Effects of pre-ganglionic decentralization or post-ganglionic excision of the superior cervical ganglia on brain edema and heat stroke in rats

The preventive effect of pre-ganglionic decentralization (Sympathetic trunk resectioN) or postganglionic excision (ganglionectomy) of the superior cervical ganglia on thermal injury induced brain edema or the development of heat stroke was assessed in rats. Brain edema was induced by cold or heat injury to the cortex in 24 rats. The results showed that decentralization, but not excision, of the superior cervical ganglia greatly inhibited the formation of brain edema which was subsequently induced. When heat stroke was induced by exposing 24 rats to an ambient temperature of 41 degree C, the latency for the onset of the heat stroke and the survival time after the heat stroke were greatly prolonged by the former surgical procedure, but shortened by the later one. The present study demonstrates the potential benefit to brain edema and heat stroke of the pretreatment with decentralization of the superior cervical ganglia.     

Ultrastructural changes in the rat pineal gland after sympathetic denervation. Quantitative study

Ultrastructural changes in the rat pineal gland were studied quantitatively 7 and 60 days after the sympathetic denervation by bilateral excission or decentralization of superior cervical ganglia. The surface occupied by pineal parenchymal cells decreased in rats of experimental groups with respect to the control group. Furthermore, profile areas of the cytoplasm, nucleus and nucleolus of the pinealocytes were also diminished. Cytoplasmic lipid droplets in the pinealocytes were markedly decreased in number and size in experimental rats. As demonstrated by the Kruskal-Wallis H test, statistically significant differences were found between rats of the control and operated groups. Rats treated by superior cervical ganglionectomy or decentralization showed morphological changes indicating a hypofunctional pineal gland, although differences were found between both groups.     

The Role of Lumbar Sympathetic Nerves in Regulation of Blood Flow to Skeletal Muscle during Anaphylactic Hypotension in Anesthetized Rats

During hypovolemic shock, skeletal muscle blood flow could be redistributed to vital organs via vasoconstriction in part evoked by activation of the innervating sympathetic nerve activity. However, it is not well known whether this mechanism operates during anaphylactic shock. We determined the femoral artery blood flow (FBF) and lumbar sympathetic nerve activity (LSNA) mainly regulating the hindquater muscle blood flow during anaphylactic hypotension in anesthetized rats. Anesthetized Sprague-Dawley rats were randomly allocated to the following groups (n = 7/group): (1) non-sensitized, (2) anaphylaxis, (3) anaphylaxis-lumbar sympathectomy (LS) and (4) anaphylaxis-sinoaortic denervation (SAD) groups. Anaphylaxis was induced by an intravenous injection of the ovalbumin antigen to the sensitized rats. The systemic arterial pressure (SAP), heart rate (HR), central venous pressure (CVP), FBF and LSNA were continuously measured. In the anaphylaxis group, LSNA and HR increased, while SAP and FBF decreased after antigen injection. In the anaphylaxis-SAD group, LSNA did not significantly change during the early phase, but the responses of SAP and FBF were similar to those in the anaphylaxis group. In the anaphylaxis-LS group, both FBF and SAP decreased similarly to the anaphylaxis group during anaphylactic hypotension. These results indicated that LSNA increased via baroreceptor reflex, but this sympathoexcitation or LS did not affect antigen-induced decreases in FBF or SAP. Lumbar sympathetic nerves are not involved in regulation of the blood flow to the hindlimb or systemic blood pressure during anaphylactic hypotension in anesthetized rats.     

Cholinesterases of rat sympathetic ganglia after immunosympathectomy, decentralization and axotomy

Abstract— Immunosympathectomy was produced in Sprague-Dawley rats by the subcutaneous injection of 300 units of nerve growth factor (NGF)-antiserum (1.56 mg of freeze-dried serum)/g/day for 6 days, the first dose being given 5–8 hr after birth. The immunosympathectomized rats and their control littermates were killed 2½ and 7 months after birth. Ganglionic acetylcholinesterase and pseudocholinesterase activities were measured by an adaption (Kungman , Kungman and Pouszczuk , 1968) of the colorimetric method of Ellman , Courtney , Andres and Featherstone (1961). Following immunosympathectomy the activities of these enzymes decreased significantly in superior cervical, stellate, thoracic chain, cardiac (abdominal), coeliac and superior mesenteric ganglia. The reduction of the acetylcholinesterase activity was greater than expected in a number of sympathetic ganglia, e.g. superior cervical, stellate, coeliac and cardiac ganglia, if one considered that only the postganglionic neurons were affected by immunosympathectomy. The activities of these enzymes were also reduced in the cervical sympathetic trunks from NGF-antiserum-treated rats. By means of decentralization and axotomy it was shown that 45 per cent of the total ganglionic acetylcholinesterase activity was associated with the preganglionic and 55 per cent with the postganglionic elements of the superior cervical ganglion from control rats. It was concluded that immunosympathectomy also affects the preganglionic sympathetic neurons. It is not known whether this is a primary effect of the NGF-antiserum or a secondary effect resulting from the absence of over 90 per cent of the postganglionic sympathetic cell bodies.     

EFFECTS OF SURGICAL DECENTRALIZATION AND NERVE GROWTH FACTOR ON THE MATURATION OF ADRENERGIC NEURONS IN A MOUSE SYMPATHETIC GANGLION

Abstract— The increase in tyrosine hydroxylase activity in mouse superior cervical ganglion during postnatal development was prevented by administration of the protein synthesis inhibitor cycloheximide. Surgical section of the preganglionic nerves in 4-day-old mice prevented the normal increases in tyrosine hydroxylase and monoamine oxidase activity in the ganglion during development. Surgical decentralization also prevented the developmental increases in ganglion size and cell numbers. The preganglionic fibres thus appear to exert a general regulatory effect on the growth and biochemical maturation of postganglionic adrenergic neurons in sympathetic ganglia. Administration of nerve growth factor to young mice failed to eliminate the differences in ganglion size, cell numbers and tyrosine hydroxylase activity between normally innervated and decentralized ganglia. Nerve growth factor, however, caused an increase in all these parameters in both control and decentralized ganglia–the magnitude of these increases being greatest in the control ganglia. Administration of carbachol and physostigmine to neonatal mice did not influence the normal development of tyrosine hydroxylase activity in the superior cervical ganglion.     

Alterations in physiological functions and in brain monoamine content in the sympathectomized rats

In the present study, we conducted pre-ganglionic decentralization (or sympathetic trunk resection) of the superior cervical ganglia and observed alterations in several physiological functions and in the monoamine content of different brain regions. Over an ambient temperature range of 8-30 degrees C, these sympathectomized rats maintained their rectal temperatures within a normal limit displayed by the intact controls. These sympathectomized animals, although showing no change in the level of spontaneous pain threshold or motor activity, did display an increased sensitivity of analgesic responses to morphine administration or locomotor stimulant responses to amphetamine administration. Biochemical examination revealed that these sympathectomized animals had a higher level of norepinephrine, dopamine or 5-hydroxytryptamine in the hypothalamus, as well as a higher level of dopamine in the corpus striatum. However, in the brainstem, these sympathectomized animals had a unaltered monoamine level. The data indicate that, in a sympathectomized condition, changes in the monoamine content of different brain regions may be correlated with the above-mentioned alterations in somatosensory and motor neural functions.     

Innervation of the rat pineal gland by nerve fibres originating in the sphenopalatine, otic and trigeminal ganglia. A retrograde in vivo neuronal tracing study.

The innervation of the rat pineal gland from the sphenopalatine, otic, superior cervical and trigeminal ganglia was investigated in animals by use of in vivo retrograde tracings. A solution of 2% Fluorogold was iontophoretically injected into the superficial pineal gland in a series of Wistar rats. After a survival time of 4-10 days, the animals were fixed by perfusion and the brains, sphenopalatine, otic, superior cervical and trigeminal ganglia were investigated with a fluorescence microscope. Many retrogradely labelled perikarya were found in the superior cervical ganglia, but a smaller number of neurones were also labelled in the sphenopalatine, otic and trigeminal ganglia. Injections of the tracer into the subarachnoidal space were used as the control for unspecific uptake and transport of the tracer. The input to the pineal gland from the parasympathetic sphenopalatine and otic ganglia might be involved in the regulation of the annual rhythms of the pineal gland. The projections from the sensory trigeminal ganglion could be involved in the control of the blood flow of the gland.     

KISS1 and KISS1R expression in the human and rat carotid body and superior cervical ganglion

KISS1 and its receptor, KISS1R, have both been found to be expressed in central nervous system, but few data are present in the literature about their distribution in peripheral nervous structures. Thus, the aim of the present study was to investigate, through immunohistochemistry, the expression and distribution of KISS1 and KISS1R in the rat and human carotid bodies and superior cervical ganglia, also with particular reference to the different cellular populations. Materials consisted of carotid bodies and superior cervical ganglia were obtained at autopsy from 10 adult subjects and sampled from 10 adult Sprague-Dawley rats. Immunohistochemistry revealed diffuse expression of KISS1 and KISS1R in type I cells of both human and rat carotid bodies, whereas type II cells were negative. In both human and rat superior cervical ganglia positive anti-KISS1 and -KISS1R immunostainings were also selectively found in ganglion cells, satellite cells being negative. Endothelial cells also showed moderate immunostaining for both KISS1 and KISS1R. The expression of both kisspeptins and kisspeptin receptors in glomic type I cells and sympathetic ganglion cells supports a modulatory role of KISS1 on peripheral chemoreception and sympathetic function. Moreover, local changes in blood flow have been considered to be involved in carotid body chemoreceptor discharge and kisspeptins and kisspeptin receptors have also been found in the endothelial cells. As a consequence, a possible role of kisspeptins in the regulation of carotid body blood flow and, indirectly, in chemoreceptor discharge may also be hypothesized.     

CHARACTERISTICS OF THE PURIFIED NERVE GROWTH FACTOR ANTIBODY

Purified nerve growth factor antibody has been shown to be competent in several different systems. The material is effective in producing immunosympathectomy in young rats and in preventing the action of nerve growth factor on explants of rat superior cervical ganglia. When injected into the brain of young rats it is without effect on brain tyrosine hydroxylase activity, but appears to escape into the system and cause a reduction of tyrosine hydroxylase activity in the superior cervical ganglia. Iodinated antibody injected subcutaneously into neonatal rats does not enter the brain and does not accumulate in superior cervical ganglia, or any of the other tissues studied. The antibody prevents the retrograde transport of nerve growth factor from the anterior chamber of the eye to the superior cervical ganglion and is not itself transported.     

Synaptic Vesicle Proteins and Neuronal Plasticity in Adrenergic Neurons

The neurons in the superior cervical ganglion are active in plasticity and re-modelling in order to adapt to requirements. However, so far, only a few studies dealing with synaptic vesicle related proteins during adaptive processes have been published. In the present paper, changes in content and expression of the synaptic vesicle related proteins in the neurons after decentralization (cutting the cervical sympathetic trunk) or axotomy (cutting the internal and external carotid nerves) were studied. Immunofluorescence studies were carried out using antibodies and antisera against integral membrane proteins, vesicle associated proteins, NPY, and the enzymes TH and PNMT. For colocalization studies, the sections were simultaneously double labelled. Confocal laser scanning microscopy was used for colocalization studies as well as for semi-quantification analysis, using the computer software. Westen blot analysis, in situ 3'-end DNA labelling, and in situ hybridization were also employed. After decentralization of the ganglia several of the synaptic vesicle proteins (synaptotagmin I, synaptophysin, SNAP-25, CLC and GAP-43) were increased in the iris nerve terminal network, but with different time patterns, while TH-immunoreactivity had clearly decreased. In the ganglia, these proteins had decreased at 1 day after decentralization, probably due to degeneration of the pre-ganglionic nerve fibres and terminals. At later intervals, these proteins, except SNAP-25, had increased in the nerve fibre bundles and re-appeared in nerve fibres outlining the principal neurons.     

A COMPARISON OF THE NEURAL REGULATION OF TYROSINE HYDROXYLASE ACTIVITY IN SYMPATHETIc GANGLIA OF ADULT MICE AND RATS

Surgical decentralization of the superior cervical ganglion (SCG) in rats and mice led to a fall in ganglionic tyrosine hydroxylase (T-OH) activity, and a loss of more than 90 per cent of the preganglionic neurone marker, choline acetyl transferase. T-OH activity was reduced by more than 50 per cent in mice SCG ten days after surgery, but fell by only 25 per cent in rat SCG after 21 days. The surgical procedure did not cause obvious histo-logical damage or loss of SCG cells in either species. Both T-OH and choline acetyl transferase activities in rat and mouse SCG recovered to normal three months after surgery. Reserpine treatment was more effective in rats in causing increased ganglionic T-OH activity than in mice. Neither decentralization nor reserpine treatment caused any changes in DOPA-decarboxylase or monoamine oxidase activities in rat SCG. These results demonstrate that T-OH activity in SCG is subject to trans-synaptic regulation in both rats and mice; this regulation does not apply to DOPA-decarboxylase or monoamine oxidase. Differences in basal sympathetic tone may explain the different results obtained in mice and rats.     

Effects of Anesthetics on the Renal Sympathetic Response to Anaphylactic Hypotension in Rats

The autonomic nervous system plays an important role in rat anaphylactic hypotension. It is well known that sympathetic nerve activity and cardiovascular function are affected by anesthetics. However, the effects of different types of anesthesia on the efferent renal sympathetic nerve activity (RSNA) during anaphylactic hypotension remain unknown. Therefore, we determined the renal sympathetic responses to anaphylactic hypotension in anesthetized and conscious rats and the roles of baroreceptors in these responses. Sprague-Dawley rats were randomly allocated to anesthetic groups that were given pentobarbital, urethane, or ketamine-xylazine and to a conscious group. The rats were sensitized using subcutaneously injected ovalbumin. The systemic arterial pressure (SAP), RSNA and heart rate (HR) were measured. The effects of sinoaortic baroreceptor denervation on RSNA during anaphylaxis were determined in pentobarbital-anesthetized and conscious rats. In all of the sensitized rats, the RSNA increased and SAP decreased after antigen injection. At the early phase within 35 min of the antigen injection, the antigen-induced sympathoexcitation in the conscious rats was significantly greater than that in the anesthetized rats. Anaphylactic hypotension was attenuated in the conscious rats compared to the anesthetized rats. The anesthetic-induced suppression of SAP and RSNA was greater in the order ketamine-xylazine >urethane = pentobarbital. Indeed, in the rats treated with ketamine-xylazine, RSNA did not increase until 40 min, and SAP remained at low levels after the antigen injection. The baroreceptor reflex, as evaluated by increases in RSNA and HR in response to the decrease in SAP induced by sodium nitroprusside (SNP), was suppressed in the anesthetized rats compared with the conscious rats. Consistent with this finding, baroreceptor denervation attenuated the excitatory responses of RSNA to anaphylaxis in the conscious rats but not in the pentobarbital-anesthetized rats. RSNA was increased markedly in conscious rats during anaphylactic hypotension. Anesthetics attenuated this antigen-induced renal sympathoexcitation through the suppression of baroreceptor function.     

Effect of myeloma IgE injections on passive and active cutaneous anaphylaxis in rats

The ability of injected rat IgE myeloma protein IR162 to inhibit passive and active cutaneous anaphylaxis in Lewis rats was investigated. IgE injected i.p. 24 hr before the sensitization with IgE anti-ovalbumin (OVA) completely inhibited both IgE- and IgG2a-induced passive cutaneous anaphylactic (PCA) reactions at a dose (2.5 mg/100 g body weight) that resulted in peak serum concentrations of 150 micrograms IgE IR162/ml. Peak IgE IR162 serum concentrations of 20 to 60 micrograms/ml inhibited the PCA reaction in approximately 50% of the rats. Intracutaneous injection of a mixture of myeloma IgE and anti-OVA IgE in a ratio of 100:1 or more also inhibited the PCA reaction. In contrast, the PCA reaction was not inhibited by seven daily doses of IgE beginning 24 hr after passive sensitization. Likewise, the cutaneous anaphylactic reaction elicited in rats 14 days after immunization with OVA and Bordetella pertussis was not prevented by daily injections of myeloma IgE despite a 1000- to 3000-fold excess of the myeloma IgE to anti-OVA IgE serum concentration. The data demonstrate that parenteral administration of myeloma IgE inhibits the PCA reaction only when given before passive sensitization and does not prevent cutaneous anaphylaxis in actively immunized rats. Because myeloma IgE failed to inhibit anaphylactic reactions in actively immunized rats, it is questionable whether administering human IgE-derived synthetic peptides or recombinant DNA-produced IgE fragments will be able to prevent allergic diseases by blocking the IgE Fc receptors on mast cells.     

The roles of mast cells and Kupffer cells in rat systemic anaphylaxis

Mast cells and other cells such as macrophages have been shown to mediate systemic anaphylaxis. We determined the roles of mast cells and Kupffer cells in hepatic and systemic anaphylaxis of rats. Roles of mast cells were examined by using the mast cell-deficient white spotting (Ws/Ws) rat; the Ws/Ws and wild type (+/+) rats were sensitized with ovalbumin (1 mg). Roles of Kupffer cells were examined by depleting Kupffer cells using gadolinium chloride or liposome-encapsulated dichloromethylene diphosphonate in the Ws/Ws and Sprague-Dawley rats. An intravenous injection of 0.6 mg ovalbumin caused substantial anaphylactic hypotension in both the Ws/Ws and +/+ rats; however, the occurrence was delayed in the Ws/Ws rats. After antigen, portal venous pressure increased by 13.1 cmH2O in the +/+ rats, while it increased only by 5.7 cmH2O in the Ws/Ws rats. In response to antigen, the isolated perfused liver of the Ws/Ws rats also showed weak venoconstriction, the magnitude of which was one tenth as large as that of the +/+ rats, indicating that hepatic anaphylaxis was primarily due to mast cells. In contrast, Kupffer cell depletion did not attenuate anaphylactic hepatic venoconstriction in isolated perfused livers. In conclusion, mast cells are involved mainly in anaphylactic hepatic presinusoidal portal venoconstriction but only in the early stage of anaphylactic systemic hypotension in rats. Macrophages, including Kupffer cells, do not participate in rat hepatic anaphylactic venoconstriction.     

Differences in neuronal lipid composition between superior cervical ganglia and nodose ganglia of the rat

The lipid content and composition of rat superior cervical ganglia containing sympathetic motor neurons and nodose ganglia containing parasympathetic sensory neurons were studied for the first time to elucidate the mechanism of the different effects of exogenous gangliosides on these neurons in the culture medium. The ganglioside content of the superior cervical ganglia was almost 3-times that of the nodose ganglia. Although both ganglia contained GM3, GD3, GD1b and GT1b as major gangliosides, the nodose ganglia additionally contained a significant amount of sialosyllactoneotetraosylceramide LM1 (10% of total sialic acids). Contrasting with nodose ganglia, vagus fiber and dorsal root ganglia of rats, superior cervical ganglia had a higher content of sulfatide than galactosylceramide. The phospholipid content was lower in superior cervical ganglia than in nodose ganglia. Superior cervical ganglia contained less ethanolamine plasmalogen and more phosphatidylcholine than nodose ganglia. Sphingomyelin in superior cervical ganglia contained mainly medium-chain fatty acids, while that in nodose ganglia contained mainly longer-chain fatty acids. Differences in the fatty acid composition of glycerophospholipids were also observed. The results indicate that the properties of neuronal cell membranes from superior cervical ganglia and nodose ganglia are quite different, and that the differences may reflect the physiological roles of these ganglia.     

Cardiovascular and lung inflammatory effects induced by systemically administered diesel exhaust particles in rats

Pollution by particulates has consistently been associated with increased cardiorespiratory morbidity and mortality. It has been suggested that ultrafine particles, of which diesel exhaust particles (DEP) are significant contributors, are able to translocate from the airways into the bloodstream in vivo. In the present study, we assessed the effect of systemic administration of DEP on cardiovascular and respiratory parameters. DEP were administered into the tail vein of rats, and heart rate, blood pressure, blood platelet activation, and lung inflammation were studied 24 h later. Doses of 0.02, 0.1, or 0.5 mg DEP/kg (8, 42, or 212 microg DEP/rat) induced a significant decrease of heart rate and blood pressure compared with saline-treated rats. Although the number of platelets was not affected, all the doses of DEP caused a shortening of the bleeding time. Similarly, in addition to triggering lung edema, the bronchoalveolar lavage analysis revealed the presence of neutrophil influx in DEP-treated rats in a dose-dependent manner. We conclude that the presence of DEP in the systemic circulation leads not only to cardiovascular and haemostatic changes but it also triggers pulmonary inflammation.     

Motor activity as an unbiased variable to assess anaphylaxis in allergic rats

The release of mediators by mast cells triggers allergic symptoms involving various physiological systems and, in the most severe cases, the development of anaphylactic shock compromising mainly the nervous and cardiovascular systems. We aimed to establish variables to objectively study the anaphylactic response (AR) after an oral challenge in an allergy model. Brown Norway rats were immunized by intraperitoneal injection of ovalbumin with alum and toxin from Bordetella pertussis. Specific immunoglobulin (Ig) E antibodies were developed in immunized animals. Forty days after immunization, the rats were orally challenged with the allergen, and motor activity, body temperature and serum mast cell protease concentration were determined. The anaphylaxis induced a reduction in body temperature and a decrease in the number of animal movements, which was inversely correlated with serum mast cell protease release. In summary, motor activity is a reliable tool for assessing AR and also an unbiased method for screening new anti-allergic drugs.     

Mouse anaphylactic shock is caused by reduced cardiac output,but not by systemic vasodilatation or pulmonary vasoconstriction,via PAF and histamine

Aims

Systemic anaphylaxis is life-threatening, and its pathophysiology is not fully clarified. Mice are frequently used for experimental study on anaphylaxis. However, the hemodynamic features and mechanisms of mouse anaphylactic hypotension remain unknown. Therefore, we determined mechanisms of systemic and pulmonary vascular response to anaphylactic hypotension in anesthetized BALB/c mice by using receptor antagonists of chemical mediators.

Main methods

Anaphylaxis was actively induced by an intravenous injection of the ovalbumin antigen into open-chest artificially ventilated sensitized mice. Mean arterial pressure (MAP), pulmonary arterial pressure (PAP), left atrial pressure, central venous pressure, and aortic blood flow (ABF) were continuously measured.

Key findings

In sensitized control mice, MAP and ABF showed initial, transient increases, followed by progressive decreases after the antigen injection. Total peripheral resistance (TPR) did not decrease, while PAP initially and transiently increased to 18.5 ± 0.5 mm Hg and pulmonary vascular resistance (PVR) also significantly increased. The antigen-induced decreases in MAP and ABF were attenuated by pretreatment with either a platelet-activating factor (PAF) receptor antagonist, CV6209, or a histamine H₁ receptor antagonist, diphenhydramine, and were abolished by their combination. Diphenhydramine augmented the initial increases in PAP and PVR, but did not affect the decrease of the corresponding MAP fall. The antagonists of either leukotriene C₄ or serotonin, alone or in combination with CV6209, exerted no significant effects.

Significance

Mouse anaphylactic hypotension is caused by a decrease in cardiac output but not vasodilatation, via actions of PAF and histamine. The slight increase in PAP is not involved in mouse anaphylactic hypotension.     

Acetyl- and pseudocholinesterase activities in sympathetic ganglia of rats

—The quantitative method of Ellman , Courtney , Andres and Featherstone (1961) was adapted to a differential assay for the determination of acetyl- and pseudocholinesterase activities of sympathetic ganglia of rats. The activities of the cholinesterases of superior cervical, stellate and thoracic chain ganglia and of the abdominal ganglionic complexes in apposition to the superior mesenteric and coeliac arteries (superior mesenteric, coeliac and cardiac ganglia) were measured. B.W.284C51 dibromide, 5 × 10^?5m , and ethopropazine hydrochloride, 3·15 × 10^?5m , were employed to inhibit selectively acetyl- and pseudocholinesterases, respectively. Linearity was shown to be maintained with enzyme concentrations corresponding to 0·12-0·5 mg of ganglion (wet wt.)/incubation. Under the experimental conditions of this assay, the rates of the reaction of ganglionic acetyl- and pseudocholinesterases were linear for time periods greater than those employed for calculating the rates of hydrolysis in the homogenates of sympathetic ganglia. Several experimental approaches were used to ascertain the specificity of the inhibitors and of the reaction. Of the total cholinesterase activity of sympathetic ganglia of rats, 55-63 per cent was due to acetylcholinesterase and 31-39 per cent to pseudocholinesterase. On the basis of the specific enzyme activity, superior cervical, stellate and superior mesenteric ganglia contained higher acetyl- and pseudocholinesterase activities than did thoracic chain, coeliac and cardiac (abdominal) ganglia. The specific activity of acetylcholinesterase was similar in rat and cat superior cervical ganglia and sympathetic cervical trunks while the pseudocholinesterase activity of these two tissues was somewhat lower in cats than in rats.     

Cerebral Autoregulation Is Minimally Influenced by the Superior Cervical Ganglion in Two- Week-Old Lambs,and Absent in Preterm Lambs Immediately Following Delivery

Cerebral vessels in the premature newborn brain are well supplied with adrenergic nerves, stemming from the superior cervical ganglia (SCG), but their role in regulation of blood flow remains uncertain. To test this function twelve premature or two-week-old lambs were instrumented with laser Doppler flow probes in the parietal cortices to measure changes in blood flow during changes in systemic blood pressure and electrical stimulation of the SCG. In lambs delivered prematurely at ∼129 days gestation cerebral perfusion and driving pressure demonstrated a direct linear relationship throughout the physiologic range, indicating lack of autoregulation. In contrast, in lambs two-weeks of age, surgical removal of one SCG resulted in ipsilateral loss of autoregulation during pronounced hypertension. Electrical stimulation of one SCG elicited unilateral increases in cerebral resistance to blood flow in both pre-term and two-week-old lambs, indicating functioning neural pathways in the instrumented, anesthetized lambs. We conclude cerebral autoregulation is non-functional in preterm lambs following cesarean delivery. Adrenergic control of cerebral vascular resistance becomes effective in newborn lambs within two-weeks after birth but SCG-dependent autoregulation is essential only during pronounced hypertension, well above the normal range of blood pressure.