SUMMARY To study the effect of histamine (HA) on brain blood flow and capillary permeability, bilateral parietal craniectomies were made in cats anesthetized with nitrous oxide and ketamine. The dura was reraored and solutions of HA in mock cerebrospinal fluid (CSF) in varying concentrations ranging from 10 ' M to 10 ' M were irrigated continuously onto the exposed brain while local cerebral blood flow was determined polarographically by hydrogen clearance. Capillary permeability was assessed by determining HA's effect on the 12s I-albumin space of the brain. Electrical activity was monitored by eiectrocorticography. HA consistently dilated pial blood vessels and produced within 15 rain a dose-related local hyperemia that subsided 30-60 min after HA was removed. Hyperemia was blocked by cimetidine. HA had no appreciable effect on either the blood-brain barrier to albumin or the electrical activity of the cortex. HA is pharmacologically capable of participating directly in the acute hyperemic response of the brain's microclrculatlon to physiologic and pathologic stimuli but has little effect on cerebrovascular permeability to protein.Stroke, Vol 11, No 5, 1980MAMMALIAN BRAIN contains biologically significant amounts of histamine (HA) in 2 principal locations: within certain neurons, particularly those of the hypothalamus, and within mast cells, which tend to be concentrated in the leptomcninges. '2 Neuronal HA probably functions as a neurotransmitter through a specific adenylate cyclase system that has pharmacologic properties of an H, receptor.3 The function of HA in the mast cells of the brain is unknown. Mast cells are often found in brain strategically located close to blood vessels where they may affect vascular tone and, in turn, cerebral blood flow.s Schwartz 4 has suggested that mast cell HA in the bnin plays a role in inflammatory processes and vascular control, as it does elsewhere in the body.The effect of HA on systemic vasculature has been well studied.1 ' 6 -' Injected intravenously, HA constricts cardiac and pulmonary arteries and dilates the capillary bed of peripheral organs where blood pools, leading to a fall in systemic arterial pressure. Concurrently, plasma is lost through the capillary endothelium, which accentuates shock.1 '' Injected subcutaneously, HA produces capillary hyperemia, increased vascular permeability and edema, thus mimicking, in part, the acute vascular response to injury. 1 ' ° Although considerable information is also available about the effect of HA on cerebrovascular smooth muscle and cerebral blood flow (CBF), much of it is contradictory. brain as it does the permeability of vessels outside of the central nervous system.Because of the continuing uncertainty regarding the preponderant effect of HA on CBF, the lack of information about the effect of HA on the permeability of cerebral blood vessels, and the evidence indicating biologically significant stores of HA in the brain, we undertook this in vivo study to determine the local response of the cerebral circulation of t...
SUMMARY It has been hypothesized that acute lesions of the brain enlarge through an autodestructive process. Serotonin (5HT), a potent cerebral vasoconstrictor, is believed by some to mediate the process by reducing cerebral blood flow (CBF) in tissue surrounding the lesion. The hypothesis was tested in cynomolgus monkeys anesthetized with ketamine and nitrous oxide. Craniectomies, 7 mm in diameter, were performed in each parietal area. The dura was opened and polarographical electrodes of thin platinum wire were inserted into the parietal lobe cortex of each hemisphere. Mock cerebrospinal fluid (CSF) was irrigated continuously onto the brain surrounding the electrodes, from which local CBF was determined repeatedly by the hydrogen-clearance technique. After baseline CBF was established, solutions of 5HT in mock CSF (in concentrations of 5 X 10-' M, 5 X 10 5 M, and 5 X 10 s M) were irrigated onto one hemisphere while the opposite hemisphere served as control. SHT failed to change CBF.Although 5HT is a potent vasoconstrictor, under physiologic conditions it apparently is unable to effect hemodynamically significant constriction of the peripheral cerebral vasculature of the anesthetized monkey brain.IN RESPONSE to central nervous system injury, biogenic amines with vasoconstrictor properties are thought to be released from neurons and blood vessels in quantities sufficient to enlarge the original lesion. According to this hypothesis, an ischemic or traumatic lesion of the brain or spinal cord may enlarge because amines released by injury reduce blood flow sufficiently to infarct tissue surrounding the lesion.'" 8 Serotonin (5-hydroxytryptamine, 5HT) has been proposed as a mediator of this hypothetical selfpropagating zone of spreading ischemia 1 ' *• *• 8 because it is both a potent cerebral vasoconstrictor 914 and present in substantial concentrations in brain 15 and blood. 16 If the hypothesis is valid, local cerebral blood flow (CBF) should decrease when an appropriately concentrated solution of 5HT is applied topically to the brain. This paper reports the results of an investigation designed to test the hypothesis. Materials and MethodsYoung, adult cynomolgus monkeys (Macaca fascicularis) of both sexes weighing between 3 and 5 kg were initially given 50 mg of ketamine and 0.2 mg of atropine sulfate intramuscularly. They were then intubated with a cuffed endotracheal tube, placed on a volume respirator, and paralyzed with an intravenous injection of 0.3 mg of pancuronium. Anesthesia was maintained for the remainder of the experiment with an inhaled gas mixture of 70% N 2 O and 30% O 2 , supplemented with a continuous intravenous infusion of ketamine at 3 mg/kg/hr. Lactated Ringer's solution, to which was added 0.8 mg/100 ml of pancuronium, was infused continuously through a femoral vein cutdown at 16 ml/hr to maintain fluid and electrolyte balance and muscular paralysis. Rectal temperature was kept between 37° and 38°C with an externally applied heated pad. The animal was moderately hyperventilated at a respir...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.