The effects of chloralose‐urethane and sodium pentobarbitone anaesthesia on the local and autonomic components of the circulatory response to arterial hypoxia

Korner, Paul I.; Langsford, G.; Starr, David S.; Uther, John B.; Ward, Wendy L.; White, Saxon William

doi:10.1113/jphysiol.1968.sp008654

Cited by 45 publications

(32 citation statements)

References 33 publications

(32 reference statements)

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“…Changes in HR and ABP produced by chemical stimuli are thus the net result of these complicated interactions and differ greatly in different experimental conditions in various animal species [24]. Responses also differ at different levels of chemical stimuli and condition of anesthesia [25]. However, in the present study, the anesthetic used was the same in both groups, and blood gas tension and pH changes due to hypoxia were also not significantly different in between the groups.…”

Section: Discussioncontrasting

confidence: 45%

Hemodynamic Responses to Hypoxia and Hypercapnia during Acute Normovolemic Hemodilution in Anesthetized Cats.

Talwar

Fahim²

2000

JJP

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Systemic changes in arterial blood gas evoke many cardio-respiratory responses mediated by central and or peripheral chemoreceptors [1]. Hypoxia causes cardiac depression in patients with acute hypoxemic respiratory failure [2] and depression in myocardial tissue and isolated hearts [3][4][5]. Hypercapnia decreases myocardial contractility. Gudipati et al. [6] and Planta et al. [7] have suggested that respiratory acidosis contributes to cardiovascular dysfunction and mortality. Acute respiratory acidosis (pH 7.09, PCO 2 92 mmHg) decreases left ventricular contractility, increases end systolic volume in anesthetized dogs [8] and causes left ventricle (LV) contractile dysfunction accompanied by an increased oxygen cost of contractility [9]. The fall in myocardial contractility during respiratory acidosis is only partially blocked by the adrenergic activation. Stein and Ellsworth [10] observed that, under the conditions of a severely limited oxygen supply resulting from a combined effect of acute fall in hematocrit and hypoxic ventilation, a diffusion limitation for oxygen resulting from the kinetics of oxygen release from the hemoglobin molecule provides an advantage for oxygen exchange within the capillary network. They suggested that oxygen content rather than PO 2 might be a critical determinant of oxygen supply at low levels of oxygen delivery. Japanese Journal of Physiology, 50, 227-234, 2000 Key words: hemodilution, hypoxia, hypercapnia.Abstract: The present study was undertaken to evaluate the effects of hypoxia and hypercapnia on circulatory parameters during acute normovolemic hemodilution. Cats anesthetized with a mixture of ␣-chloralose and urethane were maintained by positive pressure ventilation. Muscles were paralysed by intramuscular vecuronium (0.1 mg/kg) to eliminate reflex respiratory movements. Cats were exposed to hypoxia (12% O 2 and 7% O 2 ) and hypercapnia (4% CO 2 and 7% CO 2 ) at normal hematocrit (Ht 40.1Ϯ2.8%) and then at graded levels of normovolemic hemodilution (Ht 24.0Ϯ2.0% and Ht 13.0Ϯ1.5%, respectively). Left ventricular pressure (LVP), LV dP/dt max , arterial blood pressure (ABP), heart rate (HR), and right atrial pressure (RAP) were recorded on a polygraph. Cardiac output (CO) was measured using a cardiac output computer. Hemodilution per se did not produce any significant change in ABP, RAP or LV dP/dt max , however, it produced a significant rise in HR and a significant fall in total peripheral resistance (TPR). Exposure to hypoxic gas mixtures caused significant increases in HR and CO at control Ht; but after hemodilution it caused the reverse effects. Hypercapnia did not produce any significant effect on ABP, LV dP/dt max or RAP either at control Ht or after hemodilution. Hypercapnia produced a fall in HR, CO and stroke volume (SV) at normal Ht and percent fall in HR response was enhanced following hemodilution. The reversal of chronotropic response to hypoxia and enhanced bradycardia response to hypercapnia, under conditions of acute normovolemic hemodilution would be de...

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Section: Discussioncontrasting

confidence: 45%

Hemodynamic Responses to Hypoxia and Hypercapnia during Acute Normovolemic Hemodilution in Anesthetized Cats.

Talwar

Fahim²

2000

JJP

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“…was given to the animal. This dose of relaxant has no significant vagolytic action in the rabbit (Korner, Langsford, Starr, Uther, Ward & White, 1968).…”

Section: Methodsmentioning

confidence: 80%

“…Assuming that as with hypoxia (cf. Korner et al 1968) the local effects of anaesthesia are the same in both preparations, the difference in the change in total peripheral resistance reflects an increase in peripheral constrictor activity in the normal animal.…”

Section: Discussionmentioning

confidence: 91%

“…A comparison of the differences in the response during anaesthesia in normal and 'de-efferented' animals shows the approximate magnitude of the autonomic effects in the normal animal as discussed in detail in an accompanying paper (Korner et al 1968). The present results indicate that the reduction in total peripheral resistance during anaesthesia is considerably smaller in the normal than in the 'de-efferented' rabbit (Fig.…”

Section: Discussionmentioning

confidence: 95%

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Circulatory effects of chloralose‐urethane and sodium pentobarbitone anaesthesia in the rabbit

Korner¹,

Uther²,

White³

1968

The Journal of Physiology

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SUMMARY1. The effects of chloralose-urethane and sodium pentobarbitone anaesthesia on heart rate, blood pressure and cardiac output were studied in normal rabbits, in animals given atropine and in animals without functioning autonomic effectors. The findings under anaesthesia were compared during spontaneous and artificial intermittent positive pressure respiration.2. The circulatory effects of chloralose-urethane and sodium pentobarbitone anaesthesia differed significantly for the first hour after induction of anaesthesia. During the subsequent 3 hr of maintained anaesthesia differences in the circulatory effects of the two anaesthetics were small.3. The direct local effects of these anaesthetics were assessed during the maintenance phase from the responses of animals without functioning autonomic effectors. With both anaesthetics there was peripheral vasodilatation and minimal effects on heart rate.4. The autonomic activity in the normal animal was assessed by comparing the changes in normal, atropinized and 'de-efferented' rabbits without functioning autonomic effectors. During chloralose-urethane anaesthesia there was reduction in cardiac vagal efferent activity and no change in cardiac sympatho-adrenal activity. With both anaesthetics there was an increase in peripheral sympatho-adrenal constrictor activity, tending to minimize the local vasodilator effects.

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“…There is some circumstantial evidence from studies in anaesthetized animals which lend further support to this idea. It has been observed that anaesthesia augments the renin response to ACE-inhibition (Bing & Poulsen, 1975), and anaesthesia is known to depress the function of some central synapses, distorting the autonomic nervous response to various cardiovascular stimuli, in favour of sympathetic outflow (Korner et al, 1968;Zimpfer et al, 1974;Dorward et al, 1985). It would therefore seem that the renal sympathetic innervation is conveniently placed to mediate the release of renin following ACE-inhibition.…”

Section: Discussionmentioning

confidence: 99%

The effects of combined angiotensin converting enzyme inhibition and β‐adrenoceptor blockade on plasma renin activity in anaesthetized dogs

Cambridge

Whiting

Butterfield

et al. 1992

British J Pharmacology

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1 The effects of P-adrenoceptor blockade on the changes in plasma renin activity (PRA) following angiotensin enzyme (ACE) inhibition were investigated in pentobarbitone-chloralose anaesthetized dogs. 2 ACE-inhibition, with enalapril (2 mg kg-'), caused a significant reduction in systemic arterial blood pressure (BP) with little or no effect on cardiac function, and a significant elevation of plasma renin activity (PRA). By contrast P-adrenoceptor blockade with atenolol (1 mg kg-'), caused a similar reduction in BP but in addition, significantly reduced cardiac function and PRA. 3 A combination of enalapril with atenolol, caused a significant reduction in BP, cardiac function and PRA, hence there was no elevation of PRA, as was seen following ACE-inhibition with enalapril alone. 4 The observations with P-adrenoceptor blockade alone, show that there is an important homeostatic role for the renal sympathetic innervation, mediated by P-adrenoceptors, in controlling basal renin levels. Furthermore, the renal sympathetic innervation appears to be an important contributor to the renin release caused by an ACE-inhibitor as the additional presence of a P-adrenoceptor blocking agent will prevent this release.5 BW B385C (2 mg kg-'), which combines both ACE-inhibition and P-adrenoceptor blocking properties, also produced reductions in BP and cardiac function similar to those seen with the enalapril/ atenolol combination. In addition, for an equivalent degree of ACE-inhibition by BW 385C, to that seen with enalapril alone, the elevation of PRA was attenuated.6 A combination of ACE-inhibition and P-adrenoceptor blocking activity in a single entity, such as BW B385C, therefore also produces a reduced renin release when compared with an ACE-inhibitor, such as enalapril. This provides further confirmation of the importance of the renal sympathetic innervation in the renin response to ACE-inhibition, and supports the concept of combining ACEinhibition with P-adrenoceptor blockade.

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The effects of chloralose‐urethane and sodium pentobarbitone anaesthesia on the local and autonomic components of the circulatory response to arterial hypoxia

Cited by 45 publications

References 33 publications

Hemodynamic Responses to Hypoxia and Hypercapnia during Acute Normovolemic Hemodilution in Anesthetized Cats.

Hemodynamic Responses to Hypoxia and Hypercapnia during Acute Normovolemic Hemodilution in Anesthetized Cats.

Circulatory effects of chloralose‐urethane and sodium pentobarbitone anaesthesia in the rabbit

The effects of combined angiotensin converting enzyme inhibition and β‐adrenoceptor blockade on plasma renin activity in anaesthetized dogs

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