Brain Interstitial Adenosine and Sagittal Sinus Blood Flow during Systemic Hypotension in Piglet

Park, T. S.; Wylen, D. G. L. Van; Rubio, Rafael; Berne, Robert M.

doi:10.1038/jcbfm.1988.138

Cited by 28 publications

(9 citation statements)

References 22 publications

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“…It is therefore conceivable that the actual perivascular concentration of adenosine rises more rapidly and to a higher level in response to a small reduction in MABP than both CSF and interstitial fluid measure ments would suggest. The role of adenosine within the limits of autoregulation has been a matter of debate (Winn et al , 1980a;Phillis et al , 1987;Park et al , 1988;Van Wylen et al , 1988) but is supported in the present study by the dramatic effect of 8-PT on the autoregulatory curve between 70-100 and 50 mm Hg.…”

Section: Discussionsupporting

confidence: 66%

The Role of Adenosine in the Vascular Adaptation of Neonatal Cerebral Blood Flow during Hypotension

Laudignon

Beharry

Farri

et al. 1991

J Cereb Blood Flow Metab

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Summary: This study investigated the potential role of adenosine in cerebral blood flow (CBF) regulation in the neonate during moderate and severe hypotension. Exper iments were done in anesthetized, 1-to 3-day-old piglets. Regional CBF (determined by radio labeled microsphere technique) and cerebral metabolic rate for Oz (CMROz) were measured (a) during normotension and (b) during a 3-min period of moderate (58 ± 9 mm Hg) or severe (36 ± 7 mm Hg) hypotension produced by the inflation of a balloon catheter placed in the aortic root. Measurements of CBF and CMROz were performed successively after intracerebroventricular (i. c. v. ) injections of vehicle (n = 17), the adenosine receptor blocker 8-phenyltheophylline (8-PT, 10 /Lg, n = 14), and the A2-receptor agonist 5'-N-(ethylcarboxamide)adenosine (NECA, 2 ng, n = 8).After i. c. v. administration of vehicle, none of the param eters studied was significantly altered by moderate hy potension, but severe hypotension decreased the total Autoregulation (i.e., the maintenance of a con stant cerebral blood flow (CBF) over a range of systemic blood pressure) exists in the neonates (Hernandez et aI., 1980; Laptook et aI., 1982 Laptook et aI., , 1983 Papile et aI., 1985; Leffler et aI., 1986) albeit at a narrower range relative to adults. It is due to an adaptation of the cerebral resistance vessels that constrict in response to an increase in cerebral per fusion pressure and dilate in response to a decrease Received March 3, 1990; revised November 5, 1990; accepted November 9, 1990.Address correspondence and reprint requests to Dr. N. Lau dignon at Department of Pharmacology and Therapeutics, The Montreal Children's Hospital, Room A-604, 2300 Tupper Street, Montreal, Quebec, H3H IP3, Canada.Abbreviations used: CO, cardiac output; COD, cerebral oxy gen delivery; CVR, cerebral vascular resistance; EHNA, erythro-9-(2-hydroxy-3-nonyl)adenine; i. c. v. , intracerebro ventricular; NECA, 5'-N-(ethylcarboxamide)adenosine; 8-PT, 8-phenyltheophylline. 424CBF (mean ± SD) from 86 ± 24 to 40 ± 15 ml min -I 100 g-l and CMROz from 3. 2 ± 0. 8 to 1. 8 ± 1. 0 ml min -I 100 g-I (p < 0. 05). Administration of 8-PT did not alter these parameters during normotension, but significantly de creased CBF during moderate hypotension compared to postvehicle values (53 ± 11 versus 81 ± 12 ml min -I 100 g-l, P < 0. 05). This loss of autoregulation was com pletely reversed by NECA. During severe hypotension, 8-PT altered the CBF redistribution towards the brain stem. Mean normotensive CSF concentrations of adeno sine (0. 76 ± 0. 26 /LM) increased during moderate (l.40 ± 1. 78 /LM) and severe (2. 60 ± 2. 56/LM, p < 0.05) hypoten sion. These data suggest that, in the newborn, adenosine is an important mediator of the cerebral adaptive re sponse to hypotension, even within the range of autoreg ulation.

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Section: Discussionsupporting

confidence: 66%

The Role of Adenosine in the Vascular Adaptation of Neonatal Cerebral Blood Flow during Hypotension

Laudignon

Beharry

Farri

et al. 1991

J Cereb Blood Flow Metab

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“…All resid ual common carotid blood flow was then taken to reflect unilateral ICBF. A sagittal sinus catheter was placed following the methodology of Park et al [17,18], A 2-cm-diameter cranial burr hole was made in the midline halfway between the nasion and inion, and the sagittal sinus (SS) was identified. A 16-french plastic catheter (Angiocath, Deseret Medical, Sandy, Utah, USA) was placed in the SS, blood return was verified, and the SS catheter was secured to the scalp.…”

Section: Cerebral Surgerymentioning

confidence: 99%

Relative Contribution of Endothelium-Derived Relaxation Factor to Vascular Tone in the Systemic, Pulmonary, and Cerebral Circulations of Piglets

Rudinsky

Bell²,

Hipps³

et al. 1993

Dev Pharmacol Ther

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We determined the contribution of endothelium-derived relaxation factor (EDRF) to vascular tone in the systemic, pulmonary, and cerebral circulations of piglets. Methods: 11 piglets were anesthetized and mechanically ventilated. Systemic cardiac output was determined by an electromagnetic flow probe placed on the main pulmonary artery. Cerebral blood flow was assessed by determining unilateral internal carotid artery blood flow (ICBF) using a flow probe placed on the common carotid artery after ligation of the ipsilatcral external carotid circulation. Progressive inhibition of EDRF was achieved by continuous infusion of the substituted /.-arginine analog N-nitro-L-arginine (NNLA). Hemodynamic observations were compared at 0, 0.1, 1.0, 10, 30, and 80 mg/kg cumulative dose of NNLA. Results: At all NNLA doses ≥ 1 mg/kg, both systemic blood pressure and systemic vascular resistance were elevated. At all NNLA doses ≥ 10 mg/ kg, systemic cardiac output was reduced. At all NNLA doses ≥ 10 mg/kg, pulmonary artery pressure and pulmonary vascular resistance were elevated. Although cerebral vascular resistance was elevated at all NNLA doses ≥ 10 mg/kg, ICBF was maintained at or near baseline values up to a dose of 80 mg/kg. At all levels of EDRF inhibition, both the pulmonary and systemic circulations demonstrated approximately equal magnitudes of vasoconstriction. In contrast, at 30 and 80 mg/kg cumulative dose of NNLA, the cerebral circulation was relatively less constricted by NNLA than was the systemic circulation. Systemic VO(2) was significantly reduced at 30 mg/kg and 80 mg/kg cumulative NNLA dose, while cerebral VO(2) was preserved at both NNLA doses. Conclusions: EDRF contributes to resting vasodilator tone in the systemic, pulmonary, and cerebral circulations in piglets. Progessive inhibition of EDRF constricts the systemic and pulmonary circulation equally. Inhibition of EDRF does not impair the ability of the brain to vary cerebral vascular resistance in order to redistribute blood flow towards itself during a period of reduced cardiac output.

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“…The blood flow signal from the ICBF probe was calibrated volumetrically against SS emuent using a modification of the methodology of Park et al (17,18) and Traystman and Rapela (20). We attempted to ensure that NNLA or INDO administration did not affect the ICBF signal (by, for example, redirecting ICBF to extracranial sites) in the following manner.…”

Section: Materials a N D Methodsmentioning

confidence: 99%

“…An SS catheter was placed by following the methodology of Park et al ( 17,18). A 2-cm diameter cranial burr hole was made in the midline halfway between the nasion and inion, and the SS was identified.…”

Section: Materials a N D Methodsmentioning

confidence: 99%

The Role of Prostaglandins and Endothehum-Derived Relaxation Factor in the Regulation of Cerebral Blood Flow and Cerebral Oxygen Utilization in the Piglet: Operationalizing the Concept of an Essential Circulation

et al. 1994

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ABSTRACT. The brain is considered an "essential" organ, defined as one whose blood supply is preferentially maintained vis-a-vis other less-essential circulations during periods of reduced systemic cardiac output (CO). We asked whether the actions of either prostaglandins or endothelium-derived relaxation factor might underlie the essential qualities of the cerebral circulation; that is, would the absence of one or the other impair the ability of the brain to preferentially redirect systemic blood flow during a period of reduced systemic CO. We compared hemodynamics in the cerebral and systemic circulations in 33 anesthetized piglets under three conditions that reduced systemic CO equivalently: endothelium-derived relaxation factor inhibition with the substituted L-arginine analog Nnitro-L-arginine (NNLA; 25 mg/kg), prostaglandin inhibition with indomethacin (INDO, 5 mglkg), and inflation of a left atrial balloon (LAB) catheter. NNLA, INDO, and LAB each reduced CO to an equivalent value (-30% from baseline). NNLA and INDO, but not LAB elevated systemic blood pressure, cerebral perfusion pressure (CPP), systemic vascular resistance (SVR), and cerebral vascular resistance (CVR). Cerebral blood flow (CBF) was preserved after NNLA and LAB but fell after INDO (-35%).Despite the equivalent reduction in CO noted during the three experimental protocols, the proportion of systemic blood flow directed toward the brain (CBFICO) rose significantly during LAB and NNLA (+30%) but fell significantly during INDO (-12%). Similarly, relative cerebral vascular resistance (CVRISVR) fell significantly during LAB and NNLA but rose during INDO. Cerebral vascular regulation can be considered along two complementary dimensions. Vascular regulation within the cerebral circulation itself (cerebral autoregulation) is expressed as CBF versus CPP. CBF was unchanged as CPP fell during LAB and as CPP rose after NNLA in piglets. In contrast, after INDO, CBF fell as CPP rose. Vascular regulation of the cerebral circulation vis-a-vis the rest of the body (referred to here as cerebral-specific vascular regulation) can be expressed either in terms of blood flow (CBFICO) or vascular resistance (CVRISVR). After both NNLA and LAB, as CO fell, CBFICO rose and CVRISVR fell, demonstrating preservation of the "essential" status of the cerebral circulation. In contrast, after INDO as systemic CO fell, CBFICO fell and CVRISVR rose. Prostaglandins,

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Brain Interstitial Adenosine and Sagittal Sinus Blood Flow during Systemic Hypotension in Piglet

Cited by 28 publications

References 22 publications

The Role of Adenosine in the Vascular Adaptation of Neonatal Cerebral Blood Flow during Hypotension

The Role of Adenosine in the Vascular Adaptation of Neonatal Cerebral Blood Flow during Hypotension

Relative Contribution of Endothelium-Derived Relaxation Factor to Vascular Tone in the Systemic, Pulmonary, and Cerebral Circulations of Piglets

The Role of Prostaglandins and Endothehum-Derived Relaxation Factor in the Regulation of Cerebral Blood Flow and Cerebral Oxygen Utilization in the Piglet: Operationalizing the Concept of an Essential Circulation

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