Effect of angiotensin II and endothelin‐1 receptor blockade on the haemodynamic and hormonal changes after acute blood loss and after retransfusion in conscious dogs

Francis, Roland C. E.; Höhne, Claudia; Kaczmarczyk, Gabriele; Boemke, Willehad

doi:10.1111/j.1365-201x.2004.01265.x

Cited by 11 publications

(22 citation statements)

References 41 publications

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“…In the present study there was no significant difference in CO between the groups during hypoxia. Similar findings were observed in adult dogs when the renin-angiotensin system was activated by acute blood loss in the control and losartan groups [33] . In our study, the newborn piglets had normal lungs with similar changes in CO and oxygenation during hypoxia in both groups.…”

Section: Discussionsupporting

confidence: 73%

The Role of Angiotensin II Receptor-1 Blockade in the Hypoxic Pulmonary Vasoconstriction Response in Newborn Piglets

Camelo¹,

Hehre²,

Devia³

et al. 2007

Neonatology

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Background: Angiotensin-converting enzyme activity is increased in newborn infants with respiratory distress syndrome and in animals with alveolar hypoxia. Objective: To test whether angiotensin II (Ang II) mediates the pulmonary vasoconstriction induced by acute hypoxia in newborn piglets. Methods: Eight unanesthetized chronically instrumented newborn piglets (mean ± SEM; age 6.6 ± 0.6 days; weight 2,181 ± 174 g) were randomly assigned to receive a saline solution or the Ang II type 1 receptor (AT₁) antagonist, losartan, in a crossover study design, with an interval of at least 48 h between the first and second study. Pulmonary artery (Ppa), wedge, systemic arterial (Psa) and right atrial pressures, cardiac output (CO), pulmonary (PVR) and systemic (SVR) vascular resistances, and arterial blood gases were obtained in room air, before and during the saline or losartan infusion (6 mg/kg followed by 3 mg/kg/h), and during 6 h of hypoxia (FiO₂ = 0.11) and saline or losartan infusion. Data were analyzed by repeated measures analysis of variance. Results: The pulmonary vasoconstriction induced by acute hypoxia was significantly attenuated during losartan infusion, while Psa, SVR, CO, pH, PaCO₂, PaO₂ and base excess did not differ between groups. During room air, Ppa, PVR, Psa, SVR and CO values were not modified by saline or losartan infusion. Conclusion: These data suggest that the pulmonary vasoconstriction induced by acute hypoxia in newborn piglets is partially mediated by Ang II, acting via AT₁.

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Section: Discussionsupporting

confidence: 73%

The Role of Angiotensin II Receptor-1 Blockade in the Hypoxic Pulmonary Vasoconstriction Response in Newborn Piglets

Camelo¹,

Hehre²,

Devia³

et al. 2007

Neonatology

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“…We hypothesized that a combination of xenon and remifentanil results in less cardiovascular and hormonal disturbance than two widely used isoflurane-based regimens. Animal maintenance and dietary regimen Healthy, pure-bred female Beagle dogs (mean body weight: 13.4 + 1.3 kg) of, on average, two years of age were kept under highly standardized environmental conditions (airconditioning at 218C and 55 -60% humidity) and received a dietary regimen which was standardized for sodium (2.5 mmol/kg body weight per day) and water (91 mL/kg body weight per day) intake as described previously (Hö hne et al 2002, Francis et al 2004. Daily check-ups on physical health included body weight and temperature measurement.…”

Section: Discussionmentioning

confidence: 99%

“…During a training period of at least six weeks, the dogs were gradually familiarized with the laboratory environment, the staff of investigators and the experimental procedures. The training period has been described in detail previously (Hö hne et al 2002, Francis et al 2004. The staff of investigators could provide a calming influence on the dogs by voice and petting.…”

Section: Experimental Protocolsmentioning

confidence: 99%

“…That is, their catecholamine concentrations without xenon were already in a range found only after an increase during xenon/remifentanil anaesthesia in our study (Figure 2). Apart from species differences, this might reflect a certain degree of stress being put on the pigs during instrumentation as compared with our dogs that have been accustomed to the experimental situation through weeks of training (Francis et al 2004). Beyond this, xenon was used on top of an established intravenous anaesthesia with ketamine and flunitrazepam.…”

Section: Catecholamines During Xenon Anaesthesiamentioning

confidence: 99%

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The haemodynamic and catecholamine response to xenon/remifentanil anaesthesia in Beagle dogs

et al. 2008

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SummaryThe 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 (N 2 O), (2) 0.8% isoflurane/ 0.5 mg/kg/min remifentanil or (3) 63% xenon/0.5 mg/kg/min remifentanil (n ¼ 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/N 2 O (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/N 2 O 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 (þ120%) 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.

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“…We have demonstrated that the AT 1 receptor antagonist losartan enhances hypotension and impairs CO after acute hemorrhage (20 mL kg j1 ) in nonsplenectomized, conscious (7), and isoflurane/nitrous oxideYanesthetized dogs (8).…”

Section: Introductionmentioning

confidence: 99%

Xenon/Remifentanil Anesthesia Protects Against Adverse Effects of Losartan on Hemodynamic Challenges Induced by Anesthesia and Acute Blood Loss

Francis

Philippi-Höhne

Klein³

et al. 2010

Shock

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The authors aimed to test the hypothesis that xenon anesthesia limits adverse hypotensive effects of losartan during acute hemorrhage. In six conscious unsedated Beagle dogs, the systemic and pulmonary circulation were monitored invasively, and two subsequent 60-min hypotensive challenges were performed by (a) induction (propofol) and maintenance of anesthesia with isoflurane/remifentanil or xenon/remifentanil and by (b) subsequent hemorrhage (20 mL kg⁻¹ within 5 min) from a central vein. The same amount of blood was retransfused 1 h after hemorrhage. Experiments were performed with or without acute angiotensin II receptor subtype 1 blockade by i.v. losartan (100 μg·kg⁻¹·min⁻¹) starting 45 min before induction of anesthesia. Four experiments were performed in each individual dog. Xenon/remifentanil anesthesia provided higher baseline mean arterial blood pressure (85 ± 6 mmHg) than isoflurane/remifentanil anesthesia (67 ± 3 mmHg). In losartan-treated animals, isoflurane/remifentanil caused significant hypotension (42 ± 4 mmHg for isoflurane/remifentanil vs. 71 ± 6 mmHg for xenon/remifentanil). Independent of losartan, hemorrhage did not induce any further reduction of mean arterial blood pressure or cardiac output in either group. Spontaneous hemodynamic recovery was observed in all groups before retransfusion was started. Losartan did not alter the adrenaline, noradrenaline, and vasopressin response to acute hemorrhage. Losartan potentiates hypotension induced by isoflurane/remifentanil anesthesia but does not affect the hemodynamic stability during xenon/remifentanil anesthesia. Losartan does not deteriorate the hemodynamic adaptation to hemorrhage of 20 mL kg⁻¹ during xenon/remifentanil and isoflurane/remifentanil anesthesia. Therefore, xenon/remifentanil anesthesia protects against circulatory side effects of losartan pretreatment and thus may afford safer therapeutic use of losartan during acute hemorrhage.

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Effect of angiotensin II and endothelin‐1 receptor blockade on the haemodynamic and hormonal changes after acute blood loss and after retransfusion in conscious dogs

Cited by 11 publications

References 41 publications

The Role of Angiotensin II Receptor-1 Blockade in the Hypoxic Pulmonary Vasoconstriction Response in Newborn Piglets

The Role of Angiotensin II Receptor-1 Blockade in the Hypoxic Pulmonary Vasoconstriction Response in Newborn Piglets

The haemodynamic and catecholamine response to xenon/remifentanil anaesthesia in Beagle dogs

Xenon/Remifentanil Anesthesia Protects Against Adverse Effects of Losartan on Hemodynamic Challenges Induced by Anesthesia and Acute Blood Loss

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