Mechanisms of Soybean Host-Plant Resistance Against Megacopta cribraria (Hemiptera: Plataspidae).

A number of soybean varieties traditionally bred for resistance to various soybean arthropod pests have been identified as resistant to Megacopta cribraria (F.) (Hemiptera: Plataspidae). However, the mechanisms of host-plant resistance (HPR) in this system are not understood. The goal of this study was to identify the mechanisms of resistance by examining the role of plant volatile organic compounds (VOCs) and free amino acids (FAAs) among 16 soybean varieties. Choice and no-choice cage experiments identified several soybean varieties that demonstrated antixenosis as well as antibiosis. However, resistance varied over time in certain soybean varieties, such as N02-7002 and PI567352B. Mean nymph number from choice experiments had positive correlations with the FAAs asparagine, tryptophan, alanine, phenylanaline, and serine; negative correlation with leucine and threonine. Four plant volatiles, hexanal, 2-pentylfuran, beta-cyclocitral, and cis-9-hexadecenal, were positively correlated with subsequent nymph development, whereas n-hexadecenoic acid was negatively correlated with nymph number only, in adult choice cage experiments. This study contributes to understanding the mechanisms of HPR through associations with plant VOCs and FAAs in relation to M. cribraria development and provides useful knowledge for developing soybean varieties for M. cribraria management.

Soybean Host Plant Resistance to Megacopta cribraria (Hemiptera: Plataspidae) and the Potential Role of Leaf Trichome Density.

Megacopta cribraria (F.) (Hemiptera: Plataspidae) is an invasive pest of soybean that has spread across the southeastern United States since its initial discovery in 2009 in Georgia. Previous studies in the southeastern states have documented both the population dynamics of this pest and host plant resistance (HPR) among soybean varieties, although the specific mechanisms of HPR remain unknown. The objectives of this study were, therefore, to 1) quantify field resistance to M. cribraria in multiple soybean varieties in two states previously affected by severe M. cribraria infestations, North Carolina (NC) and South Carolina (SC); and 2) study the role of soybean trichome density in imparting resistance against M. cribraria. Soybean variety 'Camp' was least attractive to M. cribraria, through time and locations, suggesting consistent resistance. Other varieties showed variable performance among the locations and sampling dates. A significant difference in trichome density was evident. However, there was no correlation between trichome density and M. cribraria infestation. Compared to a previously published study in the same location, when M. cribraria adults emerging from overwintering dispersed into soybeans, in our study only first-generation adults dispersed into soybeans. Considering the current trend of significantly lower M. cribraria infestation rates in North and South Carolina, this pest may be finally succumbing to indigenous natural enemies and should be managed by incorporating integrated pest management tactics, such as HPR, that help conserve natural enemy populations.

Leukocyte reactivity as an objective means of quantifying mental loading during ergonomic evaluation.

Psychological stress evokes rapid changes to the cardiovascular and neuroendocrine systems, responses that can become habituated following repeated exposure. This study, comprising of two phases, suggests that the immune system follows a similar trend. Phase 1: 15 healthy subjects (aged between 26 and 56years) provided capillary blood samples before and after completing three basic tasks using, in turn, two automotive touch screen interfaces (Interface 1-antecedent version, Interface 2-improved version). Using a chemiluminescent technique termed leukocyte coping capacity (LCC), the ability of leukocytes to produce reactive oxygen species in vitro was assessed. Significant differences in leukocyte activity were shown between treatment groups, where the greatest post-test decrease occurred after using Interface 1. Phase 2: a randomly selected sub-group (n=4) underwent weekly repeat testing using both interfaces. Significant differences in post-test leukocyte reactivity were exhibited between test weeks for each interface-the magnitude of response decreasing with successive exposure.

Leukocyte coping capacity: a novel technique for measuring the stress response in vertebrates.

Methods used to quantify the stress response in animals are vital tools in many areas of biology. Here we describe a new method of measuring the stress response, which provides rapid results and can be used in the field or laboratory. After a stressful event, we measure the capacity of circulating leukocytes to produce a respiratory burst in vitro in response to challenge by phorbol myristate acetate (PMA). During the respiratory burst leukocytes produce oxygen free radicals, and the level of production can be measured directly as chemiluminescence. When in vitro PMA-stimulated whole blood chemiluminescence is measured directly after a stressful event, we define the response as the leukocyte coping capacity (LCC). In an experiment badgers (Meles meles), which were caught as part of an on-going population study, were either transported to a central site prior to blood sampling or blood was collected at their site of capture. Transported animals had a significantly lower LCC and showed changes in leukocyte composition that were indicative of stress. We conclude that the stress of transport reduced LCC in badgers and that LCC serves as a quantitative measure of stress. Potential applications of this method are discussed.

Isolated limb infusion for melanoma: a simple alternative to isolated limb perfusion.

OBJECTIVE: To describe initial experience with the new technique of isolated limb infusion (ILI) for in-transit melanoma. DESIGN: A prospective case series. SETTING: The major tertiary care oncology centre for the state of Victoria, Australia. PATIENTS: Nine patients having for extensive in-transit limb melanoma INTERVENTIONS: All patients received ILI (13 treatments). OUTCOME MEASURES: Patient survival, response to treatment and complications of treatment. RESULTS: There were no perioperative deaths and morbidity was limited to deep venous thrombosis and pulmonary embolism in 1 patient. Control of the in-transit metastases was achieved to some degree in all patients and was complete in 4. CONCLUSIONS: ILI is an alternative treatment modality for patients suffering from multiple, advanced in-transit melanoma metastases. It provides effective palliation with limited morbidity and offers a safe, quick, inexpensive alternative to isolated limb perfusion with comparable results.

The effect of a short-term mental stressor on neutrophil activation.

Twenty-five undergraduates and university staff (15 females, 10 males) volunteered to take part in a study examining the effects of a short-term mental stressor on the activation of neutrophils in peripheral blood, as determined by the oxidative capacity to reduced Nitro-blue Tetrazolium (NBT). Participants were assigned to one of two groups, an experimental group (n=17) and a control group (n=8). Subjects in the experimental group were subjected to a time-constrained mental stressor and finger-stick blood samples were taken on four occasions. Those in the control group did not complete a stressor task and only experienced the four finger-stick blood samples. Heart rate was recorded at 5-min intervals as a general indicator of arousal. Examination of the stained blood samples showed that a short-term stressor resulted in significant increased activation of neutrophils, which returned almost to baseline levels on completion of the experiment. In contrast, the control group's neutrophils showed no significant change in activation throughout. The results support the hypothesis that short-term, acute stressors may activate neutrophils.

Stimulating effect of an arteriovenous shunt on the in vivo growth of isografted fibroblasts: a preliminary report.

Isogenous fibroblasts derived from the skin of inbred Sprague-Dawley rats were cultured in vitro, labeled with bisbenzamide (BB) or carboxyfluorescein diacetate (CFDA), and seeded into polycarbonate growth chambers. After 24 h incubation in vitro, the chambers, either empty or containing an arteriovenous (AV) shunt, were implanted subcutaneously into the inguinal region of Sprague-Dawley rats and examined by fluorescence microscopy 2 or 7 days later. The AV shunt remained patent in all experiments. The density of labeled cells on the chamber surface in all chambers decreased in the first 2 days after insertion. At 7 days, the cell density in the empty chambers had not altered from the 2-day level, but the density in the AV shunt containing chambers had increased to almost three times the day 2 level (p = 0.013). It appears that an AV shunt can induce a significant proliferation of fibroblasts implanted adjacent to it. For at least 7 days after labeling, BB and CFDA provide a simple and effective method of quantitative detection of implanted fibroblasts. It is concluded that nutrients from the AV shunt implanted in a growth chamber result in a significant increase in the number of viable, matrix-synthesizing cells, compared with AV shunt-free controls.

Formation of new tissue from an arteriovenous loop in the absence of added extracellular matrix.

A major requirement for the microsurgical repair of contour defects of the skin, for example, following removal of a skin cancer on the face, is a mass of vascularised subcutaneous tissue. Such tissue can be generated in vivo using basic tissue engineering principles. In previous studies in our laboratory, we have used a model comprising an arteriovenous (AV) shunt loop sandwiched in artificial dermis, placed in a cylindrical plastic growth chamber, and inserted subcutaneously to grow new connective tissue progressively up to 4 weeks. To learn more about the basic growth characteristics with this model, the same AV shunt loop within a chamber without added extracellular matrix was inserted subcutaneously into the groins of rats for 2, 4, or 12 weeks (n = 5 per group). There was a progressive increase in the mass and volume of tissue such that the chamber was two-thirds full after 12 weeks. Histological examination showed that at 2 weeks there was evidence of fibroblast and vascular outgrowth from the AV shunt, with the formation of granulation tissue, surrounded by a mass of coagulated exudate. At 4 weeks the connective tissue deposition was more extensive, with a mass of more mature granulation tissue containing considerable collagen. By 12 weeks there was an extensive, well vascularized mass of mature fibrous tissue. The blood vessels and residual adventitia of the AV shunt were the likely source of growth factors and of the cells which populated the chamber with new maturing connective tissue. A patent AV shunt in an isolated chamber appears to be the minimal requirement for the generation of new vascularized tissue that is potentially suitable for microsurgical transplantation.

Activation of human leukocytes by acute hypoxia.

Exposure of human leukocytes to 12% and 6% O(2) in vitro resulted in striking ultrastructural and morphological changes. These changes included the appearance of crater-like holes, a reduction in granular size and disruption of the cellular membrane. The implications of these findings is discussed.

Etiology of sexually transmitted infections among street-based female sex workers in Dhaka, Bangladesh.

An etiological study of sexually transmitted infections (STIs) was conducted among female sex workers (FSWs) in Dhaka, Bangladesh. Endocervical swab and blood samples from 269 street-based FSWs were examined for Neisseria gonorrhoeae, Chlamydia trachomatis, and Trichomonas vaginalis as well as for antibodies to Treponema pallidum and herpes simplex virus 2 (HSV-2). Sociodemographic data and data regarding behavior were also collected. A total of 226 of the 269 FSWs (84%) were positive for the STI pathogens studied. Among the 269 FSWs, 35.5% were positive for N. gonorrhoeae, 25% were positive for C. trachomatis, 45.5% were positive for T. vaginalis, 32.6% were seropositive for T. pallidum, 62.5% were seropositive for HSV-2, and 51% had infections with two or more pathogens.

The behaviour of muscle microcirculation in chronically hypoxic rats: the role of adenosine.

1. In rats housed in a hypoxic chamber at 12% O2 for 3-5 weeks (CH) and in normal rats housed in air (N), we directly observed responses of arterial and venous vessels of the spinotrapezius muscle to changes in O2 concentration in the inspirate. Both CH and N rats were anaesthetized with Saffan. They had haematocrits of 55.0 +/- 0.9% (mean +/- S.E.M.) and 41.9 +/- 0.5%, respectively. 2. In CH rats breathing 12% O2 and N rats breathing air, arterial and venous vessels from comparable anatomical positions in the vascular tree were of similar internal diameter. They also showed similar maximum dilator responses to topical adenosine (10(-3) M); 14.1 +/- 1.1 and 16.3 +/- 1.7% in all arterioles, 15.5 +/- 1.2 and 11.5 +/- 0.6% in all venules in CH and N rats, respectively. 3. In CH rats, the change from 12% O2 to air for 3 min induced constriction in all arterioles and venules (-12.9 +/- 1.0 and -14.3 +/- 1.7%, respectively), whereas in N rats, the change from air to 12% O2 for 3 min induced net dilatation (3.9 +/- 1.8% in arterioles and 4.7 +/- 0.8% in venules). Topical application of the adenosine receptor antagonist 8-sulphophenyltheophylline (8-SPT, 10(-3) M) had no effect on control diameters in CH or N rats, nor on constrictor responses to air in CH, but reversed or reduced dilator responses to 12% O2 in N rats (to -2.4 +/- 1.3% in arterioles and 2.0 +/- 0.9% in venules). 4. In CH rats, the change from 12 to 8% O2 produced net dilatation as great as that induced in N rats by the larger change from air to 8% O2: 8.5 +/- 2.6 and 5.0 +/- 3.7% in arterioles and 10.3 +/- 1.8 and 6.4 +/- 1.9% in venules, respectively. These responses were similarly reduced by 8-SPT to -4.3 +/- 1.9 and -5.2 +/- 2.7% in arterioles and to -6.9 +/- 2.0 and -1.5 +/- 2.0% in venules, respectively. 5. These results indicate that CH rats were acclimated to 12% O2 such that the resting tone of arterial and venous vessels of muscle was comparable to that of N rats breathing air. They also suggest that adenosine had little tonic dilator influence in CH rats breathing 12% O2 despite its contribution to the dilatation induced in N rats by acute exposure to 12% O2. This may reflect the greater haematocrit in CH rats which normalized the O2 supply to muscle. However, CH rats were more sensitive than N rats to the dilator influence of acute systemic hypoxia and this was largely mediated by adenosine.

The role of adenosine in mediating vasodilatation in mesenteric circulation of the rat in acute and chronic hypoxia.

1. We have compared the roles of adenosine in mediating dilator responses to acute hypoxia in mesenteric microcirculation of control, normoxic (N) rats and in chronically hypoxic (CH) rats kept in an hypoxic chamber at 10% O2 for 3-4 weeks. 2. In fifteen N rats, acute hypoxia (breathing 6% O2 for 3 min) induced mean increases in the diameter of arterial vessels of mesentery (whose internal diameter was 10-350 microns) of 8.0 +/- 1.9% (mean +/- S.E.M.) and of venous vessels (whose internal diameter was 12-360 microns) of 10.4 +/- 2.6%. These diameter changes were reduced by approximately 30% when the adenosine receptor antagonist 8-sulpho-phenyltheophylline (8-SPT, 10(-3) M) was applied topically to the mesentery. 3. In a further six N rats, topical application of graded concentrations of adenosine (10(-7)-10(-3) M) to the mesentery evoked graded increases in the diameter of all arterial and venous vessels, maximum increases with 10(-3) M being 12.5 +/- 3.3 and 8.4 +/- 4.3%, respectively; these responses were abolished by 8-SPT. 4. By contrast, in fourteen CH rats, the smaller change in inspirate from 10 to 8% O2 induced increases in diameter of arterial and venous vessels which had control diameters that were comparable to those of N rats, of 14.1 +/- 2.4 and 12.9 +/- 2.7%, respectively, and which were virtually equivalent to the responses induced by topical application of 10(-3) M adenosine (13.3 +/- 1.3 and 16.3 +/- 2.0% in arterial and venous vessels, respectively). The changes induced by acute hypoxia were abolished by 8-SPT, as were those induced by adenosine. 5. These results suggest that in the intestinal mesentery, where the blood vessels have negligible tissue parenchyma around them, locally released or synthesized adenosine makes a substantial contribution to the dilatation that is evoked in arteriolar vessels by acute hypoxia and to the active dilatation, or passive distension of the venous vessels. The results also suggest that this contribution is accentuated in chronic hypoxia either by greater release of adenosine or greater vascular sensitivity to it.

Acute systemic hypoxia and the surface ultrastructure and morphological characteristics of rat leucocytes.

We have examined the surface ultrastructure and morphological characteristics of leucocytes obtained from control rats breathing air and rats made acutely hypoxic (breathing 6% O2, for 30 min). Striking ultrastructural and morphological changes occurred in the leucocytes of hypoxic rats. These changes included the appearance of crater-like holes, a reduction in granule size and disruption of the cell membrane. The implications of these findings are discussed.

The influence of vasopressin on the arterioles and venules of skeletal muscle of the rat during systemic hypoxia.

1. In rats anaesthetized with Saffan, the spinotrapezius muscle was prepared for in vivo microscopy. Systemic hypoxia (breathing 8% O2 for 3 min) induced a fall in arterial pressure and tachycardia, together with constriction in some arterioles and venules of each section of the vascular tree and dilatation in others. 2. The vasopressin V1-receptor antagonist d(CH2)5Tyr(Me)-arginine vasopressin (20 mg kg-1 I.V.) preferentially attenuated constrictor responses induced by hypoxia in both arterioles and venules, but had no significant effect on the dilator responses. Analysis of responses in individual sections of the vascular tree suggested that the V1-receptor antagonist reduced hypoxia-induced constrictor responses in proximal arterioles (> 13 microns diameter) though not in terminal arterioles (< 13 microns), but reduced hypoxia-induced constrictor responses in both the proximal and distal venules (9-130 microns). 3. Infusion of vasopressin at 1.4, 2.8, 5.7 and 11.4 ng min-1 kg-1 i.v. for 3 min, expected to produce plasma concentrations within the range 28-228 pg ml-1, evoked rises in arterial pressure together with decreases in heart rate. There was also vasoconstriction in the proximal arterioles of spinotrapezius that was graded with vasopressin concentration (5-35% decrease in diameter). 4. Infusion of vasopressin at 1.4 mg min-1 kg-1 i.v. for 3 min with the intention of producing a plasma concentration likely to be reached or exceeded during 8% O2, evoked constriction of all proximal arterioles, though not of terminal arterioles, and constriction of all venous vessels. The magnitude of the constriction induced by vasopressin in vessels that dilated during hypoxia was just as great as in those that constricted during hypoxia. 5. We propose that vasopressin released during systemic hypoxia exerts a constrictor influence upon the proximal arterioles and all sections of the venous tree of skeletal muscle. In individual arterioles and venules the constrictor influence of vasopressin and catecholamines may be overcome by the influence of locally released vasodilator metabolites.

Effect of acute systemic hypoxia on vascular permeability and leucocyte adherence in the anaesthetised rat.

OBJECTIVE: The aim was to investigate the effect of acute systemic hypoxia on vascular permeability to macromolecules and on leucocyte adherence to vascular endothelium in vivo. METHODS: Experiments were performed on anaesthetised rats with either the intestinal mesentery or the spinotrapezius muscle prepared for in vivo microscopy. To quantify changes in vascular permeability, fluorescein isothiocyanate conjugated with serum albumin (FITC-albumin) was given intravenously and the microcirculation was viewed using a mercury source for 30 s periods during air breathing; or before, during, and after breathing 6% O2 for 3 or 20 min. On each occasion the number of FITC leakage sites was counted. In separate experiments acridine orange was given to stain leucocytes and the microcirculation was viewed using a mercury source during air breathing and during a 3 min period of systemic hypoxia. The number of leucocytes that adhered to venular walls for > 30 s was counted. Using mesentery, the effects were tested of BW755C, a lipoxygenase inhibitor, and of SM9064, a LTB4 receptor antagonist, upon the increase in leucocyte adherence observed during hypoxia. RESULTS: In rats that breathed air throughout, the number of leakage sites for FITC-albumin in both the spinotrapezius and mesentery remained constant. Moreover, in rats that breathed 6% O2 for 3 or 20 min, the number of leakage sites was not changed in either mesentery or spinotrapezius by hypoxia, but was substantially increased in both preparations by topical application of histamine. However, the number of leucocytes that adhered to the inside of venular walls was significantly increased in both mesentery and spinotrapezius by a 3 min inhalation 6% O2 from 2.83(SEM 0.56) to 4.66(1.77) per 100 microns length of venule and from 2.44(0.33) to 3.35(0.49) respectively during the first period of hypoxia. Between periods of hypoxia the number of adherent leucocytes returned to control in both preparations. Leucocyte adherence was not affected by BW755C (50 or 500 micrograms.ml-1 applied topically or 10 mg.kg-1 intravenously) or by SM9064 (3 mg.kg-1 intravenously). CONCLUSIONS: Acute systemic hypoxia does not affect the vascular permeability to albumin. However, 3 min periods of systemic hypoxia induce significant, but reversible, increases in leucocyte adherence in both muscle and mesenteric venules which in mesentery, at least, is not mediated by LTB4 or other products of the lipoxygenase pathway.

The role of adenosine in dilator responses induced in arterioles and venules of rat skeletal muscle by systemic hypoxia.

1. In experiments on anaesthetized rats, we have studied the role of adenosine in mediating responses induced in individual arterioles and venules of the spinotrapezius muscle by systemic hypoxia. 2. During systemic hypoxia induced by breathing 6% O2 for 3 min, some arterioles and venules dilated while others constricted. Topical application of the adenosine receptor antagonist, 8 phenyl-theophylline (8-PT), to the spinotrapezius had no effect on the constrictor responses but greatly reduced the dilator responses. The vessels nearest to the capillary bed-terminal arterioles and collecting venules--were most affected; their mean changes in diameter were reduced from 39 and 8% to 11 and -1.6% respectively. 3. In accord with these results, topical application of adenosine (2 x 10(-7)-2 x 10(-3) M) produced graded dilation of all sections of the arterial and venous trees; the terminal arterioles and collecting venules were most responsive, being dilated at maximum by 31 and 15% respectively. The dilator responses induced in those vessels that constricted during hypoxia were fully comparable with those that dilated during hypoxia. 4. Histochemical analysis of the spinotrapezius revealed that oxidative fibres that most readily release adenosine, glycolytic and mixed fibres were all evenly distributed throughout the muscle. There is no reason to suppose that some vessels are preferentially influenced by oxidative fibres. 5. These results indicate that adenosine plays a major role in dilating both arterioles and venules of muscle during systemic hypoxia. But, they are consistent with the idea that the adenosine that is important is not released from muscle fibres, but synthesized by 5'-nucleotidase localized to the blood vessels; its activity may decrease proximally along the vascular tree and may vary from one vessel to another depending on the local O2 tension.

Responses observed in individual arterioles and venules of rat skeletal muscle during systemic hypoxia.

1. In rats anaesthetized with Saffan, responses induced in individual arterial and venous vessels of the spinotrapezius muscle by systemic hypoxia (breathing 12 or 6% O2 for 3 min) were directly observed by in vivo microscopy. 2. Both 12 and 6% O2 induced gradual tachycardia and a fall in arterial pressure. Concommitantly, in each section of the vascular tree, some vessels showed a gradual increase in diameter, others, a gradual decrease. 3. During 12% O2, mean diameter changes were graded from mean increases of approximately 2% in main arteries (resting diameter 40-90 microns) to approximately 20% in terminal arterioles (7-13 microns) and ranged from mean increases of 5-8% in collecting and secondary venules (9-18 microns, 18-30 microns), to a decrease of approximately 2% in main veins (65-130 microns). 4. During 6% O2, constrictor responses were more common in arterial vessels. Thus, mean changes amounted to diameter decreases of less than 5% in main arteries and secondary arterioles (13-18 microns), and increases of approximately 5% in primary arterioles (22-50 microns) and terminal arterioles. By contrast, diameter increases predominated in venous vessels being graded from approximately 20% in collecting venules to approximately 2% in main veins. 5. In seventeen rats, 6% O2 was administered for eight 3 min periods separated by 30 min control periods. The changes evoked in arterial pressure and heart rate were consistent throughout. Diameter changes evoked in individual arterial and venous vessels were consistent in the first two hypoxic periods. However, diameter changes in the third and successive periods were significantly different from those recorded in the first period: increases in diameter became more common and pronounced. 6. These changes in vessel diameter, especially their variability, are considered in relation to recordings made previously of changes in gross blood flow and vascular conductance of limb muscle during systemic hypoxia.

The roles of catecholamines in responses evoked in arterioles and venules of rat skeletal muscle by systemic hypoxia.

1. Studies have been made in the anaesthetized rat of the roles played by alpha- and beta-adrenoreceptor stimulation in determining diameter changes induced in individual arterioles and venules of the spinotrapezius muscle during systemic hypoxia (breathing 6% O2 for 3 min). 2. Topical application to the spinotrapezius of phentolamine, the alpha-adrenoreceptor antagonist, or sotalol, the beta-adrenoreceptor antagonist, had no effect on the fall in systemic arterial pressure and tachycardia induced by hypoxia. 3. All arterioles and venules showed a decrease in diameter in response to topical application of noradrenaline (10(-6) g ml-1): these responses were abolished by topical application of phentolamine. Moreover, those arterioles and venules that showed a decrease in diameter during hypoxia before phentolamine, showed a significantly smaller decrease, or an increase in diameter after phentolamine. This effect was most marked in primary and secondary arterioles (13-50 microns diameter). 4. All arterioles and venules showed an increase in diameter in response to topical application of isoprenaline (10(-6) g ml-1); these responses were abolished by topical application of sotalol. Moreover, these arterioles and venules that showed an increase in diameter during hypoxia before sotalol, showed a significantly smaller increase or even a decrease in diameter after sotalol. 5. These results suggest that during hypoxia the arterioles of skeletal muscle, especially primary and secondary arterioles, are under the constrictor influence of a reflex increase in sympathetic nerve activity while the venules, which have no sympathetic innervation, are under the constrictor influence of circulating catecholamines. They also suggest that in individual arterioles and venules, these constrictor influences may be overcome by dilatation mediated by the beta-adrenoreceptor influence of circulating catecholamines. 6. Since some arterioles and venules still showed constriction during hypoxia after phentolamine and some still showed dilatation during hypoxia after sotalol, it seems that factors other than catecholamines contribute to the diameter changes. It is suggested that locally released metabolites exert a substantial dilator influence, particularly on terminal arterioles and collecting venules, those vessels nearest to the capillary bed.

Interactions between K+ and beta 2-adrenoreceptors in determining muscle vasodilatation induced in the rat by systemic hypoxia.

In spontaneously breathing anaesthetized rats, both moderate and severe hypoxia caused increases in [K+] in venous efflux from hindlimb muscle, from 4.3 to 4.6 and from 3.8 to 4.4 mM respectively; the increases were accentuated to 5.2 and 5.7 mM after beta 2-receptor blockade with I.V. sotalol. Sotalol also potentiated the vasodilatation evoked in hindlimb muscle by moderate hypoxia, but reduced that evoked by severe hypoxia. We propose that K+ released from muscle during hypoxia contributed to the local vasodilatation. Further, we suggest that this effect was enhanced in moderate hypoxia by blockade of the beta 2-mediated uptake mechanism for K+ in skeletal muscle, but outweighed in severe hypoxia by blockade of the beta 2-mediated dilator action of circulating catecholamines on vascular muscle.