THE MEASUREMENT OF BLOOD PRESSURE, THE CRITICAL OPENING PRESSURE, AND THE CRITICAL CLOSING PRESSURE OF DIGITAL VESSELS UNDER VARIOUS CIRCUMSTANCES

1965 ◽  
Vol 43 (6) ◽  
pp. 979-993 ◽  
Author(s):  
Peter Gaskell

A spectroscopic technique for the estimation of the critical opening pressure (COP) or critical closing pressure (CCP) of small vessels in the finger is described. The spectroscopic method of estimation of the systolic blood pressure, which is part of the technique and which involves the detection of reappearance of oxyhemoglobin absorption bands in the spectrum of reflected light from the skin distal to a blood pressure cuff that is slowly deflated, was compared to the auscultatory technique in 38 subjects on 53 occasions and gave the same results. The COP of small vessels in the finger estimated by the spectroscopic technique was decreased by body heating and by digital nerve block as had been previously shown by the microscopical method. The COP of vessels in the finger after digital nerve block in 43 normotensive young women between the ages of 18 and 22 years ranged from 2 to 19 mm Hg with a mean of 9.5 ± 4.6 (S.D.) mm Hg. When the COP was estimated in many of the same subjects after preparation as for measurement of the basal metabolic rate, in most cases it fell within the range of values obtained after nerve block. The COP in 26 subjects ranged from 1 to 22 mm Hg with a mean of 10.9 ± 5.0 (S.D.). The values for CCP estimated by the spectroscopic method in 81 individuals were not significantly different from those for COP estimated on the same occasion.

1974 ◽  
Vol 52 (4) ◽  
pp. 883-886 ◽  
Author(s):  
A. C. Darke

A spectroscopic technique for the measurement of systolic blood pressure and critical opening pressure of tail vessels in conscious rats is described. The values for systolic blood pressure obtained by this indirect technique were compared with those obtained by direct recording from a cannulated carotid artery. The correlation between the two sets of measurements was highly significant and the regression coefficient was very close to unity. In a separate series of experiments the effects of intravenous infusions of angiotensin or noradrenaline on the critical opening pressure of tail vessels were investigated in conscious ganglion-blocked rats. Both drugs produced dose-dependent increases in critical opening pressure and systolic blood pressure. This contrasts with the situation in the human finger where angiotensin has been shown to produce a decrease in critical opening pressure, indicating relaxation of a least some of the vessels in the finger, while at the same time producing an overall increase in digital vascular resistance.


1964 ◽  
Vol 206 (6) ◽  
pp. 1299-1303 ◽  
Author(s):  
Albert J. Roy ◽  
Peter B. Lambert ◽  
Howard A. Frank

The vascular bed of the hamster cheek pouch was observed in vivo under the microscope as a major artery within the field was occluded. Two changes were noted: 1) an alteration in pattern of blood flow and 2) the opening of previously unseen branches on each side of the ligature. Both responses were immediate and persisting. Besides providing for new flow patterns, the newly opened arterial branches preserve additional length of the ligated artery which becomes obliterated on each side of the ligature to the nearest open branch. Comparison of in vivo with postmortem observations indicated that latent and open branches of the artery under observation were about equal in number, and that about half of the latent branches opened in response to the ligation. Induced vasoconstriction delayed the opening of latent branches, cold prevented it. Priscoline opened all latent vessels, with or without arterial ligation. In connection with Burton's data on "critical closing pressure" of fine vessels, the ligation of a large artery appears to establish a "critical opening pressure" within latent branches.


1976 ◽  
Vol 54 (3) ◽  
pp. 314-321
Author(s):  
A. C. Darke ◽  
P. G. Nair ◽  
P. Gaskell

The possible role of increased vascular reactivity in the mechanism of experimental hypertension was studied by measurements of the critical opening pressure (COP) of tail vessels in conscious rats. In hypertension induced by administration of desoxycorticosterone acetate (DOCA) and replacement of the drinking water by 1% NaCl solution (DOCA–NaCl hypertension), and in one-kidney Goldblatt renovascular hypertension, the raised level of blood pressure was associated with an increased COP of the tail vessels when measured both before and after ganglionic blockade. In rats treated with either DOCA alone or 1% NaCl alone there was no significant increase in systolic blood pressure (SBP) or COP relative to the corresponding controls. In all four experimental series intravenous infusion of angiotensin or norepinephrine in conscious ganglion-blocked rats produced dose-dependent increases in SBP and COP. In DOCA–NaCl hypertensive rats but not in renovascular hypertensives, nor in rats treated with DOCA alone or 1% NaCl alone, the increase in COP for a given increment in dose of angiotensin or norepinephrine was significantly greater than in the control rats. It is concluded that in DOCA–NaCl hypertension there is a true increase in the reactivity of the smooth muscle of the resistance vessels to angiotensin and norepinephrine. In renovascular hypertension this is not the case and other factors must therefore be involved in causing the increased blood pressure and COP.


1997 ◽  
Vol 17 (10) ◽  
pp. 1127-1131 ◽  
Author(s):  
Erik Michel ◽  
Stefanie Hillebrand ◽  
Johanna vonTwickel ◽  
Boris Zernikow ◽  
Gerd Jorch

The nonproportional relationship between instantaneous arterial blood pressure (BP) and cerebral blood flow velocity (CBFv) is well explained by the concept of critical closing pressure (CCP). We aimed to determine the frequency response of the neonatal cerebrovascular system, and to establish the exact mathematical relationship between cerebrovascular impedance and CCP under physiologic conditions. In 10 preterm neonates (gestational age, 25–32 weeks; birth weight, 685–1,730 g; age 1–7 days) we Doppler-traced CBFv of the internal carotid artery. Blood pressure was traced simultaneously. Critical closing pressure was graphically determined. Cerebrovascular impedance was calculated as the square root of the ratio of the corresponding peaks in the power spectra of BP and CBFv at zero frequency, and at heart rate (H) and harmonics (xH). Uniformly, the impedance between H and 3H (2 to 6 Hz) was reduced about fivefold, compared with the impedance at zero frequency. The cerebrovascular system behaves like a high-pass filter, leading to a reduction of the DC (direct current) component of CBFv (analogous to current) relative to that of the driving force BP (analogous to voltage). The frequency response of cerebrovascular impedance reflects the ratio of CCP and DC BP. A mathematical derivation of this relationship is given matching the observed results. Thus, both the CCP and the impedance approach are valid.


2014 ◽  
Vol 35 (2) ◽  
pp. 285-291 ◽  
Author(s):  
Georgios V Varsos ◽  
Karol P Budohoski ◽  
Marek Czosnyka ◽  
Angelos G Kolias ◽  
Nathalie Nasr ◽  
...  

The effect of cerebral vasospasm (CVS) after aneurysmal subarachnoid hemorrhage (SAH) on critical closing pressure (CrCP) has not been fully delineated. Using cerebral impedance methodology, we sought to assess the behavior of CrCP during CVS. As CrCP expresses the sum of intracranial pressure (ICP) and vascular wall tension, we also explored its role in reflecting changes in vascular tone occurring in small vessels distal to spasm. This retrospective analysis was performed using recordings from 52 patients, diagnosed with CVS through transcranial Doppler measurements. Critical closing pressure was calculated noninvasively using arterial blood pressure and blood flow velocity. Outcome was assessed at both discharge and 3 months after ictus with the Glasgow Outcome Scale. The onset of CVS caused significant decreases in CrCP ( P=0.025), without any observed significant changes in ICP ( P=0.134). Vasospasm induced asymmetry, with CrCP ipsilateral to CVS becoming significantly lower than contralateral ( P=0.025). Unfavorable outcomes were associated with a significantly lower CrCP after the onset of CVS (discharge: P=0.014; 3 months after SAH: P=0.020). Critical closing pressure is reduced in the presence of CVS in both temporal and spatial assessments. As ICP remained unchanged during CVS, reduced CrCP most probably reflects a lower wall tension in dilated small vessels distal to spasm.


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