The importance of circulating levels of salusin-α, salusin-ß, and heregulin-ß1 in atherosclerotic coronary arterial disease.

OBJECTIVE: The relationship between the severity of atherosclerotic coronary artery disease (CAD) and circulating levels of salusin-α, salusin-ß and heregulin-ß1 has been investigated. In addition, the relationship with these peptides and high sensitive C-reactive protein (hsCRP) has been investigated. METHODS: The study was conducted on 55 volunteers who had normal coronary angiography (CAG) as the control group, 35 volunteers with the degree of coronary artery stenosis below 50% in CA as the non-critical stenosis group, 37 volunteers with narrowing of one coronary artery above 50% as single vessel group and 41 volunteers with narrowing of more than one coronary artery above 50% as multi-vessel group. One hundred and thirteen volunteers have been included to CAD group. RESULTS: There was no statistically significant difference in serum salusin-α levels between groups. Serum salusin-ß ve hsCRP levels were significantly lower in control group compared to other groups and CAD group. There was no statistically significant difference in salusin-ß and salusin-α levels in reciprocal comparison of other groups other than heregulin-ß1 levels. Heregulin-ß1 levels were significantly lower in 'non-critical occlusion' and 'multiple artery occlusion' groups compared to control group. Heregulin-ß1 levels in 'single artery occlusion' group were significantly higher than control, 'non-critical occlusion' and 'multiple artery occlusion' groups. CONCLUSION: Salusin-α levels does not indicate any significant differences between any groups in our study however the relationship of salusin-α with salusin- ß and heregulin-ß1 levels drives to cogitate that these peptides can be used as biomarkers and therapeutic approaches in CAD. We think that these peptides will be used in laboratories routinely in future in addition to hsCRP for CAD.

Effects of normovolaemic haemodilution on middle cerebral artery blood flow velocity and oxygen delivery.

BACKGROUND AND OBJECTIVE: Assessment of the effects of normovolaemic haemodilution on middle cerebral artery blood flow velocity with transcranial Doppler ultrasonography, intracranial pressure, cerebral perfusion pressure, arterial oxygen content and cerebral oxygen delivery. METHODS: Normovolaemic haemodilution was induced in rabbits under general anaesthesia, and the haematocrit was allowed to decrease to 30% in Group 1 (n = 6) and to 20% in Group 2 (n = 6). Peak systolic and diastolic velocities, mean blood flow velocity, and pulsatility and resistance indices of the middle cerebral artery were measured by transcranial Doppler ultrasonography. Changes in intracranial pressure, cerebral perfusion pressure, arterial oxygen content and cerebral oxygen delivery were also assessed. RESULTS: In Group 2, middle cerebral artery blood flow velocity increased from 0.4 +/- 0.01 to 0.51 +/- 0.02 m s(-1) after the induction of normovolaemic haemodilution (P = 0.04), while arterial oxygen content decreased from 16.2 +/- 0.1 to 8.5 +/- 0.1 mLdL(-1) (P = 0.002). The decrease in cerebral oxygen delivery from 6.5 +/- 0.2 to 4.3 +/- 0.2 was also significant (P = 0.02). However, no associated changes in intracranial pressure and cerebral perfusion pressure could be demonstrated. CONCLUSIONS: Normovolaemic haemodilution resulted in an increase in the mean blood flow velocity of the middle cerebral artery. However, this increase did not compensate for the consequences of the altered oxygen delivery to the brain when the haematocrit was reduced to 20%.

Effects of pressure- and volume-controlled inverse ratio ventilation on haemodynamic variables, intracranial pressure and cerebral perfusion pressure in rabbits: a model of subarachnoid haemorrhage under isoflurane anaesthesia.

BACKGROUND AND OBJECTIVE: An inverse I : E ratio (inspiratory time > expiratory time) may have benefits in patients suffering trauma who requiring lung ventilation. However, this application may be deleterious if there is concomitant head injury. We aimed to determine the physiological effects of pressure- and volume-controlled modes of inverse ratio (I : E = 2 : 1) ventilation of the lungs, while maintaining normocapnia, in a rabbit model of raised intracranial pressure (ICP). METHODS: New Zealand White rabbits were anaesthetized with isoflurane and a tracheostomy was performed. Subarachnoid haemorrhage was simulated in two groups by injecting blood into the cisterna magna. Groups 1 and 2 (n = 6, each), controls, were compared with Groups 3 and 4 (n = 6, each) with the simulated subarachnoid haemorrhage. Each ventilation mode was used with an I : E ratio of 2 : 1 for 30 min. Mean arterial pressure (MAP), ICP, cerebral perfusion pressure (CPP), mean airway pressure (P(AW)) and arterial blood-gas status were measured. RESULTS: Both modes increased mean P(AW) (P < 0.02). This increase was greater with the volume-controlled mode (P < 0.02). The baseline value averaged 5.8 +/- 0.4 and 5.6 +/- 0.3 mmHg in Groups 3 and 4, respectively, and increased to 7.8 +/- 0.3 and 10.8 +/- 0.4 mmHg. Inducing subarachnoid haemorrhage increased ICP and MAP (P < 0.02). Baseline ICPs were 10.3 +/- 0.5 and 10.3 +/- 0.4 mmHg in Groups 1 and 2, respectively, whereas they were 25.4 +/- 1.2 and 25.8 +/- 0.8 mmHg in Groups 3 and 4. However, ICP, MAP and CPP did not differ significantly according to the mode. CONCLUSIONS: An already raised ICP was altered by the application of induced mean PAW increases as a consequence of inverse ratio ventilation of the lungs with normocapnia.