Insulin-induced hypoglycaemia increases metabolism and peripheral chemoreceptor gain in anaesthetised rats

Bin-Jaliah, Ismaeel and Maskell, Peter D and Kumar, Prem (2004) Insulin-induced hypoglycaemia increases metabolism and peripheral chemoreceptor gain in anaesthetised rats. In: Away Day of The Centre for Cardiovascular Sciences, The University Of Birmingham, 17 September 2004, The Centre for Cardiovascular Sciences, The University Of Birmingham, Birmingham, England, UK.

[img]
Preview
PDF
Bin-Jaliah et al. 2004c.pdf

Download (21kB) | Preview
Official URL | رابط موقع المجلة: https://www.birmingham.ac.uk/research/activity/car...

Abstract|ملخص البحث

Background. Alveolar ventilation rises in proportion with increasing metabolic rate such that alveolar, and hence arterial PCO2 are maintained essentially constant. This homeostatic mechanism is crucial in the maintenance of cardiorespiratory function. The mechanism by which ventilation is coupled so precisely to metabolism, however, remains unclear. One possible mechanism might be an augmentation of peripheral chemoreceptor gain during hypermetabolism e.g., exercise. We showed, recently that insulin-induced hypoglycaemia increases ventilation in a carotid body-dependent manner due to the associated increase in metabolic rate. In this study we evaluated chemoreceptor sensitivity to PCO2 during elevated metabolism. Methods. Adult Wistar rats (300-350 g, n=8) were anaesthetized (urethane; 650 mg kg-1; I.V.), vagotomized, paralysed (pancuronium bromide; 3 mg kg-1, I.V.) and artificially ventilated with O2-enriched air. Phrenic nerve activity was recorded to derive an index of ventilation. The level of artificial pulmonary ventilation (VE) was measured from integrated tracheal airflow. Altering the degree of artificial ventilation varied the PaCO2 and thus both metabolic hyperbolae (effect of VE upon PaCO2) and CO2 chemosensitivity (effect of PaCO2 upon phrenic activity) could be assessed simultaneously. Hypoglycaemia was induced with an insulin infusion (0.4 U Kg-1 min-1, I.V.). Data are expressed as means ± S.E.M. and significance (P < 0.05) tested with paired t-test. Results. Insulin infusion lowered blood glucose to 3.37 ± 0.12 mmol L-1. This hypoglycaemia was associated with significant hypokalaemia. Hypoglycaemia induced an increase in metabolism as demonstrated by a significant elevation of the PaCO2 by 4.6 ± 1.2 mmHg at a fixed (euglycaemic, eucapnic) level of VE. CO2 chemosensitivity was increased by more than two-fold (from 1.33 ± 0.13 to 3.31 ± 0.28 V min-1 kg-1 mmHg-1). This elevation was mediated via an increase in the inspiratory drive component of each breath with no change in the timing component. A conversion and normalisation procedure was then employed to the units of ventilation obtained and the normalized mean hyperbolae and linear CO2 sensitivities showed that PaCO2 remained unchanged during hypoglycaemia from the basal setting of 40 mmHg. Conclusions. These results demonstrate that hypermetabolism during insulin-induced hypoglycaemia is associated with an increase of CO2 chemosensitivity which may be important for the maintenance of eucapnia and arterial pH during mild to moderate exercise.

Item Type|تصنيف النتاج العلمي: Conference or Workshop Item | مؤتمرات وورش عمل (Poster)
Subjects | مجال موضوع النشر: Medicine and Surgery
Biology
Divisions | الكلية: College of Medicine > Physiology
Depositing User: Prof. Ismaeel Bin-Jaliah
Date Deposited: 04 Mar 2019 09:25
Last Modified: 04 Mar 2019 09:25
URI: http://eprints.kku.edu.sa/id/eprint/4085

Actions (login required)

View Item | استعراض View Item | استعراض