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Tobias, Joseph D.; Kubos, Kenneth L.; Hirshman, Carol A.
doi: N/Apmid: N/A
The effects of aminophylline on the release of endogenous catecholamines and on airway reactivity to acrosol histamine challenge were evaluated during halothane and thiopental/fentanyl anesthesia in basenji-greyhound dogs. Responses to histamine aerosol challenge (0.01, 0.03, 0.1, 0.3, 1.0, and 3.0 mg/ml) were measured during six conditions: 1) thiopental/fentanyl anesthesia (control), 2) thiopental/fentanyl with aminophylline infusion, 3) halothane anesthesia (1.5 MAC), 4) halothane anesthesia with aminophylline infusion, 5) thiopental/fentanyl anesthesia after pretreatment with iv propranolol, and 6) thiopental/fentanyl anesthesia with aminophylline infusion after pretreatment with iv propranolol. Prior to aerosol challenge baseline pulmonary resistance (RL) did not differ in the six groups. Aminophylline significantly attenuated the pulmonary response to histamine and increased catecholamine concentrations during thiopental/fentanyl anesthesia. Although halothane itself significantly attenuated the pulmonary response to histamine, the administration of aminophylline during halothane anesthesia produced no additional protective effect and no increases in catechol-amines were noted. Moreover, no protective effect was seen after aminophylline administration during thiopental/fentanyl anesthesia in the same dogs pretreated with propranolol. These data suggest that the protective effect of aminophylline on histamine reactivity results from release of endogenous catecholamines and that the use of aminophylline during halothane anesthesia, which blocks this release, is not warranted.
Palmer, Charles ; Vannucci, Robert C.; Christensen, Melanie A.; Brucklacher, Robert M.
doi: N/Apmid: N/A
To ascertain the effect of profound hypothermia on brain function and metabolism, newborn dogs were subjected to surface cooling during which regional cerebral blood flow (rCBF) and glucose utilization (rCGU) were measured with iodo-[14C]-antipyrine and 2-deoxy-[14C]-glucose, respectively. Puppies were anesthetized with nitrous oxide, paralyzed, and their lungs artificially ventilated to maintain arterial normoxia (Pao2> 60 mmHg) and normal acid-base balance (Paco2= 35–41 mmHg; pHn= 7.34–7.42). When rectal temperature was decreased from 37 to 200C, mean arterial blood pressure (MABP) decreased from 75 to 47 mmHg (P< 0.001) and heart rate from 238 to 64 beats/min (P< 0.001). Arterial Pco, was reduced from 38 to 31 mmHg (P< 0.001) (corrected to 370C), whereas pHnwas unchanged from control (7.40). The electroencephalogram slowed progressively and became isoelectric at 22–250C. During normothermia (n = 6) blood flow to 16 component structures of brain varied from 17 (occipital white matter) to 65 (medulla) ml · 100 g−1· min−1, whereas during hypothermia (n = 6) blood flow was lower in all regions (P< 0.001) at remarkably uniform levels (8.3–10.3 ml · 100 g−1· mm−1). Thus, the greatest reductions (range, 16–48% of control) in CBF occurred in those structures with the highest intrinsic flows during normothermia and were proportionately less in low flow structures. Regional CGU also decreased in all brain regions analyzed (P< 0.001). Normothermic CGU (n = 5) varied from 9 (occipital white matter) to 24 (cerebellum) μmol · 100 g−1· min−1, whereas during hypothermia rCGU (n = 5), like rCBF, was within a narrow range (0.47–0.57 μmol · 100 g−1· min−1). The percent reductions in rCGU (range, 2.0–6.5% of control) were always greater than corresponding reductions in rCBF. The findings indicate that cerebral glucose utilization is globally depressed during profound hypothermia but that CBF remains more than adequate to support the energy needs of the immature brain.
Bernards, Christopher M.; Carpenter, Randall L.; Kenter, Mark E.; Brown, David L.; Rupp, Stephen M.; Thompson, Gale E.
doi: N/Apmid: N/A
To determine what effect the addition of epinephrine has on bupivacaine toxicity, toxic doses of bupivacaine were administered to awake spontaneously breathing pigs. Twenty animals were randomized to one of two groups. One group received an infusion of bupivacaine with epinephrine (5 μg/ml) at a rate of 2 mg · kg−1· min−1; the other received an infusion of plain bupivacaine at the same rate. Bupivacaine infusion was continued until cardiovascular collapse. Following cardiovascular collapse we attempted to resuscitate the animals viaopen chest cardiac massage and a standardized resuscitation protocol. The addition of epinephrine to bupivacaine significantly increased blood pressure and systemic vascular resistance but not heart rate or cardiac output early in the bupivacaine infusion. Epinephrine had no effect on the dose of bupivacaine that caused cardiovascular collapse (P= 0.1), on the plasma concentration of bupivacaine at collapse (P= 0.9), or on the ability to resuscitate animals following cardiovascular collapse. The addition of epinephrine decreased the dose of bupivacaine required to initiate cardiac dysrhythmias (P= 0.003). The first dysrhythmia experienced by the epinephrine group was second degree heart block, which contrasts with the premature ventricular and atrial dysrhythmias experienced by the plain group. The dose of bupivacaine that produced seizures was also reduced by the addition of epinephrine (P= 0.006). The addition of epinephrine to bupivacaine did not alter the dose of bupivacaine that caused cardiovascular collapse in awake spontaneously breathing pigs but did decrease the dose of bupivacaine that caused seizures and dysrhythmias.
Riegler, Francis X.; VadeBoncouer, Timothy R.; Pelligrino, Dale A.
doi: N/Apmid: N/A
Differential somatic neural effects of interpleural bupivacaine were determined in dogs. Alterations in evoked responses were used as a marker of neural blockade. Electrode pairs were fastened to the external surface of the right seventh ribs of five male mongrel dogs (25–30 kg) at distal (D), middle (M), and proximal (P) locations. Electrodes were similarly fastened to the ipsilateral laminae of the fifth (T5L), seventh (T7L), and ninth (T9L) thoracic vertebrae, and the contralateral cranium over the sensorimotor cortex (SMC). Pediatric feeding tubes were used as interpleural catheters. Following interpleural bupivacaine (10 ml, 0.5%) intercostal nerve block was produced, as manifested by decreases in amplitude (range 12–32% of control, P< 0.05), and increases in latency (range 108–126% of control, P< 0.05), of evoked potentials recorded between T7L and rib electrodes. The block was found to localize over dependent portions of the rib with changes in animal position, indicating a strong influence of gravity. No significant changes were seen in potentials recorded between T9L and T5L, and T9L and SMC, regardless of position. T9L-T5L and T9L-SMC potentials were abolished or severely attenuated following direct subarachnoid or epidural injection of bupivacaine at T7. Thus, there are no spinal, epidural, or gross CNS effects of interpleural bupivacaine.
Eisenach, James C.; Rauck, Richard L.; Buzzanell, Charles ; Lysak, Steven Z.
doi: N/Apmid: N/A
Intrathecally administered clonidine has been reported to produce analgesia in cancer patients tolerant to intrathecal opiates. To assess the efficacy, safety, and appropriate dose of epidurally administered clonidine for the treatment of cancer pain, clonidine (range, 100–900 μg in 100-μg increments) was injected in nine patients with severe, intractable cancer pain. Clonidine produced analgesia, as measured by change in verbal pain scores, lasting more than 6 h. Clonidine also decreased blood pressure, although this effect was well tolerated and no patient met criteria for receiving iv ephedrine (>30% decrease in mean arterial pressure not responsive to 500 ml iv crystalloid infusion). Clonidine decreased heart rate 10–30% and produced transient sedation. Serum glucose and cortisol and oxyhemoglobin saturation were not altered by clonidine. Clonidine was absorbed in a dose-dependent manner into the systemic circulation, although absorption and elimination kinetics were highly variable. Following study seven patients received epidural clonidine/morphine infusions at home for periods of up to 5 months with sustained analgesia. These results suggest that epidurally administered clonidine may offer effective analgesia in patients with severe, intractable cancer pain.
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General anesthesia has been recommended to control convulsive status epilepticus that is refractory to conventional anticonvulsant therapy. Halothane has been the recommended agent, but without experimental justification. Isoflurane, which has no reported organ toxicity and produces electrographic suppression at clinically useful concentrations in normal humans, should be a better volatile anesthetic for this purpose. The efficacy and safety of isoflurane administered to control convulsive status epilepticus were assessed on 11 occasions in nine patients in seven North American hospitals. Isoflurane, administered for 1–55 h, stopped seizures in all patients and was able to be titrated to produce burst-suppression patterns on electroencephalograms. Blood pressure support with iv fluids and/or pressor infusions was required in all of the patients. Seizures resumed upon discontinuation of isoflurane on eight of 11 occasions. Six of the nine patients died. The three survivors sustained cognitive deficits. In one patient urine fluoride concentrations were elevated, although not to nephrotoxic levels. These cases suggest that isoflurane 1) is an effective, rapidly titratable anticonvulsant; 2) does not reverse underlying causes of the refractory seizures; and 3) usually necessitates hemodynamic support with fluids and/or pressors. Iso-flurane may be administered for seizures, but only when iv agents in anesthetic doses are ineffective or produce unacceptable side effects.