Cerebral blood flow during hemorrhagic hypotension in the unanesthetized goat

1977 ◽  
Vol 232 (4) ◽  
pp. H368-H372
Author(s):  
B. Gomez ◽  
A. R. Vallejo ◽  
E. Alborch ◽  
G. Dieguez ◽  
S. Lluch

Changes in cerebral blood flow (CBF), arterial blood pressure (AP), and cardiac output (CO) were studied during stepwise blood losses in 12 unanesthetized goats. Bleeding was followed by a drop in CBF, AP and CO in a nearly parallel fashion. Control values (means +/- SE) for CBF, AP, and CO were 117 +/- 5.6 ml/min per 100 g, 105 +/- 3.1 mmHg, and 2,825 +/- 124 ml/min, respectively; and after bleeding, 66 +/- 3.9 ml/min per 100 g, 57 mmHg, and 1, 383 ml/min. Arterial blood samples obtained before bleeding, during the hypotensive state, and after reinfusion did not show any significant differences in pH, PCO2, and PO2 values. In phentolamine-treated animals, bleeding produced a drop in AP and CO similar to that observed in the nontreated animals; however, the decrease in CBF was less marked. These findings show that CBF follows pari passu the fall in AP, and they indicate that the alpha-adrenergic receptors of the cerebral vessels are involved in the cerebral blood flow changes in hemorrhage.

1981 ◽  
Vol 59 (2) ◽  
pp. 204-208 ◽  
Author(s):  
R. Keeler ◽  
Anamaria Barrientos ◽  
K. Lee

A study was made of the effects of acute (4 h) or chronic (4 days) infusion of Escherichia coli endotoxin on cardiovascular function in rats. Rats with acute endotoxemia had a reduced cardiac output but maintained their arterial blood pressure. Fractional distribution of the cardiac output was increased to the liver and reduced to the gastrointestinal tract and skin. No changes in fractional distribution to the kidneys, lungs, or heart were observed although absolute blood flow to these areas was reduced.Rats with chronic endotoxemia had a reduced cardiac output and hypotension with no change in peripheral resistance. Other changes resembled those seen in acute endotoxemia apart from a low renal fraction of the cardiac output. Calculation and interpretation of blood flow changes in these animals was difficult because of a large fall in hematocrit and changes in organ weight.


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 ◽  
...  

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.


1996 ◽  
Vol 30 (6) ◽  
pp. 578-582 ◽  
Author(s):  
Neal R Cutler ◽  
John J Sramek ◽  
Azucena Luna ◽  
Ismael Mena ◽  
Eric P Brass ◽  
...  

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.


1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos

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.


PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 737-737
Author(s):  
JEFFREY M. PERLMAN ◽  
JOSEPH J. VOLPE

In Reply.— Marshall misread a critical piece of information in the text. His interpretation of the data would be correct, if the intracranial pressure, arterial blood pressure, and cerebral blood flow velocity changes occurred simultaneously. However, as we stated in the text (see section on "Temporal Features of Changes with Suctioning"), the intracranial pressure fell to base-line values immediately following suctioning, whereas the changes in arterial blood pressure and cerebral blood flow velocity occurred more slowly over an approximately two-minute period.


2001 ◽  
Vol 280 (5) ◽  
pp. H2162-H2174 ◽  
Author(s):  
Ronney B. Panerai ◽  
Suzanne L. Dawson ◽  
Penelope J. Eames ◽  
John F. Potter

The influence of different types of maneuvers that can induce sudden changes of arterial blood pressure (ABP) on the cerebral blood flow velocity (CBFV) response was studied in 56 normal subjects (mean age 62 yr, range 23–80). ABP was recorded in the finger with a Finapres device, and bilateral recordings of CBFV were performed with Doppler ultrasound of the middle cerebral arteries. Recordings were performed at rest (baseline) and during the thigh cuff test, lower body negative pressure, cold pressor test, hand grip, and Valsalva maneuver. From baseline recordings, positive and negative spontaneous transients were also selected. Stability of Pco 2 was monitored with transcutaneous measurements. Dynamic autoregulatory index (ARI), impulse, and step responses were obtained for 1-min segments of data for the eight conditions by fitting a mathematical model to the ABP-CBFV baseline and transient data (Aaslid's model) and by the Wiener-Laguerre moving-average method. Impulse responses were similar for the right- and left-side recordings, and their temporal pattern was not influenced by type of maneuver. Step responses showed a sudden rise at time 0 and then started to fall back to their original level, indicating an active autoregulation. ARI was also independent of the type of maneuver, giving an overall mean of 4.7 ± 2.9 ( n = 602 recordings). Amplitudes of the impulse and step responses, however, were significantly influenced by type of maneuver and were highly correlated with the resistance-area product before the sudden change in ABP ( r = −0.93, P < 0.0004). These results suggest that amplitude of the CBFV step response is sensitive to the point of operation of the instantaneous ABP-CBFV relationship, which can be shifted by different maneuvers. Various degrees of sympathetic nervous system activation resulting from different ABP-stimulating maneuvers were not reflected by CBFV dynamic autoregulatory responses within the physiological range of ABP.


1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.


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