ABSTRACT
A paradigm for studying relations between behavioral, neurochemical, and electrophysiologic processes is presented. Scopolamine, a centrally acting anticholinergic agent, abolished the human auditory P3 event-related potential, but had no measurable effect on the pattern reversal visual evoked potential or alpha rhythm. Recent memory was significantly impaired, but assessment of digit span, reaction time, and distant memory showed no impairment. Physostigmine, an anticholinesterase, restored the P3 and reversed the recent memory impairment. These results strongly suggest a cholinergic role in generation of P3 potential and support the concept that P3 generation is related to memory processes.
Subject(s)
Evoked Potentials, Auditory/drug effects , Evoked Potentials, Visual/drug effects , Memory/physiology , Physostigmine/pharmacology , Scopolamine/pharmacology , Adult , Attention/drug effects , Attention/physiology , Humans , Male , Memory/drug effectsABSTRACT
The coronary blood flow and vascular resistance responses to static hindlimb exercise were studied in 11 anesthetized dogs after beta- and combined alpha- and beta-adrenergic blockade to determine if this stress causes coronary vasoconstriction. After beta-blockade static exercise increased the blood pressure and double product, but decreased the right and left ventricular (LV) coronary blood flow and increased the coronary vascular resistance. These vascular changes primarily occurred in the epicardial and mid-myocardial but not the endocardial layers of the LV. Following combined alpha- and beta-adrenergic blockade, the systemic hemodynamic and coronary flow and resistance changes were abolished. These data suggest that alpha-adrenergic mediated coronary vasoconstriction occurs during static hindlimb exercise in dogs.
Subject(s)
Anesthesia , Coronary Vessels/physiology , Isometric Contraction , Physical Exertion , Receptors, Adrenergic, alpha/physiology , Receptors, Adrenergic/physiology , Reflex/physiology , Vasoconstriction , Adrenergic alpha-Antagonists/pharmacology , Adrenergic beta-Antagonists/pharmacology , Animals , Coronary Circulation/drug effects , Dogs , Hindlimb , Vascular Resistance/drug effects , Vasoconstriction/drug effectsABSTRACT
We studied 18 alpha-chloralose-anesthetized dogs to determine if alpha-adrenergic coronary vasoconstriction occurs with hindlimb static exercise. Exercise was elicited by spinal cord ventral nerve root stimulation. Regional coronary blood flow was determined by the radioactive microsphere method. Animals were studied under four experimental conditions: control rest and static exercise, rest and static exercise after beta-adrenergic blockade with propranolol (2 mg/kg), rest and exercise after alpha-adrenergic blockade with phentolamine (.35 mg/kg), and rest and exercise after combined alpha- and beta-adrenergic blockade. Myocardial oxygen consumption during exercise was determined during control and during alpha-adrenergic blockade conditions. Control hindlimb static exercise resulted in significant increases in systolic (10.6%) and diastolic (12.5%) arterial pressures, heart rate (12.2%), and double product (24.6%). Associated with the increased demand for oxygen, myocardial oxygen consumption increased (33.6%) as did left ventricular myocardial flow (29.6%). However, left ventricular coronary vascular resistance was unchanged during static exercise. After beta-adrenergic blockade, systolic (12.2%) and diastolic (11.6%) arterial pressures and double product (10.7%) still increased significantly, but heart rate did not change with static exercise. In contrast, alpha-adrenergic vasoconstriction was unmasked as left (LV) and right (RV) ventricular myocardial blood flow decreased (LV: -30.0%, RV: -25.0%) and coronary vascular resistance increased (LV: 52.5%, RV: 45.3%) with static exercise. Combined alpha- and beta-adrenergic blockade abolished the reduction in myocardial blood flow and the increase in coronary vascular resistance which occurred with static exercise after beta-adrenergic blockade. These data suggest that, during static exercise, reflexes from skeletal muscles can cause alpha-adrenergic coronary artery vasoconstriction.
Subject(s)
Constriction, Pathologic/drug therapy , Coronary Vessels/physiopathology , Adrenergic alpha-Antagonists , Animals , Dogs , Hindlimb , Oxygen Consumption , Phentolamine/pharmacology , Physical Exertion , Propranolol/pharmacology , Reflex , Regional Blood Flow , Vascular ResistanceABSTRACT
Studies were designed to characterize the distribution of cardiac output during induced isometric exercise in anesthetized dogs. The response to isometric exercise involved significant increases in heart rate (+12 +/- 3%(SE)), mean arterial pressure (+13 +/- 2%), cardiac output (+26 +/- 8%), and respiratory minute volume (+75 +/- 26%); total peripheral resistance did not change significantly. Significant changes in blood flow were observed during isometric exercise in kidneys (-18 +/- 6%) and contracting limb muscles (+453 +/- 154%). Flow to liver (hepatic artery), spleen, brain, and myocardium remained near control values. Section of spinal dorsal roots L6-L7 abolished the responses to isometric exercise except for the increase in flow to exercising limb muscles. Alpha-adrenergic receptor blockade abolished the decrease in renal blood flow during isometric exercise; however, the increase in flow to exercising limb muscles was not affected by either alpha- or beta-adrenergic blockade.
