Breathing impairments, such as an alteration in breathing
pattern, dyspnoea, and sleep apnoea, are common health deficits
recognised in Parkinson’s disease (PD). The mechanism that
underlies these disturbances, however, remains unclear. We
investigated the effect of the unilateral damage to the rat
nigrostriatal pathway on the central ventilatory response to
hypercapnia, evoked by administering 6-hydroxydopamine
(6-OHDA) into the right medial forebrain bundle (MFB). The
respiratory experiments were carried out in conscious animals in
the plethysmography chamber. The ventilatory parameters were
studied in normocapnic and hyperoxic hypercapnia before and
14 days after the neurotoxin injection. Lesion with the 6-OHDA
produced an increased tidal volume during normoxia. The
magnified response of tidal volume and a decrease of breathing
frequency to hypercapnia were observed in comparison to the
pre-lesion and sham controls. Changes in both respiratory
parameters resulted in an increase of minute ventilation of the
response to CO2 by 28 % in comparison to the pre-lesion state
at 60 s. Our results demonstrate that rats with implemented
unilateral PD model presented an altered respiratory pattern
most often during a ventilatory response to hypercapnia.
Preserved noradrenaline and specific changes in dopamine and
serotonin characteristic for this model could be responsible for
the pattern of breathing observed during hypercapnia.
People with metabolic syndrome have higher risk of cardiovascular diseases then those without. The aim of the work was to investigate whether high fat diet administered to Prague hereditary hypertriglyceridemic (HTG) rats can induce signs of metabolic syndrome (MetS). Our results showed that HTG rats fed high fat diet (HTGch) had disturbed glucose metabolism and also lipid metabolism – increased serum triacylglycerols (TAG), total cholesterol (Ch), low-density lipoprotein
-Ch (LDL-Ch), and decreased high-density lipoprotein-Ch (HDL-Ch). Their livers proved markers of developing steatosis. Moreover, HTGch had increased blood pressure, yet the vascular endothelium was not
significantly damaged. All these changes were accompanied with oxidative stress and tissue damage identified as increased liver concentrations of thiobarbituric acid reactive substances (TBARS) and activity of the lysosomal enzyme N-acetyl-D-glucosaminidase (NAGA). We assume that the model used may be suitable for the study of MetS with no evidence of obesity. Prolongation of the high fat diet duration might have a major impact on all
parameters tested, especially on vascular endothelial function.