ABSTRACT
Dopamine topically applied to the cerebral cortex (1--20 micrograms/ml) or administered i.v. (0.5--64 micrograms/kg/min) has no effects on cerebral cortical blood flow in the rat.
Subject(s)
Cerebral Cortex/blood supply , Dopamine/pharmacology , Regional Blood Flow/drug effects , Animals , Cerebral Cortex/drug effects , Dose-Response Relationship, Drug , Kinetics , RatsABSTRACT
Local blood flow was measured in renal cortex (1 mm below cortical surface) by means of the hydrogen clearance method in urethanized rats. Recording of blood pressure from femoral artery was performed. Crotalus durissus terrificus venom injection (one mg/kg i.v.) significantly decreased cortical blood flow at 10 min, without a significant arterial pressure modification. Posterior injection of mannitol 200 mg induced a significant increase in cortical blood flow, although initial values were not reached. Electron microscopy showed thromboses in the glomerular capillaries 35 minutes after venom injection. It is suggested that the precocious effect of this venom on renal cortical blood flow may be instrumental in the development of the renal acute insufficiency induced by Crotalus durissus terrificus venom.
Subject(s)
Crotalid Venoms/pharmacology , Kidney/blood supply , Animals , Blood Pressure/drug effects , Female , Femoral Artery/physiology , Kidney/ultrastructure , Kidney Cortex/blood supply , Kidney Medulla/blood supply , Male , Microscopy, Electron , Rats , Regional Blood Flow , Thrombosis/chemically inducedABSTRACT
Local blood flow was measured in renal cortex (1 mm below cortical surface) by means of the hydrogen clearance method in urethanized rats. Recording of blood pressure from femoral artery was performed. Crotalus durissus terrificus venom injection (one mg/kg i.v.) significantly decreased cortical blood flow at 10 min, without a significant arterial pressure modification. Posterior injection of mannitol 200 mg induced a significant increase in cortical blood flow, although initial values were not reached. Electron microscopy showed thromboses in the glomerular capillaries 35 minutes after venom injection. It is suggested that the precocious effect of this venom on renal cortical blood flow may be instrumental in the development of the renal acute insufficiency induced by Crotalus durissus terrificus venom.
ABSTRACT
Local blood flow was measured in renal cortex (1 mm below cortical surface) by means of the hydrogen clearance method in urethanized rats. Recording of blood pressure from femoral artery was performed. Crotalus durissus terrificus venom injection (one mg/kg i.v.) significantly decreased cortical blood flow at 10 min, without a significant arterial pressure modification. Posterior injection of mannitol 200 mg induced a significant increase in cortical blood flow, although initial values were not reached. Electron microscopy showed thromboses in the glomerular capillaries 35 minutes after venom injection. It is suggested that the precocious effect of this venom on renal cortical blood flow may be instrumental in the development of the renal acute insufficiency induced by Crotalus durissus terrificus venom.
ABSTRACT
Cerebral cortical blood flow was measured with the hydrogen clearance technique. It was found that the increase in CoBF induced by amphetamine is blocked by atropine or chlorpromazine.
Subject(s)
Amphetamine/pharmacology , Cerebral Cortex/blood supply , Vasodilation/drug effects , Animals , Atropine/pharmacology , Cerebrovascular Circulation/drug effects , Chlorpromazine/pharmacology , Epinephrine/pharmacology , Isoproterenol/pharmacology , Norepinephrine/pharmacology , RatsABSTRACT
Experiments were conducted on rats to investigate the acute effects on renal cortical blood flow and cortical autoregulation caused by intravenous administration of hypertonic solutions of sodium chloride or glucose. Local blood flow was measured in renal cortex (at 1 mm below cortical surface) by means of the hydrogen clearance method in urethanized rats. Recording of blood pressure from femoral artery was performed. In control group, renal cortical vascular resistance (R.C.V.R.)--arterial pressure relationships demonstrated typical autoregulation. An increase in plasma osmolarity of approximately 5.90%, induced by glucose, did not affect autoregulation. An increase in plasma osmolarity of approximately 4.43%, induced by NaCl, avoided autoregulation and the resistance-arterial pressure relationships became passive in appearance. In addition, NaCl administration was associated with an increase in cortical blood flow. It is suggested that in the presence of a low increment in plasma osmolarity, the sodium ion rather than the osmolarity itself, is the factor that influences cortical blood flow autoregulation in the rat.
Subject(s)
Glucose Solution, Hypertonic/pharmacology , Glucose/pharmacology , Homeostasis , Kidney Cortex/blood supply , Saline Solution, Hypertonic/pharmacology , Sodium Chloride/pharmacology , Animals , Blood Flow Velocity , Osmolar Concentration , Rats , Regional Blood Flow/drug effects , Stimulation, Chemical , Vascular ResistanceABSTRACT
Local blood flow was measured in renal cortex (at 1 mm below cortical surface) by means of the hydrogen clearance method in urethanized rats. Recording of blood pressure from femoral artery was performed. The blood flow autoregulation was studied by plotting renal cortical vascular resistance (R.C.V.R.) as a function of arterial pressure in all the experimental conditions. R.C.V.R. was calculated as arterial pressure/blood flow ratio. In control animals R.C.V.R. was linearly correlated to arterial pressure; this implies the existence of autoregulation in the studied zone. In animals pretreated with guanethidine or propranolol, and in animals injected with propranolol immediately before the experiment, the increase of arterial pressure was not followed by an increase in R.C.V.R.; this implies that autoregulation was absent. In animals pretreated with reserpine the increase of arterial pressure was not followed by a significant increase in R.C.V.R., although a tendency to increase was detected. It is suggested that the impairment of autoregulation induced by guanethidine, propranolol or reserpine may be due to an inhibition of renin release. The results obtained with guanethidine and reserpine may be partially attributable to a decrease in adrenergic activity on the vascular smooth muscle of the studied zone, although other mechanisms cannot be discarded.
Subject(s)
Antihypertensive Agents/pharmacology , Kidney Cortex/blood supply , Regional Blood Flow/drug effects , Animals , Blood Flow Velocity , Female , Guanethidine/pharmacology , Homeostasis/drug effects , Male , Propranolol/pharmacology , Rats , Reserpine/pharmacology , Vascular Resistance/drug effectsABSTRACT
Experiments were conducted on rats to investigate the acute effects on renal cortical blood flow and cortical autoregulation caused by intravenous administration of hypertonic solutions of sodium chloride or glucose. Local blood flow was measured in renal cortex (at 1 mm below cortical surface) by means of the hydrogen clearance method in urethanized rats. Recording of blood pressure from femoral artery was performed. In control group, renal cortical vascular resistance (R.C.V.R.)--arterial pressure relationships demonstrated typical autoregulation. An increase in plasma osmolarity of approximately 5.90
, induced by glucose, did not affect autoregulation. An increase in plasma osmolarity of approximately 4.43
, induced by NaCl, avoided autoregulation and the resistance-arterial pressure relationships became passive in appearance. In addition, NaCl administration was associated with an increase in cortical blood flow. It is suggested that in the presence of a low increment in plasma osmolarity, the sodium ion rather than the osmolarity itself, is the factor that influences cortical blood flow autoregulation in the rat.
ABSTRACT
Local blood flow was measured in renal cortex (at 1 mm below cortical surface) by means of the hydrogen clearance method in urethanized rats. Recording of blood pressure from femoral artery was performed. The blood flow autoregulation was studied by plotting renal cortical vascular resistance (R.C.V.R.) as a function of arterial pressure in all the experimental conditions. R.C.V.R. was calculated as arterial pressure/blood flow ratio. In control animals R.C.V.R. was linearly correlated to arterial pressure; this implies the existence of autoregulation in the studied zone. In animals pretreated with guanethidine or propranolol, and in animals injected with propranolol immediately before the experiment, the increase of arterial pressure was not followed by an increase in R.C.V.R.; this implies that autoregulation was absent. In animals pretreated with reserpine the increase of arterial pressure was not followed by a significant increase in R.C.V.R., although a tendency to increase was detected. It is suggested that the impairment of autoregulation induced by guanethidine, propranolol or reserpine may be due to an inhibition of renin release. The results obtained with guanethidine and reserpine may be partially attributable to a decrease in adrenergic activity on the vascular smooth muscle of the studied zone, although other mechanisms cannot be discarded.
ABSTRACT
Experiments were conducted on rats to investigate the acute effects on renal cortical blood flow and cortical autoregulation caused by intravenous administration of hypertonic solutions of sodium chloride or glucose. Local blood flow was measured in renal cortex (at 1 mm below cortical surface) by means of the hydrogen clearance method in urethanized rats. Recording of blood pressure from femoral artery was performed. In control group, renal cortical vascular resistance (R.C.V.R.)--arterial pressure relationships demonstrated typical autoregulation. An increase in plasma osmolarity of approximately 5.90
, induced by glucose, did not affect autoregulation. An increase in plasma osmolarity of approximately 4.43
, induced by NaCl, avoided autoregulation and the resistance-arterial pressure relationships became passive in appearance. In addition, NaCl administration was associated with an increase in cortical blood flow. It is suggested that in the presence of a low increment in plasma osmolarity, the sodium ion rather than the osmolarity itself, is the factor that influences cortical blood flow autoregulation in the rat.
ABSTRACT
Local blood flow was measured in renal cortex (at 1 mm below cortical surface) by means of the hydrogen clearance method in urethanized rats. Recording of blood pressure from femoral artery was performed. The blood flow autoregulation was studied by plotting renal cortical vascular resistance (R.C.V.R.) as a function of arterial pressure in all the experimental conditions. R.C.V.R. was calculated as arterial pressure/blood flow ratio. In control animals R.C.V.R. was linearly correlated to arterial pressure; this implies the existence of autoregulation in the studied zone. In animals pretreated with guanethidine or propranolol, and in animals injected with propranolol immediately before the experiment, the increase of arterial pressure was not followed by an increase in R.C.V.R.; this implies that autoregulation was absent. In animals pretreated with reserpine the increase of arterial pressure was not followed by a significant increase in R.C.V.R., although a tendency to increase was detected. It is suggested that the impairment of autoregulation induced by guanethidine, propranolol or reserpine may be due to an inhibition of renin release. The results obtained with guanethidine and reserpine may be partially attributable to a decrease in adrenergic activity on the vascular smooth muscle of the studied zone, although other mechanisms cannot be discarded.
ABSTRACT
The effect of vincamine on cortical blood flow was tested in control rats and after atropine administration. Cortical blood flow was measured in urethanized rats by means of the hydrogen clearance method. A significative increase in cortical blood flow and decrease in blood pressure and cortical vascular resistance was produced by vincamine iv administration in control animals. In atropinized rats significative cortical blood flow changes were not observed although some tendency to increase was detected. It is suggested that increase in cortical blood flow induced by vincamine may be due to direct action on the vascular smooth muscle and, partially, through a cholinergic mechanism.
Subject(s)
Cerebral Cortex/drug effects , Cerebrovascular Circulation/drug effects , Vinca Alkaloids/pharmacology , Administration, Topical , Animals , Blood Flow Velocity , Blood Pressure/drug effects , Cerebral Cortex/blood supply , Injections, Intravenous , Polarography/methods , Rats , Stimulation, Chemical , Vascular Resistance/drug effects , Vinca Alkaloids/administration & dosageABSTRACT
The effect of vincamine on cortical blood flow was tested in control rats and after atropine administration. Cortical blood flow was measured in urethanized rats by means of the hydrogen clearance method. A significative increase in cortical blood flow and decrease in blood pressure and cortical vascular resistance was produced by vincamine iv administration in control animals. In atropinized rats significative cortical blood flow changes were not observed although some tendency to increase was detected. It is suggested that increase in cortical blood flow induced by vincamine may be due to direct action on the vascular smooth muscle and, partially, through a cholinergic mechanism.
ABSTRACT
The effect of vincamine on cortical blood flow was tested in control rats and after atropine administration. Cortical blood flow was measured in urethanized rats by means of the hydrogen clearance method. A significative increase in cortical blood flow and decrease in blood pressure and cortical vascular resistance was produced by vincamine iv administration in control animals. In atropinized rats significative cortical blood flow changes were not observed although some tendency to increase was detected. It is suggested that increase in cortical blood flow induced by vincamine may be due to direct action on the vascular smooth muscle and, partially, through a cholinergic mechanism.
