Naloxone and TRH affect regional blood flows in the anesthetized rabbit

The cardiovascular effects of IV naloxone and a subsequent administration of TRH IV were studied in the rabbit. Naloxone caused a vasodilation in the myocardium and adrenal glands. Naloxone elicited an increment in cerebral blood flow in several regions which attenuated the cerebrovasodilating effect of TRH in a few regions. The blockade of endogenous opioids with naloxone did not modify the peripheral vasoconstricting effect of TRH or affect the vascular effects of TRH mediated by the peripheral sympathetic nerves. The results indicate that naloxone has a vasodilating effect in the myocardium and CNS in anesthetized rabbits. The major part of the cardiovascular effect of TRH is not dependent on mechanisms sensitive to naloxone.     

The effects of endogenous or exogenous catecholamines on blood respiratory status during acute hypoxia in rainbow trout (Oncorhynchus mykiss)

Summary An extracorporeal circulation of rainbow trout (Oncorhynchus mykiss) was utilized to continuously monitor the rapid and progressive effects of endogenous or exogenous catecholamines on blood respiratory/acid-base status, and to provide in vivo evidence for adrenergic retention of carbon dioxide (CO₂) in fish blood (cf. Wood and Perry 1985). Exposure of fish to severe aquatic hypoxia (final P _wO₂=40–60 torr; reached within 10–20 min) elicited an initial respiratory alkalosis resulting from hypoxia-induced hyperventilation. However, at a critical arterial oxygen tension (P _aO₂) between 15 and 25 torr, fish became agitated for approximately 5 s and a marked (0.2–0.4 pH unit) but transient arterial blood acidosis ensued. This response is characteristic of abrupt catecholamine mobilization into the circulation and subsequent adrenergic activation of red blood cell (RBC) Na⁺/H⁺ exchange (Fievet et al. 1987). Within approximately 1–2 min after the activation of RBC Na⁺/H⁺ exchange by endogenous catecholamines, there was a significant rise in arterial PCO₂ (P _aCO₂) whereas arterial PO₂ was unaltered; the elevation of P _aCO₂ could not be explained by changes in gill ventilation. Pre-treatment of fish with the -adrenoceptor antagonist phentolamine did not prevent the apparent catecholamine-mediated increase of P _aCO₂. Conversely, pre-treatment with the -adrenoceptor antagonist sotalol abolished both the activation of the RBC Na⁺/H⁺ antiporter and the associated rise in P _aCO₂, suggesting a causal relationship between the stimulation of RBC Na⁺/H⁺ exchange and the elevation of P _aCO₂. To more clearly establish that elevation of plasma catecholamine levels during severe hypoxia was indeed responsible for causing the elevation of P _aCO₂, fish were exposed to moderate hypoxia (final P _wO₂=60–80 torr) and then injected intraarterially with a bolus of adrenaline to elicit an estimated circulating level of 400 nmol·l^-1 immediately after the injection. This protocol activated RBC Na⁺/H⁺ exchange as indicated by abrupt changes in arterial pH (pHa). In all fish examined, P _aCO₂ increased after injection of exogenous adrenaline. The effects on P _aO₂ were inconsistent, although a reduction in this variable was the most frequent response. Gill ventilation frequency and amplitude were unaffected by exogenous adrenaline. Therefore, it is unlikely that ventilatory changes contributed to the consistently observed rise in P _aCO₂. Pretreatment of fish with sotalol did not alter the ventilatory response to adrenaline injection but did prevent the stimulation of RBC Na⁺/H⁺ exchange and the accompanying increases and decreases in P _aCO₂ and P _aO₂, respectively. These results suggest that adrenergic elevation of P _aCO₂, in addition to the frequently observed reduction of P _aO₂ are linked to activation of RBC Na⁺/H⁺ exchange. The physiological significance and the potential mechanisms underlying the changes in blood respiratory status after addition of endogenous or exogenous catecholamines to the circulation of hypoxic rainbow trout are discussed.Abbreviations P _aCO₂ arterial carbon dioxide tension - P _aO₂ arterial oxygen tension - P _da dorsal aortic pressure - pHa arterial pH - P _wO₂ water oxygen tension - RBC red blood cell - V _f breathing frequency     

Expansion of the canine A blood group system

A detailed study of the canine A blood group system was undertaken, resulting in the expansion of this system into a three-factor, four-allelic one with the recognition of an additional subtype, a3. The serological and extensive family data supported the proposed genetic theory of four alleles with dominance with the order being Aa1, Aa2, Aa3 and A-. Gene frequencies of the alleles were determined in various breeds of dogs with frequencies in the general Brisbane population being 0.244 (Aa1), 0.042 (Aa2), 0.045 (Aa3) and 0.669 (A-).     

Human and mouse S-protein mRNA detected in Northern blot experiments and evidence for the gene encoding S-protein in mammals by Southern blot analysis

Summary Human S-protein is a serum glycoprotein that binds and inhibits the activated complement complex, mediates coagulation through interaction with antithrombin III and plasminogen activator inhibitor I, and also functions as a cell adhesion protein through interactions with extracellular matrix and cell plasma membranes. A full length cDNA clone for human S-protein was isolated from a lambda gt11 cDNA library of mRNA from the HepG2 hepatocellular carcinoma cell line using mixed oligonucleotide sequences predicted from the amino-terminal amino acid sequence of human S-protein. The cDNA clone in lambda was subcloned into pUC18 for Southern and Northern blot experiments. Hybridization with radiolabeled human S-protein cDNA revealed a single copy gene encoding S-protein in human and mouse genomic DNA. In addition, the S-protein gene was detected in monkey, rat, dog, cow and rabbit genomic DNA. A 1.7 Kb mRNA for S-protein was detected in RNA from human liver and from the PLC/PRF5 human hepatoma cell line. No S-protein mRNA was detected in mRNA from human lung, placenta, or leukocytes or in total RNA from cultured human embryonal rhabdomyosarcoma (RD cell line) or cultured human fibroblasts from embryonic lung (IMR90 cell line) and neonatal foreskin. A 1.6 Kb mRNA for S-protein was detected in mRNA from mouse liver and brain. No S-protein mRNA was detected in mRNA from mouse skeletal muscle, kidney, heart or testis.     

Exercise performance of normothermic and hyperthermic rats: Effect of warm rearing

1. 1.|Hypothalamic and rectal temperatures were recorded in 8 warm-reared (wr) and 12 control rats. Rats ran to exhaustion at a constant speed of 1.5 km h⁻¹ but at a variable ambient temperature adjusted to stabilize their hypothalamic temperature at 38.0°C (normothermia) or 41.0°C (hyperthermia). Blood lactate concentrations were determined before and after exercise.

2. 2.|Exercise caused exhaustion in normothermic control rats after 62.08 ± 5.43 min and in wr rats after 29.64 ± 2.09 min.

3. 3.|Hyperthermia shortened to one half (to 12.24 ± 1.36 min) and to one fourth (to 16.15 ± 1.20 min) the endurance time in wr and control rats, respectively.

4. 4.|There were no correlations between lactate concentraion and hyperthermia or endurance time.

5. 5.|In conclusion, in rats and other animals which have safe refuges, hyperthermia interferes with the ability to continue exercising.

Segmental release of amino acid neurotransmitters from transcranial stimulation

The present study used microdialysis techniques in an intact rabbit model to measure the release of amino acids within the lumbar spinal cord in response to transcranial electrical stimulation. Dialysis samples from the extracellular space were obtained over a stimulation period of 90 minutes and were examined using high pressure liquid chromatography. Neuronal excitation was verified by recerding corticomotor evoked potentials (CMEPs) from the spinal cord. A significant increase in the release of glycine and taurine compared to sham animals was measured after 90 minutes of transcranial stimulation. Glutamate and aspartate release was not significantly elevated. GABA concentrations were consistently low. CMEP components repeatedly showed adequate activation of descending fiber pathways and segmental interneuron pools during dialysis sampling. Since glycine, and to a lesser extent taurine, have been shown to inhibit motor neuron activity and are closely associated with segmental interneuron pools, suprasegmental modulation of motor activity may be, in part, through these inhibitory amino acid neurotransmitters in the rabbit lumbar spinal cord.     

颈动脉内注入腺苷对呼吸,血压和肾交感神经活动的影响

在33只麻醉家兔,观察了颈动脉内注入腺苷所诱发的平均动脉压、心率,呼吸和肾交感神经活动的变化。结果如下:(1)颈动脉内注入腺苷后,平均动脉压呈剂量依赖性下降;呼吸加快,深度变化不明显,剪断窦神经后注入腺苷,仍引起平均动脉压下降,而呼吸变化消失。(2)隔离的颈动脉窦灌流液内加入腺苷后,平均动脉压下降,心率减慢;颈动脉体(CB)失活后反应消失。(3)将腺苷灌注到颈动脉窦区后,平均动脉压下降,肾交感神经传出放电活动增加,CB 失活或剪断窦神经后,反应消失。由此提示:腺苷可作为兴奋 CB 的一种物质,引起平均动脉压降低,心率减慢,呼吸加强和肾交感神经放电活动增加。     

Management of Root-knot Nematodes by Phenamiphos Applied through an Irrigation Simulator with Various Amounts of Water

Phenamiphos (6.7 kg a.i./ha) was applied via an irrigation simulator to squash at planting (AP) and 2 weeks after planting (PP), and to corn AP and 1 week PP to manage root-knot nematodes (Meloidogyne incognita). The nematicide was applied with 0.25, 0.64, 1.27, and 1.91 cm surface water/ ha to a Lakeland sand in which the soil moisture was at or near field capacity. Based on efficacy and crop response, no additional benefits resulted when phenamiphos was applied in volumes of water greater than 0.25 crn/ha. The cost of applying each 0.25 cm of water over a hectare is approximately $1.08, or a 92% reduction in nematicide application cost over conventional methods ($13.50/ha). Low root-gall indices and high yields from squash and corn indicate more effective nematode management when phenamiphos was applied AP rather than PP. Results from this method of applying phenamiphos suggest that certain nematicides could be used as salvage alternatives when nematodes are detected in crops soon after planting. For multiple-pest management, nematicides, other compatible biocides, and fertilizers could be applied simultaneously with sprinkler irrigation.     

狗的无氧阈与骨骼肌某些特征在锻炼、脱锻炼动态变化中的关系

本实验在体力锻炼与脱锻炼过程中观察了五条成年雄性杂种狗的无氧阈(AT)、骨骼肌毛细血管密度(cap/mm~2)、毛细血管数与肌纤维数之比(C:F)、肌纤维组成——慢肌纤维百分比(％ST)以及毛细血管弥散距离(弥散距离)的变化。结果表明:锻炼前AT与cap/mm~2、C:F,％ST及弥散距离均分别有显著相关。锻炼后第五周,AT、cap/mm~2、C:F和％ST分别增加了40.9％、12.2％、22.9％和2.4％,弥散距离降低6.3％,其中只有AT的增加有显著意义,锻炼十周后,AT增加68.2％(P<0.001)、cap/mm~2增加37.8％(P<0.05)、C:F增加78.1％(P<0.001),弥散距离降低17.0％(P<0.01)而％ST无显著变化。停止锻炼后第五周,AT等各指标都有降低的趋势,但无显著意义,停止锻炼后第12周,AT、cap/mm~2,C:F,％ST分别降低了18.9％、10.9％、10.5％、2.9％,弥散距离增加5.1％,其中除AT的降低有显著意义外,其余指标的变化均无显著意义。与锻炼前相比,这些指标的变化。除％ST外,仍有显著变化。在锻炼与脱锻炼的过程中,AT与cap/mm~2、C:F、弥散距离在各期或整个过程中均呈显著相关,但与％ST相关不显著。实验结果提示,骨骼肌的毛细血管供应状况是决定无氧阈的重要因素之一。     

Membrane and cytoplasmic resistivity properties of normal and sickle red blood cells

The cytoplasmic resistivities and membrane breakdown potentials of normal (AA), sickle-cell-trait (AS), and sickle (SS) red blood cells have been measured by the biophysical methodology of resistive pulse spectroscopy over a range of osmolalities. At isotonicity, the average membrane breakdown potentials are virtually identical for the three types of cells occurring at about 1150 V/cm. Average isotonic cytoplasmic resistivities are somewhat higher for the SS cells (166.7±7.49 ohm-cm) compared to the AA (147.6±1.98 ohm-cm) or AS cells (148.7±1.79 ohm-cm). As medium osmolality is varied, the differences in resistive properties become enlarged, especially at very low and very high osmolalities. At high osmolalities, both types of sickle cells show a large increase in internal resistivity compared to the normals; at low osmolality, the SS samples exhibit a distinctly different membrane breakdown characteristic, decreasing in this parameter, whereas the other two groups increase. Of the 15 SS samples tested, three displayed much higher cytoplasmic resistivities at isotonicity: 218.2±5.25 ohm-cm, compared to an average of 153.5±3.46 ohm-cm for the other 12. The relationship between these high resistivities and the subfraction of irreversibly sickled cells in the sample is discussed.