▼ Abdominelles Kompartiment Das abdominelle Kompartiment wird begrenzt von Zwerchfell, Rippen, Bauchwand, Becken, Beckenboden, Wirbelsäule und Psoasmuskulatur und schließt das Retroperitoneum ein. Ein Volumenzuwachs in diesem Kompartiment mit limitierter Compliance führt zu einem Druckanstieg, welcher je nach Ausprägung und Dauer die Durchblutung und Funktion der enthaltenen Strukturen und Organe gefährdet.

The noble gas xenon seems to have minimal cardiovascular side-effects and so may be an ideal anaesthetic agent when investigating cardiovascular physiology. In comparison with standard modern anaesthetics, we investigated the haemodynamic and hormonal effects of xenon in Beagle dogs. After a 30 min baseline period, anaesthesia was induced with propofol and maintained with either (1) 1.2% isoflurane/70% nitrous oxide (N2O), (2) 0.8% isoflurane/0.5 µg/kg/min remifentanil or (3) 63% xenon/0.5 µg/kg/min remifentanil (n = 6 per group). Haemodynamics were recorded and blood samples taken before and 60 min after induction. Mean arterial blood pressure (MAP) was higher in conscious dogs than during isoflurane/N2O (86 ± 2 vs. 65 ± 2 mmHg, mean ± SEM) and isoflurane/remifentanil anaesthesia (95 ± 2 vs. 67 ± 3 mmHg), whereas MAP did not decrease significantly in response to xenon/remifentanil anaesthesia (96 ± 4 vs. 85 ± 6 mmHg). Bradycardia was present during isoflurane/remifentanil (54 ± 2/min) and xenon/remifentanil (40 ± 3/min), but not during isoflurane/N2O anaesthesia (98 ± 3/min, P < 0.05). Xenon/remifentanil anaesthesia induced the highest reduction in cardiac output (CO) (–61%), and the highest increase in systemic vascular resistance (+120%) among all treatment groups (P < 0.05). A simultaneous increase in endogenous adrenaline and noradrenaline concentrations could only be observed in the xenon/remifentanil group, whereas angiotensin II and vasopressin concentrations increased in all groups. In conclusion, xenon/remifentanil anaesthesia maintains MAP but reduces heart rate and CO and is associated with a considerable stimulation of vasopressor hormones in Beagle dogs. Therefore, xenon/remifentanil exerts a new quality of adverse haemodynamic effects different from volatile anaesthetics and may not perform better during studies of cardiovascular physiology.

Die kardiopulmonale Reanimation (CPR) bei Kindern ist ein emotionsbehaftetes Ereignis. Laienhelfer ergreifen aus Angst, etwas falsch zu machen, oft nur verzögert oder gar keine lebensrettende Sofortmaßnahmen. Aber auch dem medizinischen Personal fehlt zuweilen die Routine im Umgang mit dem kindlichen Notfallequipment – unkoordiniertes Handeln in der Akutsituation ist die Folge. Dieser Beitrag stellt die Grundlagen der aktuellen ERC-Richtlinien einschließlich Basic und Advanced Life Support dar. Darüber hinaus nennt er Empfehlungen zur Postreanimationstherapie und zur Einbindung der Eltern.

Das Management des Atemwegs bei Neugeborenen, Säuglingen, Kleinkindern und Kindern kann aufgrund anatomischer und physiologischer Besonderheiten schwierig sein. Durch spezielle Lagerung wird dem im Vergleich zu Erwachsenen großen Hinterkopf, dem kurzen Hals und dem Larynxhochstand Rechung getragen. Bei jeder Form von Beatmung ist die physiologisch hohe Atemfrequenz, die auf einem erhöhten Sauerstoffbedarf und einer erhöhten Kohlendioxidproduktion beruht, zu berücksichtigen. Zur Sicherung des Atemweges stehen verschiedene Hilfsmittel zur Verfügung. So kann die Maskenbeatmung durch den Einsatz eines Wendl-Tubus optimiert werden. Für viele Indikationen kann zur Narkose die klassische Larynxmaske als schonendes Verfahren auch bei bestehendem Atemwegsinfekt empfohlen werden. Bei einigen Operationen und im Fall des nicht nüchternen Kindes ist die endotracheale Intubation notwendig. Hierbei muss auf die richtige Größe des Tubus und dessen Fixierungstiefe geachtet werden. Ist eine konventionelle Intubation aufgrund der Anamnese oder z. B. eines kraniofazialen Syndroms erschwert, sollte eine primär fiberoptische Intubation durchgeführt werden.

Airway management in newborns, infants, and children is a challenge to anesthesia practitioners due to the particular anatomic and physiological characteristics. The larynx is positioned more cephalad, the occiput is protuberant, and the neck is short, which makes a special position for anesthesia induction necessary. The high respiratory frequency due to high oxygen demand and carbon dioxide production has to be taken into consideration during manual as well as mechanical ventilation. Different devices are available for airway management. Simple mask ventilation can be improved by a Wendl tube. The classic laryngeal mask can be recommended as a safe airway device in many indications, specifically in children with an upper respiratory airway infection. If intubation is indicated, an optimal size and position of the endotracheal tube has to be provided. Fiberoptic endotracheal intubation is recommended if a difficult airway is known or anticipated due to a craniofacial syndrome.

Pediatric AnesthesiaVolume 16, Issue 1 p. 95-96 Anesthesia in an infant with uncorrected tetralogy of Fallot for transanal pull-through for Hirschsprung's disease Marion Haack, Marion Haack Department of Anaesthesiology and Intensive Care Medicine, Campus Virchow-Klinikum, Charité, Berlin, Germany (email: [email protected])Search for more papers by this authorAndreas Machotta, Andreas Machotta Department of Anaesthesiology and Intensive Care Medicine, Campus Virchow-Klinikum, Charité, Berlin, Germany (email: [email protected])Search for more papers by this authorWillehad Boemke, Willehad Boemke Department of Anaesthesiology and Intensive Care Medicine, Campus Virchow-Klinikum, Charité, Berlin, Germany (email: [email protected])Search for more papers by this authorClaudia Höhne, Claudia Höhne Department of Anaesthesiology and Intensive Care Medicine, Campus Virchow-Klinikum, Charité, Berlin, Germany (email: [email protected])Search for more papers by this author Marion Haack, Marion Haack Department of Anaesthesiology and Intensive Care Medicine, Campus Virchow-Klinikum, Charité, Berlin, Germany (email: [email protected])Search for more papers by this authorAndreas Machotta, Andreas Machotta Department of Anaesthesiology and Intensive Care Medicine, Campus Virchow-Klinikum, Charité, Berlin, Germany (email: [email protected])Search for more papers by this authorWillehad Boemke, Willehad Boemke Department of Anaesthesiology and Intensive Care Medicine, Campus Virchow-Klinikum, Charité, Berlin, Germany (email: [email protected])Search for more papers by this authorClaudia Höhne, Claudia Höhne Department of Anaesthesiology and Intensive Care Medicine, Campus Virchow-Klinikum, Charité, Berlin, Germany (email: [email protected])Search for more papers by this author First published: 21 December 2005 https://doi.org/10.1111/j.1460-9592.2005.01749.xCitations: 4Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1 Harjai MM. Hirschsprung's disease: revisited. J Postgrad Med 2000; 46: 52–54. CASPubMedGoogle Scholar 2 De la Torre L, Ortega A. Transanal versus open endorectal pull-through for Hirschsprung's disease. J Pediatr Surg 2000; 35: 1630–1632. 10.1053/jpsu.2000.18338 CASPubMedWeb of Science®Google Scholar 3 Gunter JB, Dunn CM, Bennie JB et al. Optimum concentration of bupivacaine for combined caudal-general anesthesia. Anesthesiology 1991; 75: 57–61. 10.1097/00000542-199107000-00010 CASPubMedWeb of Science®Google Scholar 4 Wodey E, Pladys P, Copin C et al. Comparative hemodynamic depression of sevoflurane versus halothane in infants. Anesthesiology 1997; 87: 795–800. 10.1097/00000542-199710000-00012 CASPubMedWeb of Science®Google Scholar 5 Findlow D, Doyle E. Congenital heart disease in adults. Br J Anaesth 1997; 78: 416–430. 10.1093/bja/78.4.416 CASPubMedWeb of Science®Google Scholar 6 Bichel T, Rouge JC, Schlegel S et al. Epidural sufentanil during paediatric cardiac surgery: effects on metabolic response and postoperative outcome. Paediatr Anaesth 2000; 10: 609–617. 10.1111/j.1460-9592.2000.00557.x CASPubMedWeb of Science®Google Scholar 7 Payen D, Ecoffey C, Carli P et al. Pulse Doppler ascending aortic, carotid, brachial, and femoral artery blood flows during caudal anesthesia in infants. Anesthesiology 1987; 67: 681–685. 10.1097/00000542-198711000-00011 CASPubMedWeb of Science®Google Scholar 8 Friesen RH, Veit AS, Archibald DJ et al. A comparison of remifentanil and fentanyl for fast track paediatric cardiac anaesthesia. Paediatr Anaesth 2003; 13: 122–125. 10.1046/j.1460-9592.2003.00978.x PubMedWeb of Science®Google Scholar Citing Literature Volume16, Issue1January 2006Pages 95-96 ReferencesRelatedInformation

Percutaneous central venous cannulation of small infants is a challenging procedure. The use of ultrasound guidance has been shown to increase the success rate generally in children and to decrease the incidence of associated complications. To demonstrate that this technique is also suitable in very small infants we describe the case of a preterm neonate of 850 g body weight (BW), in which percutaneous central venous cannulation was performed successfully using ultrasound imaging for guidance.

Das schwere, akute Lungenversagen (ARDS) ist eine akute inflammatorische Erkrankung, die durch eine ausgeprägte Störung des pulmonalen Gasaustausches mit einem Abfall der paO2/FIO2-Werte auf weniger als 200 mm Hg gekennzeichnet ist [1]. Die Vasokonstriktion/-okklusion in minder- bzw. nicht belüfteten Lungenarealen führt zu einer pulmonalarteriellen Hypertension. Aufgrund der Inflammation kommt es zur Bildung eines Permeabilitätsödems. Die Mechanismen, die als ursächlich für den Alveolarkollaps beim ARDS angesehen werden, sind zum einen die Gravitationskräfte in ödematösen Lungenabschnitten [2], das Gewicht des Herzens [3] [4], ein erhöhter intraabdomineller Druck [5] sowie ein Mangel und eine Dysfunktion des endogenen Surfactants [6]. Hieraus ist geschlussfolgert worden, dass ein PEEP-Niveau in der Größenordnung dieser kompressiven Kräfte notwendig ist, um die Lunge offen zu halten und den wiederholten Kollaps einzelner Alveolarbezirke zu vermeiden.

BACKGROUND:The objective of this study was to determine whether endothelin-A receptor blockade (ETAB) impairs hemodynamic and hormonal regulation compared with controls and angiotensin II receptor blockade (AT1B) during hypotensive hemorrhage in dogs under isoflurane-nitrous oxide anesthesia.METHODS:Six dogs were studied in four protocols: (1) control experiments (controls); (2) ETA blockade using ABT-627 (ETAB); (3) AT1 blockade using losartan (AT1B); and (4) combined AT1B and ETAB (AT1B + ETAB). After a 30-min awake period, isoflurane-nitrous oxide anesthesia was established (1.3 minimum anesthetic concentration). After 60 min of anesthesia, 20 ml blood/kg body weight was withdrawn within 5 min, and the dogs were observed for another hour. Thereafter, the blood was retransfused, and the dogs were observed for a final hour.RESULTS:Anesthesia: Cardiac output decreased in all protocols, whereas mean arterial pressure decreased more in AT1B and AT1B + ETAB than in controls and ETAB. Hemorrhage: After 60 min, cardiac output had decreased less in controls than in all other protocols. Mean arterial pressure decreased more during ETAB than in controls, but most severely during AT1B and AT1B + ETAB. Angiotensin II increased further only in controls and ETAB, whereas vasopressin and catecholamines increased similarly in all protocols. Retransfusion: Mean arterial pressure remained below controls in all protocols but was lowest when the AT1 receptor was blocked. Cardiac output fully recovered in all but the ETAB protocol.CONCLUSIONS:ETAB impairs long-term hemodynamic regulation after hemorrhage and retransfusion during anesthesia despite an activation of vasoconstrictive hormones. This suggests that endothelins have a role in long-term cardiovascular regulation. AT1B impairs both short- and long-term blood pressure regulation during anesthesia and after hemorrhage.

AIM:This study investigates angiotensin II and endothelin-1 mediated mechanisms involved in the haemodynamic, hormonal, and renal response towards acute hypotensive haemorrhage.METHODS:Conscious dogs were pre-treated with angiotensin II type 1 (AT1) and/or endothelin-A (ETA) receptor blockers or not. Protocol 1: After a 60-min baseline period, 25% of the dog's blood was rapidly withdrawn. The blood was retransfused 60 min later and data recorded for another hour. Protocol 2: Likewise, but preceded by AT1 blockade with i.v. Losartan. Protocol 3: Likewise, but preceded by ETA blockade with i.v. ABT-627. Protocol 4: Likewise, but with combined AT1 plus ETA blockade.RESULTS:In controls, haemorrhage decreased mean arterial pressure (MAP) by approximately 25%, cardiac output by approximately 40%, and urine volume by approximately 60%, increased angiotensin II (3.1-fold), endothelin-1 (1.13-fold), vasopressin (116-fold), and adrenaline concentrations (3.2-fold). Glomerular filtration rate and noradrenaline concentrations remained unchanged. During AT1 blockade, the MAP decrease was exaggerated (-40%) and glomerular filtration rate fell. During ETA blockade, noradrenaline increased after haemorrhage instead of adrenaline, and the MAP recovery after retransfusion was blunted. The decrease in cardiac output was similar in all protocols.CONCLUSIONS:Angiotensin II is more important than endothelin-1 for the short-term regulation of MAP and glomerular filtration rate after haemorrhage, whereas endothelin-1 seems necessary for complete MAP recovery after retransfusion. After haemorrhage, endothelin-1 seems to facilitate adrenaline release and to blunt noradrenaline release. Haemorrhage-induced compensatory mechanisms maintain blood flow more effectively than blood pressure, as the decrease in cardiac output--but not MAP--was similar in all protocols.

Acute hypoxia increases pulmonary arterial pressure and vascular resistance. Previous studies in isolated smooth muscle and perfused lungs have shown that carbonic anhydrase (CA) inhibition reduces the speed and magnitude of hypoxic pulmonary vasoconstriction (HPV). We studied whether CA inhibition by acetazolamide (Acz) is able to prevent HPV in the unanesthetized animal. Ten chronically tracheotomized, conscious dogs were investigated in three protocols. In all protocols, the dogs breathed 21% O(2) for the first hour and then 8 or 10% O(2) for the next 4 h spontaneously via a ventilator circuit. The protocols were as follows: protocol 1: controls given no Acz, inspired O(2) fraction (Fi(O(2))) = 0.10; protocol 2: Acz infused intravenously (250-mg bolus, followed by 167 microg.kg(-1).min(-1) continuously), Fi(O(2)) = 0.10; protocol 3: Acz given as above, but with Fi(O(2)) reduced to 0.08 to match the arterial Po(2) (Pa(O(2))) observed during hypoxia in controls. Pa(O(2)) was 37 Torr during hypoxia in controls, mean pulmonary arterial pressure increased from 17 +/- 1 to 23 +/- 1 mmHg, and pulmonary vascular resistance increased from 464 +/- 26 to 679 +/- 40 dyn.s(-1).cm(-5) (P < 0.05). In both Acz groups, mean pulmonary arterial pressure was 15 +/- 1 mmHg, and pulmonary vascular resistance ranged between 420 and 440 dyn.s(-1).cm(-5). These values did not change during hypoxia. In dogs given Acz at 10% O(2), the arterial Pa(O(2)) was 50 Torr owing to hyperventilation, whereas in those breathing 8% O(2) the Pa(O(2)) was 37 Torr, equivalent to controls. In conclusion, Acz prevents HPV in conscious spontaneously breathing dogs. The effect is not due to Acz-induced hyperventilation and higher alveolar Po(2), nor to changes in plasma endothelin-1, angiotensin-II, or potassium, and HPV suppression occurs despite the systemic acidosis with CA inhibition.

The pharmacokinetics of opioids are impaired in patients with liver and renal failure. Fentanyl, sufentanil, and alfentanil are metabolized in the liver. The extrahepatic metabolism by renal enzymes is gaining more importance in patients with severe liver disease. Pharmacokinetic effects of single doses of fentanyl and sufentanil are not affected in liver and renal failure; however, continuous infusion of fentanyl may result in accumulation and prolonged opioid effects. Plasma clearance and elimination of alfentanil are reduced in patients with liver failure and its clinical use can therefore not be recommended. A reduction in alfentanil dosing is not necessary in patients with renal failure. Remifentanil is the opioid of choice in patients with liver and renal failure. The clearance of morphine is reduced in liver failure. In renal failure an accumulation of morphine metabolites has been demonstrated, and thus, application of morphine is not recommended in patients with liver and renal failure. A reduction in piritramide dosing is necessary in patients with liver failure.

Acute hypoxia induces a decrease in plasma renin activity (PRA), mediated, e.g., by an increase in adenosine concentration, calcium channel activity, or inhibition of ATP-sensitive potassium channels. The decrease in PRA results in a decrease in angiotensin II (AngII) and plasma aldosterone concentration (PAC). This study investigates whether these hypoxia-induced mechanisms can be inhibited by the L-type voltage-dependent calcium channel antagonist nifedipine. Eight conscious, chronically tracheotomized dogs received a low sodium diet (0.5 mmol Na x kg body wt(-1) x day(-1)). The dogs were studied twice in randomized order, either with nifedipine infusion (1.5 microg x kg body wt(-1) x min(-1), Nifedipine) or without (Control). The dogs were breathing spontaneously: first hour, normoxia [inspiratory oxygen fraction (FiO2)=0.21]; second and third hour hypoxia (FiO2=0.1). In Controls, PRA (6.8+/-0.8 vs. 3.0+/-0.5 ngAngI x ml(-1) x min(-1)), AngII (13.3+/-1.9 vs. 7.3+/-1.9 pg/ml), and PAC (316+/-50 vs. 69+/-12 pg/ml) decreased during hypoxia (P<0.05). In Nifedipine experiments, PRA (6.5+/-0.9 vs. 10.5+/-2.4 ngAngI x ml(-1) x min(-1)) and AngII (14+/-1.1 vs. 18+/-3.9 pg/ml) increased during hypoxia, whereas the decrease in PAC (292+/-81 vs. 153+/-41 pg/ml) was blunted (P<0.05). These results foster the idea that the hypoxia-induced decrease in PRA involves L-type calcium channel activity.

Hypoxic pulmonary vasoconstriction (HPV) is encountered during ascent to high altitude. Atrial natriuretic peptide (ANP) could be an option to treat HPV because of its natriuretic, diuretic, and vasodilatory properties. Data on effects of ANP on pulmonary and systemic circulation during HVP are conflicting, partly owing to anesthesia, surgical stress or uncontrolled dietary conditions. Therefore, ten conscious, chronically tracheotomized dogs were studied under standardized dietary conditions. The dogs were trained to breathe spontaneously at a ventilator circuit. Protocol: 30min of normoxia [inspiratory oxygen fraction (FiO2)=0.21] were followed by 30min of hypoxia without ANP infusion (Hypoxia 1, FiO2=0.1) While maintaining hypoxia an intravenous infusion of atrial natriuretic peptide was started with 50ng.kg body wt(-1).min(-1) for 30min (Hypoxia+ANPI=low dose), followed by 1000ng.kg body wt(-1).min(-1) for 30min (Hypoxia+ANP2=high dose). Thereafter, ANP infusion was stopped and hypoxia maintained for a final 30min (Hypoxia 11). Compared to normoxia, mean pulmonary arterial pressure (MPAP) (16 +/- 0.7 vs. 26 +/- 1.3 mmHg) and pulmonary vascular resistance (PVR) (448 +/- 28 vs. 764 +/- 89 dyn.s(-1).cm(-5)) increased during Hypoxia I and decreased during Hypoxia+ANP 1 (MPAP 20 +/- 1 mmHg, PVR 542 +/- 55dyn.s(-1).cm(-5)) (P<0.05). The higher dose of ANP did not further decrease MPAP or PVR, but started to have a tendency to decrease mean arterial pressure and cardiac output. We conclude that low dose ANP is able to reduce HPV without affecting systemic circulation during acute hypoxia.

BACKGROUND:This study investigates whether long-term treatment with an angiotensin converting enzyme inhibitor (ACEI) impairs the hemodynamic regulation during the early phase of spinal anaesthesia.METHODS:Forty-two patients undergoing minor surgery were studied. Twenty-one patients were long-term treated (ACEI group), while the other patients served as controls (nonACEI group). All patients received a balanced electrolyte solution (6 ml kg(-1)) 20 min before spinal anaesthesia.RESULTS:Mean arterial blood pressure decreased 19% in both groups within 20 min after spinal anaesthesia. Heart rate did not change in either group. Plasma renin concentration increased from 7.3 +/- 2.1 to 12.8 +/- 4 pg ml(-1) during spinal anaesthesia in nonACEI patients (P < 0.05), whereas an elevated plasma renin level remained unchanged in the nonACEI group. The angiotensin II concentration increased in both groups during spinal anaesthesia (P < 0.05). The vasopressin concentration did not change during spinal anaesthesia in the ACEI group, but increased from 1.2 +/- 0.3 to 2.2 +/- 0.5 pg ml(-1) in patients with ACEI treatment (P < 0.05). The norepinephrine concentration increased transiently 5 min after spinal anaesthesia in both groups, and returned to baseline levels within 15 min.CONCLUSION:Long-term ACEI treatment does not further exaggerate the blood pressure decrease in the early phase of spinal anaesthesia. The increase in vasopressin concentrations in ACEI treated patients seems to be sufficient to compensate for the inhibited renin-angiotensin system. In addition, the transient increase in plasma norepinephrine, which occurs independent of preoperative ACEI treatment, seems to be involved in blood pressure regulation during spinal anaesthesia.

Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of hypoxia-induced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-sodium (LS = 0.5 mmol sodium x kg body wt-1 x day-1) or high-sodium (HS = 7.5 mmol sodium x kg body wt-1 x day-1) diet. The dogs breathed spontaneously via a ventilator circuit during the experiments: first hour, normoxia (inspiratory oxygen fraction = 0.21); second to fourth hour, hypoxia (inspiratory oxygen fraction = 0.1). During hypoxia (arterial PO2 34.4 +/- 2.1 Torr), plasma pH increased from 7.37 +/- 0.01 to 7.48 +/- 0.01 (P < 0.05) because of hyperventilation (arterial PCO2 25.6 +/- 2.4 Torr). Urinary pH and urinary bicarbonate excretion increased irrespective of the sodium intake. Sodium excretion increased more during HS than during LS, whereas the increase in potassium excretion was comparable in both groups. Thus the quick onset of bicarbonate excretion within the first hour of hypoxia-induced respiratory alkalosis was not impaired by a low sodium intake. The increased sodium excretion during hypoxia seems to be combined with a decrease in plasma aldosterone and angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.

This study compares the haemodynamic and hormonal responses during haemorrhage of conscious dogs pre-treated with an endothelin-A (ET-A) receptor inhibitor. The dogs were studied in two different randomized groups: the control group and a group that was given the ET-A receptor antagonist ABT-627 (as a bolus of 1 mg x kg of body weight(-1) followed by 0.01 mg x kg body weight(-1) x min(-1) intravenously). The time-course was the same for both groups: after a 1 h baseline period (pre-haemorrhage), blood (25 ml x kg of body weight(-1)) was withdrawn within 5 min. Haemodynamics were continuously recorded and hormone levels measured after 1 h (post-haemorrhage). Thereafter, the blood withdrawn was retransfused within 5 min and haemodynamics again observed for 1 h (post-retransfusion). In ABT-627-treated dogs, the decrease in mean arterial pressure from 87+/-3 to 64+/-3 mmHg (P<0.05 versus pre-haemorrhage), and cardiac output from 2.1+/-0.1 to 1.3+/-0.1 l x min(-1) (P<0.05 versus pre-haemorrhage) and the increase in systemic vascular resistance from 3286+/-174 to 4211+/-230 dyn.s.cm(-5) (P<0.05 versus pre-haemorrhage) during acute haemorrhage are comparable with controls. During haemorrhage in controls, vasopressin levels increased from 0+/-0 to 13+/-2 pg x ml(-1) (P<0.05 versus pre-haemorrhage), angiotensin II levels increased from 9+/-1 to 28+/-9 pg x ml(-1) (P<0.05 versus pre-haemorrhage) and adrenaline levels increased from 134+/-22 to 426+/-74 pg x ml(-1) (P<0.05 versus pre-haemorrhage) whereas noradrenaline levels did not change (approx. 200 pg x ml(-1)). In ABT-627-treated dogs, vasopressin levels increased from 0.2+/-0.0 to 22.2+/-6.1 pg x ml(-1) (P<0.05 versus pre-haemorrhage and P<0.05 versus control), angiotensin II levels increased from 8+/-1 to 37+/-8 pg x ml(-1) (P<0.05 versus pre-haemorrhage), noradrenaline levels increased from 147+/-16 to 405+/-116 pg x ml(-1) (P<0.05 versus pre-haemorrhage) and adrenaline levels did not change (200 pg x ml(-1)) during haemorrhage. We conclude from our results that dogs receiving the selective ET-A inhibitor ABT-627 seem to show a different hormonal response after haemorrhage compared with controls, displaying considerably higher noradrenaline concentrations. Independent of ET-A receptor inhibition, cardiac output during haemorrhage was maintained within the control range. This may indicate that the organism is defending blood flow (cardiac output) over blood pressure during haemorrhage, and that this defence strategy is not compromised by ET-A receptor inhibition.

This study investigated whether adenosine mediates the decrease in plasma renin activity (PRA) during acute hypoxia. Eight chronically tracheotomized, conscious beagle dogs were kept under standardized environmental conditions and received a low-sodium diet (0.5 mmol.kg body wt(-1).day(-1)). During the experiments, the dogs were breathing spontaneously via a ventilator circuit: first hour, normoxia (21% inspiratory concentration of O(2)); second and third hours, hypoxia (10% inspiratory concentration of O(2)). Each of the eight dogs was studied twice in randomized order in control and theophylline experiments. In theophylline experiments, theophylline, an A(1)-receptor antagonist, was infused intravenously during hypoxia (loading dose: 3 mg/kg within 30 min, maintenance: 0.5 mg. kg(-1). h(-1)). In theophylline experiments, PRA (5.9 +/- 0.8 ng ANG I. ml(-1). h(-1)) and ANG II plasma concentration (15.9 +/- 2.3 pg/ml) did not decrease during hypoxia, whereas plasma aldosterone concentration decreased from 277 +/- 63 to 132 +/- 23 pg/ml (P < 0.05). In control experiments, PRA decreased from 6.8 +/- 0.8 during normoxia to 3.0 +/- 0.5 ng ANG I. ml(-1). h(-1) during hypoxia, ANG II decreased from 13.3 +/- 1.9 to 7.3 +/- 1.9 pg/ml, and plasma aldosterone concentration decreased from 316 +/- 50 to 70 +/- 13 pg/ml (P < 0.05). Thus infusion of the adenosine receptor antagonist theophylline inhibited the suppression of the renin-angiotensin system during acute hypoxia. The decrease in aldosterone occurred independently and is apparently directly related to hypoxia. In conclusion, it is likely that adenosine mediates the decrease in PRA during acute hypoxia in conscious dogs.