erect subject. In this model; as lung volume increases and the diaphragm shortens, its shape changes in such a way that the ratio between transdiaphragmatic pressure and tension in the diaphragm remains nearly constant, rather than increasing with volume. Such a model can explain the observation that the length-tension relationship of the muscle is much more important than curvature in determining the effectiveness of the diaphragm as a pressure generator.     

Relationships between pulmonary inflammation, plasma transudation, and oxygen metabolite secretion by alveolar macrophages

We have previously shown that alveolar macrophages from normal rabbit lungs do not synthesize reactive oxygen intermediates unless first conditioned by culture in vitro in the presence of serum for 24 to 48 hr. This conditioning process is mediated by a serum constituent that partitions on gel exclusion columns with an apparent m.w. of 30,000 to 50,000 daltons. Alveolar macrophage conditioning in vitro requires protein synthesis, is associated with the generation of membrane NADPH oxidase activity, and is reversible. We have predicted therefore that during the course of pulmonary inflammation, as observed 3 wk after i.v. injection of M. butyricum in oil, alveolar macrophages might similarly become conditioned in vivo through exposure to plasma protein transudates reaching the alveolus. In support of this hypothesis we show that after experimental production of granulomatous pulmonary inflammation in rabbits, alveolar macrophages showed an augmented capacity to secrete superoxide anion when stimulated with phorbol ester, and this enhancement increases exponentially with increased plasma transudation. This augmented enhancement was reversible, and decreased after culture in vitro in the absence of serum. Mature alveolar macrophages were responsible for this enhanced superoxide anion production rather than freshly emigrated monocytes. Moreover, superoxide anion production in this model of pulmonary inflammation appears to be an "all-or-none" phenomenon, with superoxide anion production associated with a subpopulation of optimally conditioned alveolar macrophages, whereas the remaining unconditioned alveolar macrophages produce little or none. We feel that these two classes of alveolar macrophages may be derived from inflamed and noninflamed regions of the lung, respectively, thereby reflecting the discontinuous nature of the inflammatory lesions themselves. Thus we propose that measurements of reactive oxygen intermediate production by lavaged alveolar macrophages may provide a semi-quantitative measure of chronic pulmonary inflammation.     

Relationships between plant photosynthesis,radial oxygen loss and nutrient removal in constructed wetland microcosms

The objective of this study was to investigate the relationships between root radial oxygen loss (ROL), photosynthesis, and nutrient removal, based on the hypothesis that ROL is primarily an active process which is affected positively by photosynthesis, and is correlated positively with nutrient removal. Four common wetland plants were studied in small-scale monoculture wetlands. Higher ROL coincided with faster growth among the four monocultures. Significant correlation between ROL and photosynthetic rate existed in Cyperus flabelliformis wetland (P < 0.01). Both ROL and photosynthesis represented close correlations with nutrient removal rates in all four monocultures. Significant differences in ROL, photosynthetic rate, removal rates of NH₄⁺, and soluble reactive phosphorus (SRP) were found among the four species. ROL and photosynthetic rates showed single-peak daily and seasonal patterns, with maximum daily values around noon, and with maximum yearly values in summer or autumn for the four monocultures. The results suggest that the ROL of wetland plants is related to active physiological processes. Both ROL and photosynthetic rate are indices which can be used to identify wetland plants with a higher nutrient removal capacity.     

Prostaglandin E2 and cyclic AMP in the coronary vasodilatation due to cardiac hyperactivity.

In the isolated perfused rat heart, the dose-related cardiostimulation produced by norepinephrine (NE) or calcium chloride (Ca2+) was followed by a corresponding increase in coronary flow (CF) and in the cardiac level of adenosine 3',5'-cyclic phosphate (cAMP). Prolonged prostaglandin E2 (pge2) infusion did not change the basic force of contraction, CF, or cAMP level but when NE or Ca2+ were administered, only the responses of the CF and the cAMP were diminished. A phosphodiesterase inhibitor, diazoxide (Dx), caused insignificant increase in the basal cAMP, without affecting the force of contraction or CF. With NE or Ca2+, during Dx both the changes in CF and cAMP were augmented compared to the nontreated hearts. The inhibitory effects of NE or Ca2+ remained unchanged. Propranolol abolished the NE but not the Ca2+ effects. It is suggested that PGE2 modulates the cardiac cAMP level and that the latter plays an important role in the adaptive regulation of the CF. It is also postulated that changes in cAMP levels may be brought about by the hyperactivity per se produced by a variety of cardiostimulating agents.     

Swimming performance, venous oxygen tension and cardiac performance of coronary-ligated rainbow trout, Oncorhynchus mykiss, exposed to progressive hypoxia

We performed in vivo studies to examine the idea that cardiac work is impaired in rainbow trout (Oncorhynchus mykiss) below a certain venous PO2 threshold. We hypothesized that coronary-ligated fish, swimming continuously at a reasonably high water velocity (1.5 body lengths x s(-1)) and exposed to progressive hypoxia, would fatigue at higher venous PO2 and ambient water PO2 compared with sham-operated fish. However, we found that both the lowest venous PO2 that supported hypoxic swimming (9.9 torr for coronary-ligated fish and 11.1 torr for sham-operated fish) and the venous PO2 at fatigue (7.8 torr and 8.6 torr, respectively) were the same for coronary-ligated and sham-operated fish. Also, both groups quit swimming at the same water PO2 heart rate and hematocrit. Nevertheless, significant differences in cardiac performance did exist between the two groups. Whereas ventral aortic blood pressure (Pva) increased significantly with hypoxic swimming in sham-operated fish, there was no such increase in coronary-ligated fish. In addition, cardiac arrhythmias occurred in coronary-ligated fish at fatigue, and these fish were slower to recover from exhaustion. We believe that the venous PO2 threshold to support cardiac performance in the absence of a coronary supply was between 7.8 and 9.9 torr. Furthermore, we suspect that the low PO2 in coronary-ligated fish effectively lowered their myocardial O2 demand. Uncertainty still exists regarding whether or not the venous PO2 threshold lies between 8.6 and 11.1 torr in sham-operated fish.