Suspension culture of gametophytes of transgenic kelp in a photobioreactor

Transgenic Laminaria japonica gametophytes producing a recombinant tissue-type plasminogen activator (rtPA) protein, which is an effective third-generation thrombolytic agent for acute myocardial infarction (AMI), were cultured in an illuminated bubble column bioreactor. A maximum final dry cell weight of 1120 mg l⁻¹ was obtained in batch culture with an initial dry cell weight of 126 mg l⁻¹ and with aeration rate of 1.2 l air min⁻¹ l⁻¹ culture, nitrate at 1.5 mM and phosphate at 0.17 mM. The yield of rtPA was 56 μg g⁻¹ dry cell wt. This is the first report regarding cultivation of a transgenic macroalga in a bioreactor.Revisions requested 27 January 2005 and 14 April 2005; Revisions received 6 April 2005 and 17 May 2005     

Use of Controlled Diaphragmatic Breathing for the Management of Motion Sickness in a Virtual Reality Environment

Evidence indicates that activation of the parasympathetic nervous system (PNS) suppresses physiological responses associated with motion sickness. Research also shows paced breathing increases PNS activation; the current study examines the use of paced diaphragmatic breathing (DB) training to quell motion sickness symptoms. Healthy participants (N = 60) were pre-screened for motion sickness susceptibility. Participants were then randomly assigned to either a control condition, focusing on environmental awareness, or to an experimental condition implementing paced DB. Following this, participants were exposed to a virtual reality (VR) motion sickness experience, while heart rate variability, breathing rate (RPM), and motion sickness ratings were collected. Results demonstrated participants in the DB condition had higher PNS activation and reported fewer motion sickness symptoms during the VR experience than the participants in the control condition. Results suggest that the DB protocol can be used to significantly increase PNS tone and decrease the development of motion sickness symptoms.     

Glutamate and GABA in the medial amygdala induce selective central sympathetic/parasympathetic cardiovascular responses

Glutamate and γ-aminobutyric acid (GABA) participate in central cardiovascular control, and are found in the rat posterodorsal medial amygdala (MePD), an area of the forebrain that modulates emotional/social behaviors. Here we tested whether these neurotransmitters in the MePD could change the basal activity, chemoreflex, and baroreflex cardiovascular responses in awake rats. Power spectral analysis and symbolic analysis were used to evaluate these responses. Microinjections of saline, glutamate (2 μg), or GABA (61 ng or 100 μg; n = 5-7 rats per group) did not affect basal parameters or chemoreflex responses. However, baroreflex responses showed marked changes. Glutamate increased power spectral and symbolic sympathetic indexes related to both cardiac and vascular modulations (P < 0.05). In turn, the displacement of the baroreflex half-maximal heart rate (HR) response was associated with a GABA (61 ng) mediated decrease in the upper plateau (P < 0.05). Administration of GABA (61 ng, but not 100 μg) also increased HR variability (P < 0.05), in association with parasympathetic activation. These data add novel evidence that the MePD can promote selective responses in the central regulation of the cardiovascular system, i.e., glutamate in the MePD evoked activation of a central sympathetic reflex adjustment, whereas GABA activated a central parasympathetic one.     

Cardiovascular responses to an orthostatic challenge and electrical-stimulation-induced leg muscle contractions in individuals with paraplegia

The purpose of this study was to investigate the cardiovascular and haemodynamic responses that occur during moderate orthostatic challenge in people with paraplegia, and the effect of electrical stimulation (ES)-induced leg muscle contractions on their responses to orthostatic challenge. Eight males with complete spinal lesions between the 5th and 12th thoracic vertebrae (PARA) and eight able-bodied individuals (AB) volunteered for this study. Changes in heart rate (fc), stroke volume (SV), cardiac output (Qc), mean arterial pressure (MAP), total peripheral resistance (TPR), limb volumes and indices of neural modulation of fc, [parasympathetic (PNS) and sympathetic (SNS) nervous system indicators] were assessed during: (1) supine rest (REST), (2) REST with lower-body negative pressure at -30 torr (LBNP -30, where 1 torr = 133.32 N/m2), and (3) for PARA only, LBNP -30 with ES-induced leg muscle contractions (LBNP + ES). LBNP -30 elicited a decrease in SV (by 23% and 22%), Qc (by 15% and 18%) and the PNS indicator, but an increase in fc (by 10% and 9%), TPR (by 23% and 17%) and calf volume (by 1.51% and 4.04%) in both PARA and AB subjects, respectively. The SNS indicator was increased in the AB group only. Compared to LBNP -30, LBNP + ES increased SV (by 20%) and Qc (by 16%), and decreased TPR (by 12%) in the PARA group. MAP was unchanged from REST during all trials, for both groups. The orthostatic challenge induced by LBNP -30 elicited similar cardiovascular adaptations in PARA and AB subjects. ES-induced muscle contractions during LBNP -30 augmented the cardiovascular responses exhibited by the PARA group, probably via reactivation of the skeletal muscle pump and improved venous return.     

The Effects of Drugs Used to Treat Obesity on the Autonomic Nervous System

Objective: Body fatness is partly under hypothalamic control with effector limbs, which include the endocrine system and the autonomic nervous system (ANS). In previous studies we have shown, in both obese and never‐obese subjects, that weight increase leads to increased sympathetic and decreased parasympathetic activity, whereas weight decrease leads to decreased sympathetic and increased parasympathetic activity. We now report on the involvement of such ANS mechanisms in the action of anti‐obesity drugs, independent of change in weight. Research Methods and Procedures: Normal weight males (ages 22 to 38 years) were fed a solid food diet, carefully measured to maintain body weight, for at least 2 weeks, as inpatients at the Rockefeller University General Clinical Research Center. In a single‐blind, placebo/drug/placebo design, eight subjects received dexfenfluramine, seven phentermine (PHE), and seven sibutramine (SIB). ANS measures of parasympathetic and sympathetic activity included: determination of amount of parasympathetic control (PC) and sympathetic control (SC) of heart period (interbeat interval), using sequential pharmacological blockade by intravenous administration of atropine and esmolol. These autonomic controls of heart period are used to estimate the overall level of parasympathetic and sympathetic activities. Norepinephrine, dopamine, and epinephrine levels in 24‐hour urine collections were measured and also resting metabolic rate (RMR). Results: Sufficient food intake maintained constant body weight in all groups. PHE and SIB produced significant increases in SC but no change in PC or in RMR. In contrast, dexfenfluramine produced marked decreases in SC, PC, and RMR. For all three drugs, the effects on urine catecholamines directly paralleled changes in cardiac measures of SC. Discussion: ANS responses to PHE and SIB were anticipated. The large, and unanticipated, response to dexfenfluramine suggests further study to determine whether there could be any relation of these ANS changes to the adverse cardiovascular effects of treatment with dexfenfluramine.     

Daytime cardiac autonomic activity during one week of continuous night shift

Shift workers encounter an increased risk of cardiovascular disease compared to their day working counterparts. To explore this phenomenon, the effects of one week of simulated night shift on cardiac sympathetic (SNS) and parasympathetic (PNS) activity were assessed. Ten (5m; 5f) healthy subjects aged 18-29 years attended an adaptation and baseline night before commencing one week of night shift (2300-0700 h). Sleep was recorded using a standard polysomnogram and circadian phase was tracked using salivary melatonin data. During sleep, heart rate (HR), cardiac PNS activity (RMSSD) and cardiac SNS activity (pre-ejection period) were recorded. Night shift did not influence seep quality, but reduced sleep duration by a mean of 52 +/- 29 min. One week of night shift evoked a small chronic sleep debt of 5 h 14 +/- 56 min and a cumulative circadian phase delay of 5 h +/- 14 min. Night shift had no significant effect on mean HR, but mean cardiac SNS activity during sleep was consistently higher and mean cardiac PNS activity during sleep declined gradually across the week. These results suggest that shiftwork has direct and unfavourable effects on cardiac autonomic activity and that this might be one mechanism via which shiftwork increases the risk of cardiovascular disease. It is postulated that sleep loss could be one mediator of the association between shiftwork and cardiovascular health.     

Autonomic regulation of the heart rate in humans under conditions of acute experimental hypoxia

Autonomic regulation of the heart rate (HR) was studied in young healthy volunteers under conditions of experimental acute normobaric hypoxia. Spectral analysis of the HR variability (HRV) was performed with differential sphygmography. The total spectral power (TP) of the HRV and its low and high frequency components (LF and HF, respectively) were assessed, and the sympathovagal balance (LFn/HFn) was calculated. Acute hypoxia increased the sympathetic and decreased the parasympathetic effects on the heart and was accompanied in the majority of subjects by a significant increase in HR and a decrease in HRV. The change in the autonomic regulation of the cardiac rhythm was assumed to be a mechanism of heart activity adaptation to acute hypoxia.Translated from Fiziologiya Cheloveka, Vol. 31, No. 1, 2005, pp. 82–87.Original Russian Text Copyright © 2005 by Nesterov.     

Production of poly(3-hydroxybutyrate) from whey by fed-batch culture of recombinant Escherichia coli in a pilot-scale fermenter

Production of poly(3-hydroxybutyrate) [P(3HB)] from wheyby fed-batch culture of recombinant Escherichia coli CGSC 4401 harboring a plasmid containing the Alcaligenes latus polyhydroxyalkanoate (PHA) biosynthesis genes was examined in a 30 l fermenter supplying air only. With lactose below 2 g l^–1, cells grew to 12 g dry cell l^–1 with 9% (w/w) P(3HB) content. Accumulation of P(3HB) could be triggered by increasing lactose to 20 g l^–1. By employing this strategy, 51 g dry cell l^–1 was obtained with a 70% (w/w) P(3HB) content after 26 h. The productivity was 1.35 g P(3HB) l^–1 h^–1. The same fermentation strategy was used in a 300 l fermenter, and 30 g dry cell l^–1 with 67% (w/w) P(3HB) content was obtained in 20 h.     

Effects of angiotensin II antagonists on the contractile and hydrosmotic effect of AT II and AT III in the toad (Bufo arenarum)

The effects of peptide and non-peptide angiotensin II receptor antagonists on the responses to angiotensin II were examined using aortic rings and skin isolated from the toad. The contractile responses of aortic rings to (Ala-Pro-Gly) angiotensin II were inhibited by the angiotensin II analogue Leu⁸ angiotensin II, with a pA₂ value of 7.6. Similarly, the concentration response curve for (Ala-Pro-Gly) angiotensin II was displaced to the right by the specific angiotensin receptor subtype antagonist DuP 753, with a pA₂ value of 6.0. In contrast, the angiotensin receptor subtype 2 antagonists PD 123177 and CGP 42112A did not modify the contractile response to (Ala-Pro-Gly) angiotensin II. None of the antagonists was able to alter the contractile response to norepinephrine. Both Leu⁸ angiotensin II (10^-8 mol·l^-1) and DuP 753 (10^-6 mol·l^-1) partially inhibited angiotensin III-induced contractions in toad aorta. Angiotensin III, in turn, exhibited lower activity than [Asn¹-Val⁵] angiotensin II in this preparation, its molar potency ratio being 0.293. Previous work from this laboratory reported that osmotic water permeability in the skin of the toad Bufo arenarum was increased by angiotensin II, the effect being blocked by the peptide antagonist Leu⁸ angiotensin II. The hydrosmotic response to [Asn¹-Val⁵] angiotensin II (10^-7 mol·l^-1) was significantly inhibited by DuP 753 (10^-6 and 5×10^-6 mol·l^-1), whereas the response was not inhibited by a tenfold higher concentration of either PD 123177 or CGP 42112A. DuP 753 (10^-6 mol·l^-1) also inhibited the hydrosmotic response to angiotensin III (10^-7 mol·l^-1). These results suggest that receptors for angiotensin II present in isolated toad aorta and skin exhibit pharmacological features similar to those characterized as angiotensin subtype 1 in mammalian tissues.Abbreviations AT ₁ angiotensin receptor subtype 1 - AT ₂ angiotensin receptor subtype 2 - AT II angiotensin II - AT III angiotensin III - CDRC cumulative doseresponse curve(s) - NE norepinephrine - SCC short-circuit current     

Plasma catecholamine and nephrine responses to brief intermittent maximal intensity exercise

Catecholamines (noradrenaline, NA; adrenaline, AD; dopamine, DA) influence the metabolic and cardiovascular responses to exercise. However, changes in catecholamine metabolism during exercise are unclear. Plasma normetanephrine (NMET), metanephrine (MET) and catecholamine responses to a laboratory-based model of games-type exercise were examined. Twelve healthy men completed a resting control trial and a trial consisting of ten 6 s cycle ergometer sprints interspersed with 30 s recovery, in randomised order. Resting and post-sprint venous blood samples were taken. Plasma NA and AD increased after each sprint but DA was unaltered. Plasma nephrines increased significantly from sprint 4 onwards with peak NMET increasing 60% to 0.76 ± 0.19 nmol l⁻¹ and MET 230% to 0.37 ± 0.16 nmol l⁻¹ from resting values (P < 0.05). The results demonstrate increased catecholamine metabolism via elevated catechol-O-methyl transferase activity during intermittent sprinting. The results may aid regulation of the metabolic and cardiovascular responses to exercise by maintaining tissue adrenoceptor sensitivity to circulating catecholamines.     

Angiotensin II type-1 receptor antagonist attenuates LPS-induced acute lung injury

Angiotensin II is able to trigger inflammatory responses through an angiotensin II type 1 (AT1) receptor. The role of AT1 receptor in acute lung injury (ALI) is poorly understood. Mice were randomly divided into three groups (n = 40 each groups): NS group; LPS group (2 mg/kg LPS intratracheally); and LPS + ZD 7155 group, 10 mg/kg ZD 7155 (an AT1 receptor antagonist) intraperitoneally 30 min prior to LPS exposure. Samples from the lung were isolated and assayed for histopathology analyses or proinflammatory gene expressions, angiotensin II receptors expressions and nuclear factors activities. LPS exposure resulted in severe ALI, elevated levels of TNF-α and IL-1β mRNA expressions, and increased activities of NF-κB and activated protein (AP)-1. Upregulation of AT1 receptor and down-regulation of AT2 receptor were also observed after LPS challenge. Pretreatment with ZD 7155 significantly inhibited the increase of AT1 receptor expression and upregulated AT2 receptor expression. ZD 7155 also reduced the mRNA expression of TNF-α and IL-1β, inhibited the activation of NF-κB and AP-1, and improved lung histopathology. These findings suggest that antagonism of AT1 receptor inhibits the activation of NF-κB and AP-1 in the lung, which may mediate the release of TNF-α and IL-1β and contribute to LPS-induced ALI.     

Cartilage oligomeric matrix protein is an endogenous β-arrestin-2-selective allosteric modulator of AT1 receptor counteracting vascular injury

Compelling evidence has revealed that biased activation of G protein-coupled receptor (GPCR) signaling, including angiotensin II (AngII) receptor type 1 (AT1) signaling, plays pivotal roles in vascular homeostasis and injury, but whether a clinically relevant endogenous biased antagonism of AT1 signaling exists under physiological and pathophysiological conditions has not been clearly elucidated. Here, we show that an extracellular matrix protein, cartilage oligomeric matrix protein (COMP), acts as an endogenous allosteric biased modulator of the AT1 receptor and its deficiency is clinically associated with abdominal aortic aneurysm (AAA) development. COMP directly interacts with the extracellular N-terminus of the AT1 via its EGF domain and inhibits AT1-β-arrestin-2 signaling, but not Gq or Gi signaling, in a selective manner through allosteric regulation of AT1 intracellular conformational states. COMP deficiency results in activation of AT1a-β-arrestin-2 signaling and subsequent exclusive AAA formation in response to AngII infusion. AAAs in COMP^–/– or ApoE^–/– mice are rescued by AT1a or β-arrestin-2 deficiency, or the application of a peptidomimetic mimicking the AT1-binding motif of COMP. Explorations of the endogenous biased antagonism of AT1 receptor or other GPCRs may reveal novel therapeutic strategies for cardiovascular diseases.Subject terms: Extracellular signalling molecules, Mechanisms of disease     

Acute modulation of myocardial function by angiotensin 1–7

Angiotensin 1–7 is a bioactive heptapeptide of the renin–angiotensin system. Its cardiovascular actions have recently acquired growing relevance, mainly due to its counter-regulatory actions in the angiotensin cascade. The aim of the present study was to evaluate the actions of angiotensin 1–7 on myocardial function. Increasing concentrations of angiotensin 1–7 (10⁻⁹ to 10⁻⁵ M) were added to rabbit right papillary muscles: (1) in baseline conditions with intact endocardial endothelium (EE); (2) after selective removal of the EE with Triton X-100 (1 s, 0.01%); (3) with intact EE in the presence of the Mas receptor antagonist A-779, the AT₁ receptor antagonist ZD-7155, the AT₂ receptor antagonist PD-123,319 or the nitric oxide synthesis inhibitor NG-nitro-l-arginine (l-NA). Concerning the effects on contractility, we observed a significant decrease on active tension, dT/dt_max, peak shortening and dL/dt_max of −10.5 ± 3.6%, −8.0 ± 3.0%, −5.3 ± 2.6% and −5.7 ± 2.3%, respectively. There was no change on relaxation parameters, namely dT/dt_min or dL/dt_min. Time to half relaxation was significantly decreased. The presence of ZD-7155 or PD-123,319 did not change these effects. However, angiotensin 1–7 effects on myocardial properties were abolished after selective EE removal and in the presence of A-779 or l-NA. In conclusion, in this animal species, angiotensin 1–7 through its binding to Mas receptor induces a negative inotropic effect modulated by the EE and nitric oxide and independent of AT₁ or AT₂ receptors activation. As the effects described in the present work were influenced by the endocardial endothelium, they may be disrupted in situations associated to endothelial dysfunction, as in heart failure or myocardial ischemia.     

Analysis and evaluation of trans,trans-muconic acid as a biomarker for benzene exposure

Benzene is an important industrial chemical and, due to its occurrence in mineral oil and its formation in many combustion processes, a widespread environmental pollutant. Since benzene is hematoxic and has been classified as a human carcinogen, monitoring and control of benzene exposure is of importance. Although trans,trans-muconic acid (ttMA) was identified as a urinary metabolite of benzene at the beginning of this century, only recently has its application as a biomarker for occupational and environmental benzene exposure been investigated. The range of metabolic conversion of benzene to ttMA is about 2–25% and dependent on the benzene exposure level, simultaneous exposure to toluene, and probably also to genetic factors. For the quantitation of ttMA in urine, HPLC methods using UV and diode array detection as well as GC methods combined with MS or FID detection have been described. Sample pretreatment for both HPLC and GC analysis comprises centrifugation and enrichment by solid-phase extraction on anion-exchange sorbents. Described derivatization procedures prior to GC analysis include reaction with N,O-bis(trimethysilyl)acetamide, N,O-bis(trimethylsilyl)trifluoroacetamide, pentafluorobenzyl bromide and borontrifluoride–methanol. Reported limits of detection for HPLC methods range from 0.1 to 0.003 mg l⁻¹, whereas those reported for GC methods are 0.03–0.01 mg l⁻¹. Due to its higher specificity, GC methods appear to be more suitable for determination of low urinary ttMA levels caused by environmental exposure to benzene. In studies with occupational exposure to benzene (>0.1 ppm), good correlations between urinary ttMA excretion and benzene levels in breathing air are observed. From the reported regressions for these variables, mean excretion rates of ttMA of 1.9 mg g⁻¹ creatinine or 2.5 mg l⁻¹ at an exposure dose of 1 ppm over 8 h can be calculated. The smoking-related increase in urinary ttMA excretion reported in twelve studies ranged from 0.022 to 0.2 mg g⁻¹ creatinine. Only a few studies have investigated the effect of exposure to environmental levels of benzene (<0.01 ppm) on urinary ttMA excretion. A trend for slightly increased ttMA levels in subjects living in areas with high automobile traffic density was observed, whereas exposure to environmental tobacco smoke did not significantly increase the urinary ttMA excretion. It is concluded that urinary ttMA is a suitable biomarker for benzene exposure at occupational levels as low as 0.1 ppm. Biomonitoring of exposure to environmental benzene levels (<0.01 ppm) using urinary ttMA appears to be possible only if the ingestion of dietary sorbic acid, another precursor to urinary ttMA, is taken into account.     

Mechanisms of Virtual Reality Exposure Therapy: The Role of the Behavioral Activation and Behavioral Inhibition Systems

J. A. Gray’s (1975) theory distinguishes between two motivational systems, which he refers to as the behavioral activation system (BAS) and the behavioral inhibition system (BIS). D. C. Fowles (1980) has shown that heart rate responses reflect activity of the BAS, and electrodermal responses reflect activity of the BIS. Both BAS and BIS are reliably activated during in-vivo exposure to fearful situations (F. H. Wilhelm & W. T. Roth, 1998). However, due to the constraints imposed by virtual reality (VR), we hypothesized that VR exposure to fearful situations would activate the BIS alone. To test this hypothesis, a VR free-standing elevator simulation was presented to participants selected for high and low fear of heights. As predicted, the high-anxious group strongly responded electrodermally (effect size d = 1.53), but showed only minimal HR elevations during exposure (d = 0.12), and little other cardiovascular or respiratory changes. The low-anxious control group showed little electrodermal and HR reactivity (d = 0.28 and 0.12). A comparison with data from a previous study demonstrated that this pattern was in stark contrast to the large electrodermal and cardiovascular response observed during situational in-vivo exposure outside the laboratory. We conclude that the BIS, but not BAS, is selectively activated during VR exposure, causing discordance between self-report and commonly used physiological measures of anxiety. Results are discussed within the framework of E. B. Foa & M. J. Kozak’s (1986) emotional processing theory of fear modification, suggesting different mechanisms underlying VR and in-vivo exposure treatments.     

Serological evidence of an antibody response in farmed southern bluefin tuna naturally infected with the blood fluke Cardicola forsteri

In this study, adaptive immune response was investigated in farmed southern bluefin tuna, Thunnus maccoyii, infected with a sanguinicolid Cardicola forsteri. A cohort (Cohort₂₀₀₅) of southern bluefin tuna was sampled between March 2005 and August 2006. Samples were taken at the transfer of wild caught tuna to sea cages and then at regular intervals. Parasite intensity, abundance and prevalence data were recorded. An ELISA was developed to detect and quantify an antibody response against the blood fluke in southern bluefin tuna serum. Intensity and prevalence of the blood fluke were shown to peak in May 2005 at 10.9 flukes per infected fish (SE = 1.72) and 97.5% prevalence and then decreased to low prevalence (10%) and intensity (1.0). There were no significant changes in prevalence or intensity in 2006. Antibody titres and seroprevalence increased from 1.37 U μl⁻¹ and 10% at transfer in March 2005 to reach a peak in December 2005 of 25.86 U μl⁻¹ (SE = 6.26 U μl⁻¹) and 66.66%. No significant changes were observed in antibody titres for the same cohort of fish during 2006. Parasitological and serological values from Cohort₂₀₀₅ were compared to a 2006 cohort (Cohort₂₀₀₆) in March 2006 and August 2006 to determine if prior infection in Cohort₂₀₀₅ elicited any protection against infection in 2006. Although significant differences were not observed in intensities between cohorts it was shown that Cohort₂₀₀₅ had significantly lower abundances and prevalences of blood fluke infection than Cohort₂₀₀₆. Although there was no significant difference in mean antibody titres between cohorts in March 2006, the mean antibody titre of Cohort₂₀₀₆ was significantly greater than that of Cohort₂₀₀₅ in August 2006. No significant differences were observed in seroprevalence. This is one of the few studies to demonstrate the development of acquired resistance in fish against a parasite in an aquaculture environment under natural infection conditions.     

Peptidergic modulation of cardiovascular dynamics in the Dungeness crab,Cancer magister

Decapod crustacean pericardial organs contain extensive neurohormonal reserves which can be released directly into the haemolymph to act as physiological modulators. The present paper concerns the in vivo effects of two pericardial peptides, proctolin and crustacean cardioactive peptide, on cardiovascular dynamics in the crab Cancer magister. Infusion of proctolin into the pericardial sinus caused a slight decrease in heart rate concurrent with a large increase in cardiac stroke volume. It decreased haemolymph flow anteriorly through the paired anterolateral arteries and increased flow posteriorly and ventrally through the posterior aorta and sternal artery, respectively. The threshold for responses occurred at circulating concentrations of 10^-9 mol·l^-1, and haemolymph flows remained elevated for up to 30 min after peptide infusion. The effects of crustacean cardioactive peptide were less dramatic. Heart rate was not affected but a significant increase in stroke volume was observed. Crustacean cardioactive peptide increased haemolymph flow through the anterolateral arteries and increased scaphognathite rate. The threshold for crustacean cardioactive peptide activity was higher than for proctolin (10^-7 mol·l^-1 and 10^-6 mol·l^-1) but the responses to crustacean cardioactive peptide were of longer duration. The effects of proctolin on regional haemeolymph distribution in Cancer magister closely resemble the cardiovascular responses of this species when exposed to hypoxic conditions. These peptides may be implicated as cardiovascular regulators during environmental perturbations.     

Cardiovascular responses to exercise and muscle metaboreflex activation during the recovery from pacing-induced heart failure.

Rapid recovery of resting hemodynamics from tachycardia- or arrhythmia-induced heart failure (HF) has been demonstrated in both humans and animals. However, little is known about cardiovascular responses to exercise in animals or about reflex control of the cardiovascular system during exercise while recovering from HF. Inasmuch as the reduced cardiac output (CO) during exercise in HF has been shown to lead to underperfusion of active skeletal muscle and tonic activation of the muscle metaboreflex, an improved CO during exercise in subjects recovering from HF may lead to higher skeletal muscle blood flows and to relief of this metabolic stimulus. We investigated cardiovascular responses to graded treadmill exercise and metaboreflex activation [evoked by imposed graded reductions in hindlimb blood flow (HLBF) during mild and moderate exercise] in chronically instrumented dogs during control, mild to moderate HF (induced by rapid ventricular pacing), and recovery from HF. Most hemodynamic responses to graded exercise returned to control within 24 h of disconnecting the pacemaker. After 2 wk of recovery, CO and HLBF at each workload were significantly higher than control. In addition, whereas the increase in CO that normally occurs with metaboreflex activation was markedly attenuated in HF, it completely returned in the recovery experiments. We conclude that cardiovascular responses to graded exercise during the recovery from pacing-induced HF return rapidly to near or above control and that the increased CO and HLBF in recovery likely relieved the metabolic stimulus and tonic metaboreflex activation that may have occurred during moderate exercise in HF.     

Influence of medium composition and aeration on the synthesis of biosurfactants produced by Candida antarctica

Candida antarctica synthesised surface-active mannosylerythritol lipids at 46 g l^–1 by adding 80 g soybean oil l^–1 to the medium and maintaining the pO₂ at 50% with an air flow rate 1 vvm. Two-stage culturing of C. antarctica avoided medium foaming but the yield of biosurfactants synthesis was 28 g l^–1. The biosurfactants decreased the surface tension of water to 35 mN m^–1.