The effects of induced acute hyperglycemia in the cat on the retinal capillary blood flow.
OBJECTIVE
To study the effect of acute hyperglycemia on the erythrocyte flow in specific retinal capillary paths.


METHODS
A technique for fluorescent labeling of a known fraction of the erythrocyte moiety of systemic blood was combined with fluorescence viewing of the retinal capillary network in live cats. This technique was developed to enable visualization of the erythrocyte flow in the retinal capillary network and used to acquire video recording of the retinal capillary erythrocyte flow in normal feline eyes. The pattern of capillary erythrocyte flow under normal blood glucose levels and normal systemic blood pressure served as baseline. Acute hyperglycemia was induced by intravenous injection of glucose while monitoring the systemic blood pressure. Two subsets of functional capillary pathways previously defined as S (simple) and C (complex) were identified in the recorded data. The relationship between erythrocyte flux in random selections of these two pathways and the level of hyperglycemia and systemic blood pressure was determined.


RESULTS
Induction of acute hyperglycemia led to acute elevation of the systemic blood pressure that returned to baseline levels within few minutes, while blood glucose remained high. The capillary erythrocyte flux in S paths was significantly higher than in C paths at all values of systemic blood pressure. The capillary erythrocyte flux in the S paths was directly proportional to the systemic blood pressure whereas the flux in C paths was minimally affected by acute hyperglycemia for the systemic blood pressure range between 110 and 160 mm Hg.


CONCLUSIONS
The erythrocyte flux in S paths is affected by the changes of the systemic blood pressure and these paths act as 'shunt vessels' when acute elevation of the systemic blood pressure occurs. C paths maintain stable perfusion under changing conditions, most probably in an effort to minimally alter the basic metabolic needs of the retinal tissue. Hyperglycemia per se was not responsible for changes of the cell flux in these capillary paths.
Ben-Nun
J
J
Department of Ophthalmology, 'Assaff-Hroffee' Medical Center, Tzriffin, Israel.
Alder
V A
VA
Constable
I J
IJ
D000208:Acute Disease; D000818:Animals; D001783:Blood Flow Velocity / Q000502:physiology; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D002196:Capillaries / Q000503:physiopathology; D002415:Cats; D004912:Erythrocytes / Q000502:physiology*; D005947:Glucose / Q000633:toxicity; D006943:Hyperglycemia / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology*; D008856:Microscopy, Fluorescence; D012160:Retina / Q000503:physiopathology*; D012171:Retinal Vessels / Q000503:physiopathology*; D014741:Video Recording
D001786:Blood Glucose; D005947:Glucose