Physiological responses to acute stress in alloxan and streptozotocin diabetic rats

Abstract

Physiological responses to acute stress were assessed in alloxan diabetic, streptozotocin diabetic and control laboratory rats. Rats were prepared with indwelling tail artery catheters to allow for direct measurement of mean arterial pressure (MAP, mmHg) and heart rate (HR, beats per minute) and remote sampling of blood. Within 24 hours after surgery, basal values of MAP and HR were determined. Two days after surgery, rats were subjected to 5 minutes of intermittent footshock. Blood samples were collected before footshock stress and immediately and 15 minutes after termination of footshock. Plasma levels of norepinephrine (NE) and epinephrine (EPI) increased significantly above basal values in all animals exposed to acute footshock stress. However, in approximately one-half of alloxan and streptozotocin diabetic rats, plasma levels of EPI under basal conditions and following footshock stress were elevated significantly compared to controls and the remaining diabetic animals. We have denoted these subgroups of diabetic animals as reactive responders (plasma EPI greater than controls) and nonreactive responders (plasma EPI similar to controls), respectively. Plasma levels of NE under basal conditions and following footshock stress were similar in reactive responders and nonreactive responders compared to matched controls. Baseline blood glucose levels were elevated in alloxan and streptozotocin diabetic rats compared to controls. Blood glucose levels increased reliably in all animals following footshock stress. Basal MAPs were reduced significantly in both subgroups of alloxan and streptozotocin diabetic rats compared to matched controls. In contrast, resting HRs were similar between diabetic rats and their corresponding controls. These data indicate that a distinct subgroup of animals with chemically-induced diabetes exists which maintains elevated basal circulating levels of EPI and has exaggerated plasma EPI responses to acute stress. These reactive responders may have greater difficulty with glycemic control, especially during periods of stressful stimulation.