Analysis of the ICP pulse-pressure relationship as a function of arterial blood pressure clinical validation of a mathematical model

1982 ◽  
Vol 66 (1-2) ◽  
pp. 1-21 ◽  
Author(s):  
O. Hoffmann ◽  
J. T. Zierski
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Arterial Blood Pressure ◽  
Pulse Pressure ◽  
Clinical Validation ◽  
Arterial Blood

scholarly journals Physiological Association between Limb Ballistocardiogram and Arterial Blood Pressure Waveforms: A Mathematical Model-Based Analysis

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Peyman Yousefian ◽  
Sungtae Shin ◽  
Azin Sadat Mousavi ◽  
Chang-Sei Kim ◽  
Barry Finegan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Arterial Blood Pressure ◽  
Model Based ◽  
Arterial Blood ◽  
Model Based Analysis

Cardiovascular responses to bladder distension in patients with spinal transection

1975 ◽  
Vol 228 (4) ◽  
pp. 1288-1292 ◽  
Author(s):  
RD Wurster ◽  
WC Randall
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Pulse Pressure ◽  
Cardiovascular Responses ◽  
Sympathetic Nerves ◽  
Bladder Pressure ◽  
Bladder Distension ◽  
Arterial Blood

Arterial blood pressure, heart rate, and cutaneous volume pulses were recorded during controlled elevation of urinary bladder pressure in a group of seven patients with spinal cord transsection above vertebral level T5 and in another group of four patients below T5. Profound elevations in systolic blood pressure and pulse pressure were induced by bladder distension when the lesion was situated above T5. Lesser elevations occurred in patients with lesions below T5. Marked vasoconstriction characterized skin areas innervated by the "isolated" spinal cord, while passive dilatation occurred in areas supplied by the proximal cord. Only three of seven patients with lesions above T5 level had decreased heart rate during marked elevations in arterial blood pressure. The marked elevations in pulse pressure in patients with lesions above T5 could not be explained solelyby increased vasoconstriction and decreased heart rate, but involves also inotropic cardiac responses. These inotropic responses are mediated by cardiac sympathetic nerves which leave the spinal cord above the T5 level.

Cardiovascular actions of dogfish urotensin II in the dogfish Scyliorhinus canicula

1993 ◽  
Vol 265 (3) ◽  
pp. R573-R576 ◽  
Author(s):  
N. Hazon ◽  
C. Bjenning ◽  
J. M. Conlon
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Pulse Pressure ◽  
Bolus Injection ◽  
Urotensin Ii ◽  
Scyliorhinus Canicula ◽  
Arterial Blood ◽  
Dose Dependent

Bolus injections of synthetic dogfish urotensin II (0.1-1.0 nmol) into the celiac artery of the conscious dogfish Scyliorhinus canicula (n = 8) resulted in sustained and dose-dependent increases in arterial blood pressure and pulse pressure. A maximum rise in mean arterial pressure of 10.5 +/- 1.2 mmHg (equivalent to 38.6 +/- 4.2% over mean basal values) and a maximum increase in pulse pressure of 3.9 +/- 0.8 mmHg was elicited by injection of 0.5 nmol of peptide. In comparison, a bolus injection of epinephrine (5 nmol) elicited a rise of 24.8 +/- 3.3% in mean arterial pressure. Bolus injection of 0.5 nmol synthetic goby (Gillichthys mirabilis) urotensin II under the same conditions did not elicit a significant hypertensive response. When dogfish urotensin II (0.5 nmol) was administered 3 min after an intra-arterial injection of phentolamine, the rise in arterial blood pressure was completely abolished. Dogfish urotensin II produced a dose-dependent contraction (pD2 = 6.58 +/- 0.07; n = 8) of isolated rings of vascular muscle prepared from the first afferent branchial artery of the dogfish. A maximum contractile force of 1.3 mN was produced by 10(-5) M peptide. The urotensin II-induced contraction of the vascular rings was unaffected by pretreatment with tetrodotoxin (1 microM) or indomethacin (14 microM). It is concluded that urotensin II has potent hypertensive activity in the dogfish that is mediated, at least in part, through release of catecholamines, but the sustained nature of the pressor response suggests that the peptide may have a direct action on the heart.

The reversal of hemorrhagic hypotension by naloxone in conscious rabbits

1981 ◽  
Vol 59 (12) ◽  
pp. 1208-1213 ◽  
Author(s):  
James C. Schadt ◽  
Donald H. York
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Pulse Pressure ◽  
Halothane Anesthesia ◽  
Endogenous Opiates ◽  
Pentobarbital Anesthesia ◽  
Arterial Blood ◽  
Initial Surgery

The effects of naloxone on blood pressure and heart rate were studied in consious, chronically prepared rabbits. In addition, the effects of barbiturate anesthesia on the response to naloxone were investigated. Initial surgery to implant arterial and venous catheters was performed under halothane anesthesia. Experiments were begun 10 days to 2 weeks later. The rabbits were divided into two groups: a normotensive group and a group made hypotensive by hemorrhage. In the normotensive rabbits, naloxone (2 mg/kg i.v.) did not alter mean arterial blood pressure [Formula: see text], pulse pressure, (PP), or heart rate (HR). However, a 5 mg/kg dose increased [Formula: see text] and PP, and decreased HR. In the hypotensive group, naloxone in a dose of 2, 3, or 5 mg/kg i.v. significantly increased [Formula: see text] and PP while decreasing HR in a dose-related manner. A dose of 0.2 mg/kg did not significantly alter any of the measured parameters. Pentobarbital anesthesia significantly reduced the effects of the 3 mg/kg naloxone dose in the hypotensive group. These actions of naloxone may be mediated through antagonism of endogenous opiates.

Resonant and notch behavior in intracranial pressure dynamics

2009 ◽  
Vol 3 (5) ◽  
pp. 354-364 ◽  
Author(s):  
Mark E. Wagshul ◽  
Erin J. Kelly ◽  
Hui Jing Yu ◽  
Barbara Garlick ◽  
Tom Zimmerman ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Transfer Function ◽  
Arterial Blood Pressure ◽  
Pulse Pressure ◽  
Function Analysis ◽  
Isotonic Saline ◽  
Pressure Amplitude ◽  
Arterial Blood ◽  
Transfer Function Analysis

Object The intracranial pulse pressure is often increased when neuropathology is present, particularly in cases of increased intracranial pressure (ICP) such as occurs in hydrocephalus. This pulse pressure is assumed to originate from arterial blood pressure oscillations entering the cranium; the fact that there is a coupling between the arterial blood pressure and the ICP is undisputed. In this study, the nature of this coupling and how it changes under conditions of increased ICP are investigated. Methods In 12 normal dogs, intracarotid and parenchymal pulse pressure were measured and their coupling was characterized using amplitude and phase transfer function analysis. Mean intracranial ICP was manipulated via infusions of isotonic saline into the spinal subarachnoid space, and changes in transfer function were monitored. Results Under normal conditions, the ICP wave led the arterial wave, and there was a minimum in the pulse pressure amplitude near the frequency of the heart rate. Under conditions of decreased intracranial compliance, the ICP wave began to lag behind the arterial wave and increased significantly in amplitude. Most interestingly, in many animals the pulse pressure exhibited a minimum in amplitude at a mean pressure that coincided with the transition from a leading to lagging ICP wave. Conclusions This transfer function behavior is characteristic of a resonant notch system. This may represent a component of the intracranial Windkessel mechanism, which protects the microvasculature from arterial pulsatility. The impairment of this resonant notch system may play a role in the altered pulse pressure in conditions such as hydrocephalus and traumatic brain swelling. New models of intracranial dynamics are needed for understanding the frequency-sensitive behavior elucidated in these studies and could open a path for development of new therapies that are geared toward addressing the pulsation dysfunction in pathological conditions, such as hydrocephalus and traumatic brain injury, affecting ICP and flow dynamics.

scholarly journals Association of central arterial blood pressure and left ventricular hypertrophy in patients with chronic kidney disease

2021 ◽  
Author(s):  
Ruyi Cai ◽  
Lina Shao ◽  
Yifan Zhu ◽  
Jinshi Zhang ◽  
Yueming Liu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Left Ventricular Hypertrophy ◽  
Arterial Blood Pressure ◽  
Pulse Pressure ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Arterial Blood ◽  
Central Pulse Pressure

Abstract Aims: In the general population, central arterial blood pressure has proved to be more closely related to left ventricular hypertrophy than brachial arterial blood pressure. We aimed to investigate whether this relationship was true in patients with chronic kidney disease. Methods: In this retrospective study, we reviewed the medical records of 289 adult patients with chronic kidney disease from the Zhejiang Provincial People’s Hospital in Zhejiang, China. Demographic, echocardiographic, and brachial and central blood pressure parameters were retrieved from medical records. Central blood pressure was measured using the SphygmoCor® CvMS (AtCor, Australia) device and its corresponding software. Multivariate logistic regression analyses were performed to identify independent predictors of left ventricular hypertrophy. Receiver operating characteristic curves were used to determine the ability of central and brachial blood pressure to predict left ventricular hypertrophy.Results: The left ventricular mass index was positively associated with both central and brachial blood pressures. However, multiple logistic regression analysis demonstrated that a central pulse pressure ≥ 58 mm Hg was an independent risk factor for left ventricular hypertrophy (OR=5.597, 95%CI 2.363-13.259, P <0.001). Brachial pulse pressure is not superior to central pulse pressure in predicting left ventricular hypertrophy (AUC = 0.695, 95%CI 0.634-0.756, P < 0.001 vs. AUC = 0.687, 95%CI: 0.626 to 0.748, P < 0.001, respectively; P = 0.4824).Conclusions: Our results suggested that, similarly to the general population, central pulse pressure is a better parameter for predicting the occurrence of left ventricular hypertrophy in patients with chronic kidney disease.

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