Pulmonary Vascular Response to Carotid Sinus Hypotension in the Awake and Anaesthetized Dog (original) (raw)
Related papers
British Journal of Anaesthesia, 1999
Inhaled nitric oxide, a selective pulmonary vasodilator, is known to improve arterial oxygenation after cardiopulmonary bypass and during acute respiratory distress syndrome in humans. During general anaesthesia with spontaneous ventilation, healthy adult horses develop large alveolar-arterial oxygen tension differences. In this study, we have determined the effects of inhaled nitric oxide (10 parts per million (ppm)) on venous admixture and pulmonary haemodynamics in horses anaesthetized with halothane. Seven adult horses were studied twice in random sequence. After premedication with romifidine 100 µg kg -1 , anaesthesia was induced with ketamine 2.2 mg kg -1 and maintained with 1.1 MAC (0.95%) of halothane in oxygen. Horses breathed spontaneously. After 65 min, each horse had nitric oxide 10 ppm added to the inspired gas for 20 min (procedure HAϩNO) or anaesthesia was continued with halothane in oxygen (procedure HA). Cardiac output, minute ventilation, arterial and mixed venous oxygen and carbon dioxide tensions, and mean pulmonary and carotid arterial pressures were measured for 100 min. Shunt fraction and pulmonary and systemic vascular resistances were calculated. Shunt fraction (SF) and mean pulmonary artery pressure (P PA mean ) were not different between the two groups after 65 min of general anaesthesia (HA: SF 0.20 (SD 0.06), P PA mean 45 (8) mm Hg; HAϩNO: SF 0.21 (0.04), P PA mean 44 (7) mm Hg) or after 85 min (HA: SF 0.22 (0.07), P PA mean 45 (8) mm Hg; HAϩNO: SF 0.20 (0.03), P PA mean 43 (7) mm Hg). There were no significant effects of time or nitric oxide inhalation on any other variable. There was a significant correlation (rϭ0.80, PϽ 0.05) between calculated shunt fraction 65 min after induction of anaesthesia and body weight. 1999; 83: 321-4
Baroreceptor Control of Regional Haemodynamics During Halothane Anaesthesia in the Dog
BJA: British Journal of Anaesthesia, 1977
Regional haemodynamic control by the cardiovascular baroreceptors was examined in dogs anaesthetized with 1 + MAC of halothane in oxygen (1%). The open-loop relationships between carotid sinus pressure (CSP) and regional haemodynamics in the iliac, renal, mesenteric, aortic and coeliac beds were examined before vagotomy, following vagotomy and following thoracotomy. Around the carotid sinus reflex set point, the ratio of the reflex decrease in systemic arterial pressure to an increase in CSP (reflex gain) was-0.744 + 0.089 (mean ±SEM): the latter increased to-1.275 ± 0.093 following vagotomy. Reflex resistance changes were greatest in the renal bed and least in the coeliac bed, reflecting blood flow homeostasis which was well preserved in the renal bed but minimal in the coeliac bed. Thoracotomy in the dogs in which vagotomy had been performed resulted in no significant changes in the dependent variables studied. It is concluded that, in these dogs anaesthetized with 1 + MAC of halothane, baroreceptor control of regional pressure flow relationships is well preserved.
Veterinary Anaesthesia and Analgesia, 2007
Objective To compare the cardiorespiratory changes induced by equipotent concentrations of halothane (HAL), isoflurane (ISO) and sevoflurane (SEVO) before and after hemorrhage.Study design Prospective, randomized clinical trial.Animals Twenty-four healthy adult dogs weighing 15.4 ± 3.4 kg (mean ± SD).Methods Animals were randomly allocated to one of three groups (n = 8 per group). In each group, anesthesia was maintained with 1.5 minimum alveolar concentration of HAL (1.3%), ISO (1.9%) and SEVO (3.5%) in oxygen. Controlled ventilation was performed to maintain eucapnia. Cardiorespiratory variables were evaluated at baseline (between 60 and 90 minutes after induction), immediately after and 30 minutes after the withdrawal of 32 mL kg−1 of blood (40% of the estimated blood volume) over a 30-minute period.Results During baseline conditions, ISO and SEVO resulted in higher cardiac index (CI) than HAL. Heart rates were higher with SEVO at baseline, while mean arterial pressure (MAP) and mean pulmonary arterial pressure did not differ between groups. Although heart rate values were higher for ISO and SEVO after hemorrhage, only ISO resulted in a higher CI when compared with HAL. In ISO-anesthetized dogs, MAP was higher immediately after hemorrhage, and this was related to better maintenance of CI and to an increase in systemic vascular resistance index from baseline.Conclusions Although the hemodynamic responses of ISO and SEVO are similar in normovolaemic dogs, ISO results in better maintenance of circulatory function during the early period following a massive blood loss.Clinical relevance Inhaled anesthetics should be used judiciously in animals presented with blood loss. However, if an inhalational agent is to be used under these circumstances, ISO may provide better hemodynamic stability than SEVO or HAL.
Chemoreceptor influence on pulmonary blood flow during unilateral hypoxia in dogs
Respiration physiology, 1977
Dogs anesthetized with 30 mg/kg pentobarbital were artificially respired after differential cannulation of the main stem bronchi. Following median sternotomy, blood flow was monitored by electromagnetic flow probes on the left pulmonary artery (QL) and on the pulmonary trunk or aorta, QT. Following 10 min of bilateral 100% O2, QL was 42.5 +/- 7% of QT. When 6% O2, was substituted as the gas mixture inspired by the left lung while the right lung remained on 100% O2, PaO2 was above 70 mm Hg and QL fell to 24.5 +/- 5% of QT. Room air was then used to ventilate the right lung while the left lung remained on 6% O2. This caused PaO2 to fall to 42.3 +/- 3 MM Hg and QL to rise to 38.3 +/- 6% QT. This increase in blood flow to the unilaterally hypoxic lung during systemic hypoxemia did not occur in dogs after peripheral chemoreceptor denervation. Therefore, interference with the local response to alveolar hypoxia during systemic hypoxemia appears to be mediated by the arterial chemoreceptors.
Hypoxic pulmonary vasoconstriction and the pharmacologically denervated lung
Anaesthesia, 1982
The roles of the autonomic nervous system and cardiac output on h,yoxicpulmonary vasoconstriction were studied in 15 mongrel dogs anaesthetised with intravenous pentobarbitone (30 rriglkg) and the lungs mechanically ventilated to maintain normal arterial blood gases. After a hypoxic challenge in Group I (n = 6 ) and Group II (n = 3) animals, autonomic denervation M.'US achieved by total spinal block with tetracaine (20 mg) injected into the cisterna magna. Group I animals receiveda large volume of intravenous j u i d (80 mltkg normal saline) before the block while Group II animals were given minimum fluid. When Group I animals were exposed to 10% inspired oxygen, mean pulmonary arterial pressure increased by 88 and by 72% before and after the block, respectively. The cardiac output increased by 279. ; with hypoxia before the block while it didnot change significantly with hypoxia after the block. The pulmonary vascular resistance increased by 65 and by 152% with hypoxia before and after the block. Group 11 animu1.r were also exposed to 10% inspired oxygen. They showed u similar response to Group I anima1.s before the block. However, after the block irreversible hypotension developed with hypoxia.
Effects of halothane on respiratory mechanics and lung histopathology in normal rats
British Journal of Anaesthesia, 2000
It is generally accepted that halothane reduces airway and tissue resistance in lungs with preexisting airway tone. However, under conditions of resting airway tone, pulmonary resistance remains unaltered. In this study, we have determined the effects of halothane on respiratory system, pulmonary and chest wall resistive, elastic and viscoelastic mechanical properties, and related the results to findings from lung histology in intact normal rats. Sixteen adult male Wistar rats were allocated randomly to one of two groups (nϭ8 in each group): control or halothane group. In the control group, animals were sedated with diazepam 5 mg i.p. and anaesthetized with pentobarbital 20 mg kg-1 i.p. In the halothane group, the anaesthetic was administered at an end-tidal concentration of 1 MAC throughout the study. Rats were paralysed and underwent mechanical ventilation. Halothane decreased airway resistance but increased the tissue component of resistance (caused by viscoelastic elements and lung inhomogeneity). Static and dynamic elastance also increased with halothane anaesthesia. Pulmonary resistance remained unchanged. Lung histopathology demonstrated airway dilatation and a greater degree of lung collapse and hyperinflation in the halothane group. We conclude that halothane anaesthesia acts both on airway and lung tissue. In airway tissue, dilatation occurs but the lung periphery stiffens. Consequently, these opposing effects result in no overall apparent change in mechanical properties, although changes are observed during halothane anaesthesia in normal animals and subjects.
Ankara Üniversitesi Veteriner Fakültesi Dergisi, 2009
The objective of this study was to investigate the cardiopulmonary effects of sevoflurane (SEV), isoflurane (ISO) and halothane (HAL) anesthesia during spontaneous ventilation (SV) or controlled ventilation (CV) in dogs. An experimental study was designed. Sixty healthy cross breed dogs were used for the study. Dogs were randomly allocated to six anesthesia groups (n = 10 in each group): SEV/SV; SEV/CV; ISO/SV; ISO/CV; HAL/SV; HAL/CV. After premedication with xylazine HCl, anesthesia was induced with thiopental sodium. Inhalation anesthesia was maintained for 90 minutes with SEV, ISO, or HAL. Cardiopulmonary parameters [heart rate (HR), respiratory rate (RR), mean arterial blood pressure (MAP), end tidal carbon dioxide level (ETCO 2), oxygen saturation (SpO 2), central venous pressure (CVP), body temperature, arterial partial pressure of oxygen (PaO 2), arterial partial pressure of carbon dioxide (PaCO 2), and arterial pH] were measured after induction of anesthesia; the first measurement was taken one minute after the loss of consciousness with SEV, ISO, or HAL and the others were done at 15th, 30th, 45th, 60th and 90th minutes. There was not any significant difference in HR between anesthetics among SV and CV. RR decreased significantly during ISO and HAL anesthesia in SV (p<0.001). MAP decreased significantly in all groups but there was not any significant difference between the ventilation modes. There was a significant decrease in ETCO 2 during CV compared to SV (p<0.001). The CVP values during anesthesia with SEV in SV were lower than those of other anesthetics (p<0.001). Body temperature decreased significantly during ISO and HAL anesthesia compared to SEV anesthesia (p<0.001). Compared with SV, CV prevented the increase in PaCO 2 (p<0.001) and no decrease in pH was observed (p<0.05). It is concluded that SEV anesthesia was appeared to have minimum complications on cardiopulmonary parameters in the healthy dogs which were premedicated with xylazine HCL and inducted with thiopental sodium. In the study, the use of CV was not associated with cardiovascular embarrassment during inhalation anesthesia and it was provide a more stable plane of anesthesia.
European Journal of Pharmacology, 1997
This study examined whether a clinically relevant concentration of the volatile anaesthetic halothane modifies the endothelium-depen-Ž. Ž. Ž. dent relaxation produced by acetylcholine 3 nM-10 mM , histamine 1 pM-0.1 mM and anti-human immunoglobulin E 1:1000 in human isolated pulmonary arteries submaximally precontracted with noradrenaline. An inhibitor of nitric oxide formation, N G-nitro-L-Ž. arginine 100 mM , attenuated acetylcholine-induced relaxation but failed to inhibit histamine-and anti-human immunoglobulin Ž. E-induced relaxation. Indomethacin 2.8 mM, a cyclooxygenase inhibitor preferentially reduced the relaxation to histamine and Ž. anti-human IgE. Halothane 2% significantly attenuated the relaxation to acetylcholine but had no significant effect on the relaxation Ž. elicited by histamine and anti-human IgE. Halothane 2% enhanced the basal release of prostaglandin I by human pulmonary arteries 2 Ž y1 y1. Ž. control 0.31 " 0.04 ng mg ; treated tissues 0.50 " 0.06 ng mg ; n s 5; P-0.05. Halothane 2% did not alter the responsiveness Ž. Ž and sensitivity of preparations to relaxants acting through activation of adenylyl cyclase forskolin or guanylyl cyclase sodium. Ž. nitroprusside or by the opening of K channels cromakalim. In conclusion, halothane inhibits the endothelium-dependent relaxation ATP of human pulmonary arteries to acetylcholine by interfering with the nitric oxide pathway at a site before activation of soluble guanylyl cyclase in vascular smooth muscle.
Anaesthesia, 2010
The relative order of potency of anaesthetic agents on the hypoxic ventilatory response has been tested in humans, but animal data are sparse. We examined the effects of 1.4, 1.6, 1.8, and 2.0 MAC halothane, isoflurane, and sevoflurane on phrenic nerve activity in euoxia (baseline) and during acute normocapnic hypoxia (inspired oxygen fraction 0.09) in adult male Sprague-Dawley rats. With halothane, all animals became apnoeic even in euoxia, and the hypoxic response was completely abolished at all anaesthetic levels. With isoflurane, 5 of 14 animals exhibited phrenic nerve activity in euoxia at 1.4 MAC and demonstrated a hypoxic response (302% of baseline activity), but all became apnoeic and lost the hypoxic response at higher doses. With sevoflurane, phrenic nerve activity and a hypoxic response was preserved in at least some animals at all doses (i.e. even the highest dose of 2.0 MAC). Similar to the rank order of potency previously observed in humans, the relative order of potency of depression of the hypoxic ventilatory response in rats was halothane (most depressive) > isoflurane > sevoflurane (p = 0.01 for differences between agents).