The pharmacology of chloralose

Balis, George U.; Monroe, Russell R.

doi:10.1007/bf00710911

Cited by 141 publications

(56 citation statements)

References 53 publications

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“…This probably reflects this anaesthetic's ability to sensitize the carotid sinus baroreceptors (Balis & Monroe, 1964). Inhibition of the reflex bradycardia by ketamine may be due to a vagolytic action of this agent (Traber, Wilson & Priano, 1970) or a direct inhibitory action on the baroreceptors (Dowdy & Kaya, 1968).…”

Section: Discussionmentioning

confidence: 99%

“…Anaesthetics affect a number of autonomic and haemodynamic parameters (Alper & Flacke, 1969;Priano et at., 1969;Balis & Monroe, 1964;Price, 1960;Garfield, Alper, Gillis & Flacke, 1968). Few investigators, however, have considered how the responsiveness of the cardiovascular system to drugs in the conscious animal is influenced by these agents.…”

Section: Discussionmentioning

confidence: 99%

“…Each of these agents causes specific alterations in various haemodynamic parameters (Alper & Flacke, 1969;Priano, Traber & Wilson, 1969;Balis & Monroe, 1964;Brown & Hilton, 1956). In addition, responses to cardiovascular drugs may differ qualitatively when tested under different anaesthetic agents (Giles & Burch, 1971).…”

Section: Introductionmentioning

confidence: 99%

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Cardiovascular responses to noradrenaline in the rat before and after administration of various anaesthetics

Brezenoff

1973

British J Pharmacology

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Summary1. Cardiovascular responses to intravenously administered noradrenaline were monitored in the rat in the conscious state and again following anaesthesia. Injections and pressure recordings were made via permanently implanted venous and arterial catheters. 2. The pressor response to noradrenaline was inhibited by diethyl ether, urethane and deep pentobarbitone anaesthesia. It was unchanged by ketamine and was potentiated by chloralose and light pentobarbitone anaesthesia. 3. Reflex bradycardia was potentiated by chloralose, blocked by ketamine and reduced by pentobarbitone. It was either reduced or unchanged by ether or urethane.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Cardiovascular responses to noradrenaline in the rat before and after administration of various anaesthetics

Brezenoff

1973

British J Pharmacology

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“…This is prob ably due to the fact that chloralose, in contrast to other anesthetics, does not block but rather en hances the afferent input to the cortex. In fact, the primary sensory areas of cerebral cortex are an in tegral part of a reflex loop that facilitates the sen sory-evoked myoclonic startle response typical for this type of anesthesia (Balis and Monroe, 1964;Hossmann et aI., 1971). The laminar pattern of the hemodynamic and metabolic response in the pri mary somatosensory cortex after electrical stimula tion under chloralose was similar to that in the awake animal after whisker stimulation (Dietrich et aI., 1986) and suggests that under chloralose the same intracortical circuits are activated as in the awake state.…”

Section: Discussionmentioning

confidence: 99%

Functional Activation of Cerebral Blood Flow and Metabolism before and after Global Ischemia of Rat Brain

Ueki

Linn

Hossmann

1988

J Cereb Blood Flow Metab

214

137

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Summary: The effect of somatosensory stimulation on the local CBF (LCBF), CMRglu (LCMRglu), tissue pH, and tissue content of AT P, glucose, and lactate was studied in chloralose-anesthetized rats before and after 30 min of near-complete forebrain ischemia. In nonischemic rats LCBF in primary somatosensory cortex increased by 33%, LCMRglu increased by 55%, tissue glucose content decreased by 21%, and lactate increased by 30%. Local AT P and tissue pH did not change. Functional activation of the intact chloralose-anesthetized rat, in consequence, is associated with the stimulation of "aerobic"glycolysis but does not result in disturbances of energy or acid-base homeostasis. After 30-min ischemia and 3-h recircula-The coupling between neuronal activity, blood flow, and glucose utilization is a well-documented phenomenon that has been extensively studied in the past and that provides the basis for the meta bolic mapping of functional activity of the brain (Sokoloff, 1981). The general concept of metabolic coupling is based on the assumption that the activa tion of neuronal circuits is associated with an in crease of energy and transmitter turnover that has to be fueled by an increased supply of glucose and oxygen. Recently, evidence has been provided that a period of transient cerebral ischemia suppresses the stimulation-evoked increase of glucose utiliza tion for up to several days after the ischemic impact (Dietrich et aI., 1986). The responsiveness of blood flow to changes of Pco2, which is thought to con- tribute to the flow-metabolism couple, is also sup pressed for days, if not months, after ischemia even if spontaneous and evoked electrical activity return to normal (Schmidt-Kastner et aI., 1986).If functional activation of the brain after ischemia requires the same amount of energy as in the intact brain, and if neither blood flow nor glucose con sumption is increased during activation, the brain will have to cover the increased energy demands by utilizing its energy stores. This process should lead to measurable alterations in the regional content of energy metabolites. To test this hypothesis we have studied the effect of functional activation before and after global ischemia of rat brain by combining autoradiographic measurements of local CBF (LCBF) and CMRg\u (LCMRglu) with methods for the pictorial evaluation of energy metabolites and of the acid-base state of the brain ("multiparame tric brain imaging") (Hossmann et aI., 1985).The results obtained demonstrate that following a period of severe forebrain ischemia, activation of blood flow or glucose utilization is completely sup pressed although EEG and evoked potentials re cover. Surprisingly, this dissociation does not cause any disturbances of the regional energy state of the brain, which raises the fundamental question of the

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“…Halothane, 0.25%, was given as an adjunct to oa-chloralose. The work of Bagshaw & Cox (1977) suggests that, at this concentration, its cardiovascular effects are minimal and halothane largely prevents the unwanted movements which have been described under chloralose anaesthesia (Balis & Monroe, 1964 …”

Section: Discussionmentioning

confidence: 99%

A new canine model of endotoxin shock

Evans

Hinds

Varley

1984

British J Pharmacology

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1 A new canine model of endotoxin shock has been developed in which spontaneous recovery of cardiovascular function is largely prevented, the haemodynamic effects of anaesthesia are minimized and intravascular volume replacement is given. 2 This model has been evaluated using two groups of five adult mongrel dogs anaesthetized with ca-chloralose and breathing spontaneously. Animals in one group were anaesthetized, instrumented and given Escherichia coli (E. coli) endotoxin intravenously, whilst those in the control group were subjected only to anaesthesia and instrumentation.3 E. coli endotoxin was given to dogs in the shock group as a bolus dose of 5 mg kg-lfollowed by a continuous infusion at 2 mg kg-1 h -1. This produced immediate, severe, cardiovascular depression, with precipitous falls in mean arterial pressure (MAP), cardiac index (CI), stroke index (SI) and left ventricular (LV) dp/dt max. There were associated increases in systemic and pulmonary vascular resistances. Arterio-venous oxygen content difference (C(a-v)O2) increased after induction of shock, and animals developed a progressive metabolic acidosis. Increasing haemoconcentration occurred, as evidenced by a rising haematocrit (PCV). Hypovolaemia was reflected by a concurrent fall in pulmonary capillary wedge pressure (PCWP). 4 One hour after induction of shock, intravascular volume replacement was given in the form of a colloidal gelatin solution, as a bolus dose of 10 ml kg-, followed by a continuous infusion at 10 ml kg-1 h-1. Volume replacement reversed haemoconcentration, restored PCWP and produced some haemodynamic improvement, although in general, severe cardiovascular depression persisted throughout a three hour observation period. 5 This severe endotoxin shock model has proved to be stable, reproducible and economical. It provides a useful preliminary test for new methods of treatment in hypodynamic endotoxin shock, as well as allowing investigation of acute metabolic and physiological changes. IntroductionAnimal models have been widely used for the investigation of septic shock, a condition which in man still carries a mortality of up to 50% (Schumer, 1979).Many workers have performed endotoxin-based experiments, and there is a wealth of literature describing the effects of endotoxin in different species of experimental animals (Halmagyi et al., 1963;Brockman et al., 1967; Kuida etal., 1971; Balis etal., 1978;Morris et al., 1979). This subject has been comprehensively reviewed by Gilbert (1960).However, concern has recently been expressed with regard to the clinical relevance of endotoxin models (Wichterman et al., 1980) and alternatives which attempt to represent more exactly the clinical situation have been suggested. These have included 1Correspondence. the intravenous infusion of live bacteria into mongrel dogs, sheep, pigs and rhesus monkeys (Pool et al., 1977;Hinshaw et al., 1979;Fairman & Glauser, 1980;Gahos et al., 1982). Other models have involved the induction of peritonitis, for example, by implantation of a septic sponge or ...

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The pharmacology of chloralose

Cited by 141 publications

References 53 publications

Cardiovascular responses to noradrenaline in the rat before and after administration of various anaesthetics

Cardiovascular responses to noradrenaline in the rat before and after administration of various anaesthetics

Functional Activation of Cerebral Blood Flow and Metabolism before and after Global Ischemia of Rat Brain

A new canine model of endotoxin shock

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