Severe hypoxaemia in field-anaesthetised white rhinoceros (Ceratotherium simum) and effects of using tracheal insufflation of oxygen

White rhinoceros anaesthetised with etorphine and azaperone combination develop adverse physiological changes including hypoxia, hypercapnia, acidosis, tachycardia and hypertension. These changes are more marked in field-anaesthetised rhinoceros. This study was designed to develop a technique to improve safety for field-anaesthetised white rhinoceros by tracheal intubation and oxygen insufflation. Twenty-five free-ranging white rhinoceros were anaesthetised with an etorphine and azaperone combination for translocation or placing microchips in their horns. Once anaesthetised the rhinoceros were monitored prior to crating for transportation or during microchip placement. Physiological measurements included heart and respiratory rate, blood pressure and arterial blood gas samples. Eighteen rhinoceros were intubated using an equine nasogastric tube passed nasally into the trachea and monitored before and after tracheal insufflation with oxygen. Seven rhinoceros were not intubated or insufflated with oxygen and served as controls. All anaesthetised rhinoceros were initially hypoxaemic (percentage arterial haemoglobin oxygen saturation (% O2Sa) = 49 % + 16 (mean + SD) and PaO2 = 4.666 + 1.200 kPa (35 + 9 mm Hg)), hypercapnic (PaCO2 = 8.265 + 1.600 kPa (62 + 12 mm Hg)) and acidaemic (pHa = 7.171 + 0.073 ). Base excess was -6.7 + 3.9 mmol/ℓ, indicating a mild to moderate metabolic acidosis. The rhinoceros were also hypertensive (systolic blood pressure = 21.861 + 5.465 kPa (164 + 41 mm Hg)) and tachycardic (HR = 107 + 31/min). Following nasal tracheal intubation and insufflation, the % O2Sa and PaO2 increased while blood pHa and PaCO2 remained unchanged.Tracheal intubation via the nose is not difficult, and when oxygen is insufflated, the PaO2 and the % O2Sa increases, markedly improving the safety of anaesthesia, but this technique does not correct the hypercapnoea or acidosis. After regaining their feet following reversal of the anaesthesia, the animals' blood gas values return towards normality.

Electronic Analysis of Intrinsic Laryngeal Muscles in Canine Sound Production

This study explores the relationship between voice production and intrinsic laryngeal muscle (ILM) activities as expressed by orderly recruitment of their specific motor units. In 5 dogs, both the recurrent laryngeal nerve (RLN) and the vagus nerve (cranial nerve X) were stimulated via tripolar electrodes with stimulating frequencies (Fs) of 10 to 60 Hz and 0 to 7 mA during application of symmetric 600 Hz, 7 to 0 mA blocking currents. The fundamental frequency (F0) and the intensity (I) of sounds generated by tracheal insufflation of humidified air were recorded while electromyograms of the cricothyroideus (CT), thyroarytenoideus (TA), and posterior cricoarytenoideus (PCA) were obtained via surface electrodes. Contractions of the CT were concurrently induced by stimulating the superior laryngeal nerve (SLN). The recruitment rates were highly specific and were affected by which nerve was stimulated. For the RLN, PCA ramping was lowest for Fs of ≤50 Hz. For Fs of 10 to 30 Hz, the recruitment rate of the TA was significantly steeper than that for the other ILMs, and the CT had the highest rate for Fs of 40 to 50 Hz. Conversely, for the vagus nerve, PCA recruitment was highest for Fs of ≥30 Hz. The average F0 was significantly higher with the RLN than with the vagus nerve. When the TA recruited faster than the CT (ie, via the RLN, but not the vagus nerve), the F0 was higher. While only CT ramping was significantly related to changes in sound intensity, there was a trend toward a decrease when PCA ramping was higher than CT ramping, as occurred when only the vagus nerve was stimulated. Stimulation of the SLN always increased F0 and loudness. We conclude that changes in F0 occur mainly through RLN-mediated CT and TA contraction. Loudness is controlled by the CT. The PCA exerts reciprocal coupling on both functions via the vagus nerve, and they are boosted across the board by the SLN. These findings may allow artificial manipulation of voice.

Intra-airway gas transport during high-frequency chest vibration with tracheal insufflation in dogs

High-frequency external chest vibration with tracheal insufflation (high-frequency vibration ventilation) has previously been shown to be an effective mode of artificial ventilation in experimental animals. To investigate the intra-airway gas mixing during high-frequency vibration ventilation (frequency 30 Hz, amplitude 0.4 cm), we used an analysis of the single-breath washout curve that gives the vibration-induced mixing coefficient distribution relative to the no-vibration situation. Data from four anesthetized dogs were collected during constant-flow insufflation at six rates (0.05–0.4 l.min-1.kg-1), at three insufflation durations (2, 4, and 7 s), and with the insufflation catheter outlet at three positions (carina, trachea, and a bronchus) while the vibration was on and off. Vibration enhanced intra-airway gas mixing 14.1 +/- 3.9-fold, with the peak of the enhancement distribution located 125 +/- 29 ml from the airway opening and a distribution width of 121 +/- 29 ml. As insufflation flow increased, the position of the peak enhancement shifted toward the alveolar zone and diminished in peak amplitude. Changing the insufflation duration and the catheter position did not affect the intra-airway mixing induced by vibration. External chest vibration causes a substantial increase of intra-airway gas mixing, bringing alveolar gas to central airways. This leads to overall increased pulmonary gas transport when fresh gas is insufflating the tracheal carina area.

Cellular distribution of pulmonary Mn and CuZn superoxide dismutase: effect of hyperoxia and interleukin-1.

Pulmonary superoxide dismutase (SOD) plays an important role in the lung defense against O2 toxicity. We have previously demonstrated that tracheal insufflation of interleukin-1 alpha (IL-1) selectively enhances pulmonary MnSOD and protects rats against O2 toxicity. However, little is known about the cellular distribution of pulmonary MnSOD- and CuZnSOD-specific proteins. We performed immunohistochemistry in plastic sections (2 microns thick) to determine the effects of hyperoxia and IL-1 on the cellular distribution of pulmonary MnSOD and CuZnSOD in rats. MnSOD and CuZnSOD were present in all lung cells. Smooth muscle and endothelial cells appeared to contain higher immunoreactive MnSOD and CuZnSOD proteins than other lung cell types. Exposure of rats to 100% O2 for 24 hr had no effect on the cellular distribution and intensity of pulmonary MnSOD. However, at 50 hr after O2 exposure the intensity of pulmonary MnSOD was reduced. In contrast, tracheal insufflation of IL-1 markedly enhanced the intensity of pulmonary MnSOD in rats exposed to O2 for 50 hr. Neither O2 exposure nor IL-1 insufflation had any apparent effect on the distribution and intensity of pulmonary CuZnSOD. We conclude that IL-1 selectively enhances pulmonary MnSOD and that this effect is manifested in most lung cells, particularly smooth muscle and endothelial cells.