A comparison of the haemodynamic effects of isoflurane and halothane anaesthesia in horses

The purpose of this study was to compare the haemodynamic effects of equipotent isoflurane and halothane anaesthesia. Six adult horses were investigated on two separate occasions at least 4 weeks apart. On both occasions anaesthesia was induced by ketamine 2.2 mg/kg bwt given 5 min after i.v. administration 100 microg/kg bwt romifidine. Anaesthesia was maintained either by halothane or isoflurane (end-tidal concentrations 0.9-1.0% and 1.3-1.4%, respectively). Horses were ventilated by intermittent positive pressure to maintain PaCO2 between 40-50 mmHg. Haemodynamic variables were measured using catheter-mounted strain gauge transducers in the left and right ventricle, aorta, and right atrium. Cardiac output (CO), velocity time integral (VTI), maximal aortic blood flow velocity (Vmax) and acceleration (dv/dt(max)), left ventricular pre-ejection period (PEP) and ejection time (ET) were measured from aortic blood flow velocity waveforms obtained by transoesophageal Doppler echocardiography. Flow velocity waveforms were recorded from the femoral arteries and veins using low pulse repetition frequency Doppler ultrasound. Time-averaged mean velocity (TAV), velocity of component a (TaVa), velocity of component b (TaVb) and early diastolic deceleration slope (EDDS) were measured. Pulsatility index (PI) and volumetric flow were calculated. Microvascular blood flow was measured in the left and right semimembranosus muscles by laser Doppler flowmetry. Maximal rate of rise of LV pressure (LVdp/dt(max)), CO, Vmax, dv/dt(max), ET, VTI were significantly higher at all time points during isoflurane anaesthesia compared to halothane anaesthesia. Pre-ejection period and diastolic aortic blood pressure were significantly less throughout isoflurane anaesthesia compared to halothane. Isoflurane anaesthesia was associated with significantly lower systemic vascular resistance than halothane anaesthesia. Femoral arterial and venous blood flow were significantly higher and EDDS and PI were significantly lower during isoflurane anaesthesia compared to halothane anaesthesia. In addition during both halothane and isoflurane anaesthesia, femoral arterial flow was higher and EDDS and PI lower in the left (dependent) artery compared to the right (nondependent) artery. This study supports previous work demonstrating improved left ventricular systolic function during isoflurane compared to halothane anaesthesia. This improvement was still evident after premedication with a potent-long acting alpha2-adrenoreceptor agonist, romifidine, and induction of anaesthesia with ketamine. There was also evidence of increased hindlimb blood flow during isoflurane anaesthesia. However, there were differences observed in flow between the left and right hindlimb during maintenance of anaesthesia with each agent, suggesting that there were differences in regional perfusion in anaesthetised horses caused by factors unrelated to agents administered.     

Assessing fitness in endurance horses

A field test and a standardized treadmill test were used to assess fitness in endurance horses. These tests discriminated horses of different race levels: horses participating in races of 120 km and more showed higher values of VLA4 (velocity at which blood lactate reached 4 mmol/L) and V200 (velocity at which heart rates reached 200 beats per min) than horses of lower race levels.     

Spirometric performance in Belgian Blue calves: II. Analysis of environmental factors and estimation of genetic parameters

Genetic parameters and environmental effects for spirometric variables (SV) in calves were estimated using 734 Belgian Blue calves (15 to 297 d of age), sired by 20 AI bulls. For each calf, the following SV were measured: 1) the average ventilation (l/min) recorded during the 15 s of maximal ventilatory changes induced by lobeline administration (0.25 mg/kg, i.v.) (15-s MV(L)); 2) the vital capacity, and the maximal peak expiratory and inspiratory flows recorded after lobeline administration; and 3) the ventilatory reserve (15-s MV(L) - ventilation at rest). Analysis of environmental factors showed age of calf, herd, sex, and vaccination status had significant effects on SV. A sire model and a multiple-trait derivative-free REML procedure were used to estimate genetic parameters for SV, body weight, and muscling score. Heritabilities for SV ranged from 0.28 +/- 0.11 to 0.44 +/- 0.16. Genetic correlations among SV varied from 0.76 to 0.98 and environmental correlations from 0.69 to 0.80. Genetic correlations of SV with body weight (0.25 to 0.56) and with muscling score (0.21 to 0.76) were positive, as were environmental correlations of SV with body weight (0.44 to 0.70) and muscling score (0.09 to 0.25). These results suggest that selection may improve SV without impairing other traits of economic importance.     

p65 Homodimer activity in distal airway cells determines lung dysfunction in equine heaves

Nuclear factor-κB (NF-κB) activity, which is a key regulator of inflammatory gene expression, is increased in bronchial epithelial cells from horses suffering from heaves (a hypersensitivity-associated inflammatory condition of the lung). To determine whether this increased activity extends to distal airways and to other pulmonary cells, cells recovered by broncho-alveolar lavage (BAL) in healthy and heaves-affected horses were assessed for NF-κB activity. NF-κB activity was much higher in BAL cells from heaves-affected horses, especially during crisis (disease exacerbation), than in cells from healthy horses. Moreover, the level of NF-κB activity found in BAL cells was positively correlated to total lung resistance and to the proportion of neutrophils present in BAL fluid. Finally, prototypical p65–p50 NF-κB heterodimers were absent from BAL cells, which mostly contained p65 homodimers. These results (1) show that increased NF-κB activity is a general feature of heaves lung; (2) demonstrate the importance of p65 homodimers in neutrophilic inflammation; and (3) suggest that the use of specific NF-κB inhibitors could improve lung function in heaves-affected horses.     

Partitioning of pulmonary resistance in Friesian calves

Eight right cranial lobes of healthy Friesian calves were suspended in an airtight box. They were inflated at a constant transpulmonary pressure (Ptp) and ventilated from the outside by modifying pressures in the box with a quasi-sinusoidal pump at a frequency of 30 counts per minute. Peak-to-peak changes were 0.5 kPa. Lobar resistance (Rl) was partitioned into three components: central airway resistance (Rc), small airway resistance (Rp) and tissue resistance (Rt). Partitioning of R1 was realised at six different lung volumes. Minimal R1 was observed for a value of Ptp between 0.5 and 0.7 kPa. At a Ptp of 0.5 kPa, Rc, Rp, Rt represent 30, 15 and 55 per cent of R1, respectively. Lobar resistance increases at high and low lung volumes. Small airway resistance is small and independent of the level of lung inflation, except at low lung volumes where a marked increase is observed. Tissue resistance is relatively high and responsible for the increase of R1 at high lung volumes. Central airway resistance does not change significantly with lung volumes.     

Equine pulmonary and systemic haemodynamic responses to endothelin-1 and a selective ET(A) receptor antagonist

Based on previous in vitro studies, we hypothesised that endothelin (ET) would induce vasoconstriction in the pulmonary circululation of the horse and that this action would be mediated via ET(A) receptors. Pulmonary and systemic haemodynamic responses to endothelin-1 (ET-1), a potent vasoactive endogenous peptide, were investigated in 6 conscious, nonsedated horses at rest. Bolus i.v. injections of exogenous ET-1 (0.1, 0.2 and 0.4 microg/kg bwt) caused significant increases in pulmonary (PAP) and carotid (CAP) artery pressures, with peak increases of 79% and 51% for mean PAP and CAP, respectively. The effect of ET-1 on PAP and CAP was rapid and transient for PAP (-10 min) but prolonged for CAP (up to 60 min). ET-1 significantly decreased cardiac output by up to 35% and significantly increased systemic vascular resistance (SVR) by up to 104%. Pulmonary vascular resistance (PVR) showed a trend (P>0.05) to increase with 0.2 and 0.4 microg/kg bwt ET-1. Infusion of a selective ET(A) receptor antagonist (TBC11251) completely inhibited the responses to a subsequent bolus of 0.2 microg/kg bwt ET-1. We conclude that exogenous ET-1 exerts a potent vasoconstrictive action on the pulmonary and systemic circulations of the horse. These effects appear to be mediated largely through ET(A) receptors in both circulations. Endothelin may play a role in hypertensive conditions in the horse.     

Endothelin in the equine hypoxic pulmonary vasoconstrictive response to acute hypoxia

Elevated concentrations of endothelin (ET), a potent endothelium-derived vasoactive peptide, have been reported in a number of pathophysiological conditions associated with pulmonary hypertension, both in the horse and other species. We have previously shown, both in vitro and in vivo, that the pulmonary and systemic vascular response to exogenous ET is mediated predominantly via ET(A) receptors. Our hypothesis in the present study was that ET is involved in the equine hypoxic pulmonary vasoconstrictive response to acute hypoxia. In this study, we investigated the effects of a selective ET(A) receptor antagonist on hypoxic pulmonary hypertension in the mature horse. Horses were exposed to a 10 min period of hypoxia (F(I)O2 approximately 0.11) on 2 occasions, with and without pretreatment with the selective ET(A) receptor antagonist TBC11251 (10 mg/kg bwt i.v.). Hypoxia increased mean pulmonary artery pressure (PAP) from 18.3+/-0.9 (mean +/- s.e. normoxia) to 28.0+/-0.8 mmHg (hypoxia) in the session without ET(A) receptor antagonism. Carotid arterial pressure (CAP) also increased progressively throughout the period of hypoxic challenge and at the end was 153+/-5 mmHg (hypoxia) compared to during normoxia (140+/-5 mmHg). There was no significant overall effect of ET(A) receptor antagonism on the haemodynamic or ventilatory responses to acute hypoxia. However, between 5 and 10 min of hypoxia there was a trend for the mean PAP to diverge in the 2 treatments, which just failed to reach significance at 10 min of hypoxia (P = 0.053). In conclusion, this study describes the haemodynamic and ventilatory changes in response to a period of acute hypoxia in the adult horse. The results do not support a role for ET as a mediator of acute HPV in the horse, but suggest that it may be involved as a modulator or in the slower (>10 min) phase of HPV.