PubMed · 4871155
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E J Campbell. 1968. Respiration.. https://doi.org/10.1146/annurev.ph.30.030168.000541
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OBJECTIVE: To evaluate anesthetic and cardiorespiratory effects of an intramuscular injection of a tiletamine-zolazepam-medetomidine combination in cheetahs. DESIGN: Prospective study. ANIMALS: 17 adult captive cheetahs. PROCEDURE: The anesthetic combination was administered intramuscularly via a dart. Induction quality, duration of lateral recumbency, duration of recovery, and quality of anesthetic reversal with atipamezole were assessed. Cardiorespiratory variables (arterial blood gas partial pressures, arterial blood pressure, heart and respiratory rates, end-tidal CO2, oxygen saturation, and rectal temperature) were measured during anesthesia. RESULTS: Sedation and lateral recumbency developed within 1.9 +/- 1.0 (mean +/- SD) and 4.3 +/- 2.0 minutes of drug administration, respectively. Clinically acceptable cardiorespiratory and blood gas values were recorded for at least 87 minutes after drug administration in all but 1 cheetah. Hypoxemia and arrhythmias developed in 1 cheetah breathing room air but resolved after treatment with oxygen. Hypertension developed in all cheetahs. Significant differences in heart and respiratory rates, mean arterial blood pressure, arterial pH, partial pressure of oxygen, and hemoglobin saturation were found between cheetahs that did and did not receive oxygen supplementation. After administration of atipamezole, sternal recumbency and mobility returned within 6.9 +/- 5.8 and 47.5 +/- 102.2 minutes, respectively. Postreversal sedation, which lasted approximately 4 hours, developed in 4 cheetahs. CLINICAL IMPLICATIONS: Tiletamine-zolazepam-medetomidine delivered via a dart provided an alternative method for induction and maintenance of anesthesia in cheetahs. Atipamezole at the dose used was effective for reversal of this combination in the initial phase of anesthesia.
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The mechanisms that control the periodicity of spontaneous epileptiform cortical potentials were investigated in the in vitro isolated guinea pig brain preparation. A brief intracortical application of bicuculline in the piriform cortex induced spontaneous interictal spikes (sISs) that recurred with high periodicity (8.5 +/- 3.1 sec, mean +/- SD). Intracellular recordings from principal neurons showed that the early phase of the inter-sIS period is caused by a GABAb receptor-mediated inhibitory potential. The late component of the interspike period correlated to a slowly decaying depolarization abolished at membrane potentials positive to -32.1 +/- 5.3 mV and was not associated with membrane conductance changes. Specific pharmacological tests excluded the contribution of synaptic and intrinsic conductances to the late inter-sIS interval. Recordings with ion-sensitive electrodes demonstrated that sISs determined both a rapid increase in extracellular K+ concentration (0.5-1 mM) and an extracellular alkalinization (0.05-0.08 pH units) that slowly decayed during the inter-sIS period and returned to control values just before a subsequent sIS was generated. These observations were not congruous with the presence of a silent period, because both extracellular increase in K+ and alkalinization are commonly associated with an increase in neuronal excitability. Extracellular alkalinization could be correlated to an sIS-induced intracellular acidification, a phenomenon that reduces cell coupling by impairing gap junction function. When intracellular acidification was transiently prevented by arterial perfusion with NH4Cl (10-20 mM), spontaneous ictal-like epileptiform discharges were induced. In addition, the gap junction blockers octanol (0.2-2 mM) and 18-alpha-glycyrrethinic acid (20 microM) applied either via the arterial system or locally in the cortex completely and reversibly abolished the sIS. The results reported here suggest that the massive cell discharge associated with an sIS induce a strong inhibition, possibly secondary to a pH-dependent uncoupling of gap junctions, that regulates sIS periodicity.