Cortical cerebral blood flow cycling: anesthesia and arterial blood pressure

1995 ◽  
Vol 268 (2) ◽  
pp. H569-H575 ◽  
Author(s):  
S. C. Jones ◽  
J. L. Williams ◽  
M. Shea ◽  
K. A. Easley ◽  
D. Wei
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Pressure Change ◽  
Sprague Dawley ◽  
Doppler Flowmetry ◽  
Blood Withdrawal ◽  
Cranial Window ◽  
Arterial Blood ◽  
Mean Pressure

Cycling of various cerebral metabolic substances, arterial vascular diameter, and flow has been noted by many workers at a frequency near 0.1 Hz. Suspicion that this phenomenon is dependent on the type of anesthesia led us to investigate the occurrence of cerebral blood flow (CBF) cycling with different anesthetics. Fifteen Sprague-Dawley rats were anesthetized with either pentobarbital (n = 5, 40–50 mg/kg), alpha-chloralose (n = 5, 60 mg/kg), or halothane (n = 5, 1–0.5%). Body temperature was maintained at 37 degrees C. Femoral arterial and venous catheters were placed, and a tracheotomy was performed, permitting artificial ventilation with 30% O2–70% N2. A closed cranial window was formed over a 3-mm diameter craniotomy. Mean arterial pressure (MABP), arterial partial pressures of CO2 and O2 (PaCO2 and PaO2), and pH were controlled and stabilized at normal values. CBF was determined using laser Doppler flowmetry. To induce cycling, MABP was transiently and repeatedly lowered by exsanguination. Fast Fourier analysis of selected 64-s flow recordings (n = 38) was performed. CBF cycling was observed, independent of the type of anesthesia, in all animals. In 36 epochs, cycling was induced when MABP was reduced to a mean pressure of 65 +/- 1.5 mmHg. The mean frequency and amplitude were 0.094 +/- 0.003 Hz and 6.6 +/- 0.5%, respectively. Cycling occurred without blood withdrawal in two epochs. With the use of the blood-withdrawal epochs (n = 36), all three anesthetics shared a common linear slope between amplitude and blood pressure (P < 0.02) and blood pressure change (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Cerebrovascular Responses under Controlled and Monitored Physiological Conditions in the Anesthetized Mouse

1995 ◽  
Vol 15 (4) ◽  
pp. 631-638 ◽  
Author(s):  
T. Dalkara ◽  
K. Irikura ◽  
Z. Huang ◽  
N. Panahian ◽  
M. A. Moskowitz
Keyword(s):  
Blood Pressure ◽  
Respiratory Control ◽  
Blood Gases ◽  
Cerebrovascular Reactivity ◽  
Sprague Dawley ◽  
Physiological Control ◽  
Doppler Flowmetry ◽  
Cranial Window ◽  
Arterial Blood ◽  
End Tidal

Control of physiological parameters such as respiration, blood pressure, and arterial blood gases has been difficult in the mouse due to the lack of technology required to monitor these parameters in small animals. Here we report that anesthetized and artificially ventilated mice can be maintained under physiological control for several hours with apparently normal cerebrovascular reactivity to hypercapnia and mechanical vibrissal stimulation. SV-129 mice were anesthetized with urethane (750 mg/kg i.p.) and α-chloralose (50 mg/kg i.p.), intubated, paralyzed, and artificially ventilated. Respiratory control was maintained within physiological range by reducing the inspiratory phase of the respiratory cycle to <0.1 s and by adjusting end-tidal CO2 to give a Pco2 of 35 ± 3 mm Hg. In these mice, mean arterial pressure (95 ± 9 mm Hg), heart rate (545 ± 78 beats/min), and arterial pH (7.27 ± 0.10) could be maintained for several hours. Body temperature was kept at 36.5–37.5°C. We observed stable regional CBF (rCBF) measurements (as determined by laser–Doppler flowmetry) when systemic arterial blood pressure was varied between 40 and 130 mm Hg. Hypercapnia led to a 38 ± 15% (5% CO2) and 77 ± 34% (10% CO2) increase in rCBF. Mechanical stimulation of contralateral vibrissae for 1 min increased rCBF by 14 ± 4%. Changes in rCBF compare favorably with those observed previously in another rodent species, the Sprague–Dawley rat. After placement of a closed cranial window, cerebrovascular reactivity to hypercapnia and whisker stimulation was intact and well maintained during 2-h superfusion with artificial CSF.

Alteration of pial vessel responses to blood pressure changes in rats after hypoxia

1987 ◽  
Vol 65 (11) ◽  
pp. 2265-2268 ◽  
Author(s):  
B. Y. Ong ◽  
J. J. Kettler ◽  
D. Bose
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Pial Arteries ◽  
Similar Time ◽  
Vascular Responses ◽  
Cranial Window ◽  
Arterial Blood ◽  
Cerebral Blood Flow Autoregulation ◽  
Pial Vessel

Previous studies in newborn lamb have shown impairment of cerebral blood flow autoregulation after hypoxia followed by reoxygenation. The present study was done to see if such a phenomenon existed in the adult rat and if it could be demonstrated at the level of the pial arterioles. Using an open cranial window preparation, we assessed the changes in pial vessel diameter during blood pressure alterations induced by hemorrhage and reinfusion of blood, before and after 30 s of hypoxia, in 15 male Sprague–Dawley rats. Mean diameters of pial arteries in the study group of rats were 128 ± 54 μm before hypoxia and 141 ± 61 μm after normoxia following hypoxia. The corresponding diameters in rats serving as time controls were 136 ± 52 and 138 ± 52 μm. Slopes of pial vessel diameters as a function of mean arterial blood pressures descreased significantly (p < 0.05) after hypoxia from −0.86 ± 0.45 to 0.03 ± 0.66 (mean ± SD). In the control rats not subjected to hypoxia, the slopes remained unchanged over a similar time period (−0.60 ± 0.16 and −0.42 ± 0.19). The negative slopes indicate that pial vessels dilate during hypotension and constrict during hypertension. Such vascular responses may play a role in autoregulation of cerebral blood flow. We found that a relatively brief period of hypoxia can cause a long-lasting impairment of vascular responses even after restoration of normoxia. These findings are consistent with a previous report of persistent impairment of cerebral blood flow autoregulation after a brief period of hypoxia.

Variability in the Magnitude of the Cerebral Blood Flow Response and the Shape of the Cerebral Blood Flow: Pressure Autoregulation Curve during Hypotension in Normal Rats

2002 ◽  
Vol 97 (2) ◽  
pp. 488-496 ◽  
Author(s):  
Stephen C. Jones ◽  
Carol R. Radinsky ◽  
Anthony J. Furlan ◽  
Douglas Chyatte ◽  
Yinsheng Qu ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Lower Limit ◽  
Vascular Reactivity ◽  
Surgical Trauma ◽  
Sprague Dawley ◽  
Doppler Flowmetry ◽  
Cranial Window ◽  
Pressure Autoregulation

Background The maintenance of constant cerebral blood flow (CBF) as mean cerebral perfusion pressure (CPP) varies is commonly referred to as CBF-pressure autoregulation. The lower limit of autoregulation is the CPP at which the vasodilatory capacity is exhausted and flow falls with pressure. We evaluated variability in the magnitude of percent change in CBF during the hypotensive portion of the autoregulatory curve. We hypothesize that this variability, in normal animals, obeys a Gaussian distribution and characterizes a vasodilatory mechanism that is inherently different from that described by the lower limit. Methods Sixty-five male Sprague-Dawley rats were anesthetized with 0.5-1% halothane and 70% nitrous oxide in oxygen. Body temperature was maintained at 37 degrees C. Using a closed, superfused cranial window, CBF (as % of control) was determined using laser Doppler flowmetry (LDF) through the window with the intracranial pressure set at 10 mmHg. Animals with low vascular reactivity to inhaled carbon dioxide and superfused adenosine diphosphate (ADP) or acetylcholine were excluded. MABP was sequentially lowered by exsanguination to 100, 85, 70, 55, and 40 mmHg. Using the %CBF versus CPP plots for each curve (1) the lower limit of autoregulation was identified; (2) the pattern of autoregulation was classified as "peak" (a rise in LDF flow of at least 15% as arterial pressure was dropped), "classic" (plateau with a fall), or "none" (a fall in LDF flow of greater than 15%); (3) the area under the autoregulatory curve between CPPs of 30 and 90 mmHg was calculated; and (4) the magnitude of the %CBF response to hypotension was assessed by determining the %CBF at a CPP of 60 mmHg (%CBFCPP60). Results Of the 65 curves, 21 had the peak pattern, 33 the classic pattern, and 11 the none pattern. The %CBFCPP60 and autoregulatory area displayed Gaussian distributions, consistent with normal variability. Although %CBFCPP60, autoregulatory area, and pattern were significantly correlated (r or rho &gt; 0.84, P &lt; 0.001), the lower limit correlated weakly with autoregulatory area (r = 0.34, P = 0.012), and not at all with autoregulatory pattern or %CBFCPP60. Conclusions The %CBFCPP60 measures an aspect of the autoregulatory curve that is distinct from the lower limit. The peak autoregulatory pattern indicates that vessels are dilating more than is necessary to maintain a plateau in response to the pressure decrease, whereas the none pattern existed in spite of acceptable vascular responses to inhaled carbon dioxide and superfused ADP or ACh and the lack of surgical trauma. These results provide a different view of autoregulation during hypotension, are most likely dependent on the highly regional CBF method used, and could have implications concerning potential cerebral ischemia and hypotension during anesthesia.

Cortical NOS inhibition raises the lower limit of cerebral blood flow-arterial pressure autoregulation

1999 ◽  
Vol 276 (4) ◽  
pp. H1253-H1262 ◽  
Author(s):  
Stephen C. Jones ◽  
Carol R. Radinsky ◽  
Anthony J. Furlan ◽  
Douglas Chyatte ◽  
Alejandro D. Perez-Trepichio
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Lower Limit ◽  
Blood Withdrawal ◽  
Arterial Blood ◽  
Pressure Autoregulation

The maintenance of constant cerebral blood flow (CBF) as arterial blood pressure is reduced, commonly referred to as CBF-pressure autoregulation, is typically characterized by a plateau until the vasodilatory capacity is exhausted at the lower limit, after which flow falls linearly with pressure. We investigated the effect of cortical, as opposed to systemic, nitric oxide synthase (NOS) inhibition on the lower limit of CBF-pressure autoregulation. Forty-four Sprague-Dawley rats were anesthetized with halothane and N2O in O2. With a closed cranial window placed the previous day in a ventilated and physiologically stable preparation, we determined the CBF using laser-Doppler flowmetry. Animals with low reactivity to inhaled CO2 and suffused ADP or ACh were excluded. Five arterial pressures from 100 to 40 mmHg were obtained with controlled hemorrhagic hypotension under cortical suffusion with artificial cerebrospinal fluid (aCSF) and then again after suffusion for 35 ( n = 5) and 105 min ( n = 10) with aCSF, 10−3 M N ω-nitro-l-arginine (l-NNA; n = 12), or 10−3 M N ω-nitro-d-arginine (d-NNA; n = 5). An additional group ( n = 7) was studied after a 105-min suffusion of l-NNA followed by a single blood withdrawal procedure. The lower limit of autoregulation was identified visually by four blinded reviewers as a change in the slope of the five-point plot of CBF vs. mean arterial blood pressure. The lower limit of 90 ± 4.3 mmHg after 105 min of 1 mMl-NNA suffusion was increased compared with the value in the time-control group of 75 ± 5.3 mmHg ( P < 0.01; ANOVA) and the initial value of 67 ± 3.7 mmHg ( P < 0.001). The lower limit of 84 ± 5.9 mmHg in seven animals with 105 min of suffusion of 1 mM l-NNA without previous blood withdrawal was significantly increased ( P < 0.01) in comparison with 70 ± 1.9 mmHg from those with just aCSF suffusion ( n = 37). No changes in lower limit for the other agents or conditions, including 105 or 35 min of aCSF or 35 min of l-NNA suffusion, were detected. The lack of effect on the lower limit withd-NNA suffusion suggests an enzymatic mechanism, and the lengthyl-NNA exposure of 105 min, but not 35 min, suggests inhibition of a diffusionally distant NOS source that mediates autoregulation. Thus cortical suffusion ofl-NNA raises the lower limit of autoregulation, strongly suggesting that nitric oxide is at least one of the vasodilators active during hypotension as arterial pressure is reduced from normal.

Acute vasoconstriction: decrease and recovery of cerebral blood flow after various intensities of experimental subarachnoid hemorrhage in rats

2009 ◽  
Vol 110 (5) ◽  
pp. 996-1002 ◽  
Author(s):  
Thomas Westermaier ◽  
Alina Jauss ◽  
Jörg Eriskat ◽  
Ekkehard Kunze ◽  
Klaus Roosen
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Therapeutic Potential ◽  
Experimental Studies ◽  
Acute Type ◽  
Sprague Dawley ◽  
Early Recovery ◽  
Doppler Flowmetry ◽  
Arterial Blood

Object Immediate vasoconstriction after subarachnoid hemorrhage (SAH) has been observed in a number of experimental studies. However, it has not yet been examined which pattern this acute-type vascular reaction follows and whether it correlates with the intensity of SAH. It was the purpose of the present study to vary the extent of SAH using the endovascular filament model of SAH with increasing filament sizes and to compare the course of intracranial pressure (ICP), cerebral perfusion pressure (CPP), and regional cerebral blood flow (rCBF). Methods Male Sprague-Dawley rats were subjected to SAH using the endovascular filament model. Subarachnoid hemorrhage was induced using a 3-0, 4-0, or 5-0 Prolene monofilament (8 rats in each group). Eight animals served as controls. Bilateral rCBF (laser Doppler flowmetry), mean arterial blood pressure, and ICP were continuously monitored. Thereafter, the rats were allowed to wake up. Twenty-four hours later, the animals were killed, their brains were removed, and the extent of SAH was determined. Results After induction of SAH, ICP steeply increased while CPP and rCBF rapidly declined in all groups. With increasing size of the filament, the increase of ICP and the decrease of CPP were more pronounced. However, the decline of rCBF exceeded the decline of CPP in all SAH groups. In a number of animals with minor SAH, an oscillating pattern of rCBF was observed during induction of SAH and during early recovery. Conclusions The disparity between the decline and recovery of CPP and rCBF suggests that acute vasoconstriction occurs even in SAH of a minor extent. Acute vasoconstriction may contribute significantly to a perfusion deficit in the acute stage after SAH. The oscillating pattern of rCBF in the period of early recovery after SAH resembles the pattern of synchronized vasomotion, which has been thoroughly examined for other vascular territories and may yield therapeutic potential.

Diurnal variation in time to presyncope and associated circulatory changes during a controlled orthostatic challenge

2010 ◽  
Vol 299 (1) ◽  
pp. R55-R61 ◽  
Author(s):  
N. C. S. Lewis ◽  
G. Atkinson ◽  
S. J. E. Lucas ◽  
E. J. M. Grant ◽  
H. Jones ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Diurnal Variation ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Orthostatic Challenge ◽  
Arterial Blood ◽  
Neurally Mediated Syncope

Epidemiological data indicate that the risk of neurally mediated syncope is substantially higher in the morning. Syncope is precipitated by cerebral hypoperfusion, yet no chronobiological experiment has been undertaken to examine whether the major circulatory factors, which influence perfusion, show diurnal variation during a controlled orthostatic challenge. Therefore, we examined the diurnal variation in orthostatic tolerance and circulatory function measured at baseline and at presyncope. In a repeated-measures experiment, conducted at 0600 and 1600, 17 normotensive volunteers, aged 26 ± 4 yr (mean ± SD), rested supine at baseline and then underwent a 60° head-up tilt with 5-min incremental stages of lower body negative pressure until standardized symptoms of presyncope were apparent. Pretest hydration status was similar at both times of day. Continuous beat-to-beat measurements of cerebral blood flow velocity, blood pressure, heart rate, stroke volume, cardiac output, and end-tidal Pco2 were obtained. At baseline, mean cerebral blood flow velocity was 9 ± 2 cm/s (15%) lower in the morning than the afternoon ( P < 0.0001). The mean time to presyncope was shorter in the morning than in the afternoon (27.2 ± 10.5 min vs. 33.1 ± 7.9 min; 95% CI: 0.4 to 11.4 min, P = 0.01). All measurements made at presyncope did not show diurnal variation ( P > 0.05), but the changes over time (from baseline to presyncope time) in arterial blood pressure, estimated peripheral vascular resistance, and α-index baroreflex sensitivity were greater during the morning tests ( P < 0.05). These data indicate that tolerance to an incremental orthostatic challenge is markedly reduced in the morning due to diurnal variations in the time-based decline in blood pressure and the initial cerebral blood flow velocity “reserve” rather than the circulatory status at eventual presyncope. Such information may be used to help identify individuals who are particularly prone to orthostatic intolerance in the morning.

Effect of the Ace Inhibitor Ceronapril on Cerebral Blood flow in Hypertensive Patients

1996 ◽  
Vol 30 (6) ◽  
pp. 578-582 ◽  
Author(s):  
Neal R Cutler ◽  
John J Sramek ◽  
Azucena Luna ◽  
Ismael Mena ◽  
Eric P Brass ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Diastolic Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Enzyme Inhibitor ◽  
Blood Pressure Response ◽  
Combined Therapy ◽  
Arterial Blood

Objective To assess the effect of the angiotensin-converting enzyme inhibitor ceronapril on cerebral blood flow (CBF) in patients with moderate hypertension. Design Patients received chlorthalidone 25 mg for 4 weeks, and if diastolic blood pressure remained in the range of 100–115 mm Hg, they were given titrated doses of ceronapril (10–40 mg/d based on blood pressure response) in addition to chlorthalidone for 9 weeks. Setting Outpatient research clinic. Subjects Eligible patients had moderate essential hypertension (diastolic blood pressure 100–115 mm Hg) assessed when the patients were receiving no medications. Thirteen patients were entered into the study; 1 withdrew for reasons unrelated to the study drug. Twelve patients (11 men, 1 woman; mean age 52 y) completed the study. Intervention Ceronapril, given with chlorthalidone. Main Outcome Measures CBF measurements were taken at the start and end of ceronapril therapy using intravenous 133Xe; blood pressures were determined weekly. Results Mean arterial blood pressure decreased from 130 ± 4 to 120 ±7 mm Hg after 4 weeks of chlorthalidone administration, and fell further to 108 ± 8 mm Hg after an additional 9 weeks of combined chlorthalidone-ceronapril therapy (p < 0.05). CBF fell from 44 ± 15 to 34 ± 5 mL/min/100 g during the 9 weeks of combined therapy (p = 0.05). No adverse effects consistent with decreased CBF were observed. The decrease in CBF was not linearly correlated with the change in systemic blood pressure, but was strongly correlated (r = –0.937; p < 0.001) with the initial CBF. Conclusions The decrease in mean arterial blood pressure was not associated with a decrease in CBF. Patients with high CBF may be predisposed to a decrease in CBF when treated with ceronapril and chlorthalidone.

Vasoactive intestinal polypeptide reduces hydrochloric acid-induced duodenal mucosal permeability

1993 ◽  
Vol 264 (2) ◽  
pp. G272-G279 ◽  
Author(s):  
O. Nylander ◽  
E. Wilander ◽  
G. M. Larson ◽  
L. Holm
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Vasoactive Intestinal Polypeptide ◽  
Lesion Score ◽  
Morphological Examination ◽  
Mucosal Permeability ◽  
Doppler Flowmetry ◽  
Arterial Blood ◽  
51Cr Edta ◽  
Intestinal Polypeptide

The duodenum in anesthetized rats was perfused with HCl, and mucosal integrity was assessed by measuring the clearance of 51Cr-labeled EDTA from blood to lumen and/or by morphological examination (lesion score). Duodenal blood flow was determined by laser Doppler flowmetry and luminal alkalinization as well as H+ disappearance by backtitration. Intravenous infusion of vasoactive intestinal polypeptide (VIP; 13.5 micrograms.kg-1.h-1) increased luminal alkalinization threefold and decreased clearance of 51Cr-EDTA by 50%. VIP also decreased arterial blood pressure and induced a small and irregular decrease in duodenal blood flow. Perfusion with 10 mM HCl increased clearance of 51Cr-EDTA 2.1-fold, but the lesion score was not different from that in saline-perfused animals. Perfusion with 20 mM HCl increased clearance of 51Cr-EDTA four-fold and induced a greater lesion score than did 10 mM. Perfusion with either 10 or 20 mM HCl did not affect the duodenal blood flow. VIP reduced the rise in clearance of 51Cr-EDTA in response to 10 mM but not that to 20 mM HCl. Intravenous injection of prazosin (50 micrograms/kg) decreased luminal alkalinization, clearance of 51Cr-EDTA, blood pressure, and duodenal blood flow. In prazosin-pretreated rats, perfusion with 10 mM HCl increased clearance of 51Cr-EDTA 2.6-fold, and the lesion score was greater in this group than in animals infused with VIP. A positive linear correlation was obtained between HCO3- secretion and the mean rate of H+ disappearance.(ABSTRACT TRUNCATED AT 250 WORDS)

Vasodilation of cat cerebral arterioles by prostaglandins D2, E2, G2, and I2

1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Standard Error ◽  
Arterial Blood ◽  
Cerebral Arterioles ◽  
The Mean ◽  
Dose Dependent ◽  
The Brain

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.

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