The effect of nimodipine on intracranial pressure

1987 ◽  
Vol 67 (3) ◽  
pp. 387-393 ◽  
Author(s):  
Mark N. Hadley ◽  
Robert F. Spetzler ◽  
Mary S. Fifield ◽  
William D. Bichard ◽  
John A. Hodak

✓ Nimodipine was administered by intravenous infusion to six male baboons before, during, and after 6 hours of middle cerebral artery occlusion. Intracranial pressure (ICP) and systemic blood pressure were monitored continuously. An epidural balloon was inflated at regular intervals at three levels of arterial CO2 tension (25, 35, and 50 mm Hg) before and after the administration of nimodipine, and volume-pressure curves were generated. In every case, curves generated after intravenous nimodipine infusion were lower and shifted more to the right than the same set of curves generated before nimodipine administration, regardless of the baseline ICP. The reduction in ICP following nimodipine infusion was not due to a reduction in mean arterial blood pressure and was statistically significant at all three levels of pCO2 (p < 0.01). These results suggest that, in the presence of elevated ICP due to cerebral infarction, there is no increased risk of exacerbating intracranial hypertension with the addition of nimodipine.

1992 ◽  
Vol 76 (3) ◽  
pp. 415-421 ◽  
Author(s):  
David W. Newell ◽  
Rune Aaslid ◽  
Renate Stooss ◽  
Hans J. Reulen

✓ Intracranial pressure (ICP) and continuous transcranial Doppler ultrasound signals were monitored in 20 head-injured patients and simultaneous synchronous fluctuations of middle cerebral artery (MCA) velocity and B waves of the ICP were observed. Continuous simultaneous monitoring of MCA velocity, ICP, arterial blood pressure, and expired CO2 revealed that both velocity waves and B waves occurred despite a constant CO2 concentration in ventilated patients and were usually not accompanied by fluctuations in the arterial blood pressure. Additional recordings from the extracranial carotid artery during the ICP B waves revealed similar synchronous fluctuations in the velocity of this artery, strongly supporting the hypothesis that blood flow fluctuations produce the velocity waves. The ratio between ICP wave amplitude and velocity wave amplitude was highly correlated to the ICP (r = 0.81, p < 0.001). Velocity waves of similar characteristics and frequency, but usually of shorter duration, were observed in seven of 10 normal subjects in whom MCA velocity was recorded for 1 hour. The findings in this report strongly suggest that B waves in the ICP are a secondary effect of vasomotor waves, producing cerebral blood flow fluctuations that become amplified in the ICP tracing, in states of reduced intracranial compliance.


1979 ◽  
Vol 51 (2) ◽  
pp. 206-210 ◽  
Author(s):  
Gündüz Gücer ◽  
Lawrence J. Viernstein

✓ Intracranial pressure (ICP) was recorded continuously by telemetry in seven normal monkeys trained to eat, sleep, and live in a primate chair. Electroencephalography, electromyography, and blood pressure were also measured by conventional means. During wakefulness and all stages of sleep except desynchronized sleep, the ICP record showed small short-term variations in pressure. However, during desynchronized sleep, the mean ICP rose on the average to 170 ± 6 mm H2O above the ICP levels in the other states of sleep, and the pulsation pressure variation increased by a factor of three. The episodes occurred 10 ± 2 times during the night and lasted for 6.8 ± 1.4 minutes, during which the average systemic blood pressure decreased by 19 ± 1.6 mm Hg. These ICP waves occurring during desynchronized sleep resemble the plateau waves described by Lundberg, but are of smaller magnitude and they appear to be a normal characteristic of sleep in the macaque monkey. Bilateral sympathectomy of the superior cervical ganglia in four of the monkeys did not alter significantly the duration, amplitude, or frequency of occurrence of the ICP waves during desynchronized sleep.


2019 ◽  
Vol 127 (4) ◽  
pp. 1050-1057
Author(s):  
Katelyn N. Wood ◽  
Danielle K. Greaves ◽  
Richard L. Hughson

We tested the hypothesis that acute changes in arterial blood pressure (BP) when astronauts moved between supine and standing posture before and after spaceflight can be tracked by beat-to-beat changes in pulse arrival time (PAT). Nine male crewmembers (45 ± 7 yr of age; mean mission length: 165 ± 13 days) participated in a standardized supine-to-sit-to-stand test (5 min-30 s-3 min) before flight and 1 day following return to Earth with continuous monitoring of ECG and finger arterial BP. PAT was determined from the R-wave of the ECG to the foot of the BP waveform. On average, modest cardiovascular deconditioning was detected by ~10 beats/min increase in heart rate in supine and standing posture after spaceflight ( P < 0.05). When looking across the full data collection period, the r2 values between inverse of PAT (1/PAT) and systolic (SBP) and diastolic BP (DBP) varied considerably between individuals (SBP preflight 0.142 ± 0.186, postflight 0.262 ± 0.243). Individual variability was consistent during periods of transition (SBP preflight 0.284 ± 0.324, postflight 0.297 ± 0.269); however, when SBP dropped >20 mmHg, r2 was significant in 5 of 5 preflight tests and 5 of 7 postflight tests. The standard error of the estimate based on a simple linear model during both pre- and postflight testing was 9–11 mmHg for SBP and 6–7 mmHg for DBP. Overall, the results support the hypothesis that PAT tracked dynamic changes in BP. PAT as a noninvasive, nonintrusive surrogate for changes in BP could be developed as an indicator of risk for syncope on return from spaceflight or other Earth-based applications. NEW & NOTEWORTHY Astronauts returning to Earth’s gravity are at increased risk of low blood pressure on standing. Arterial pulse arrival time tracked the decrease in arterial blood pressure on moving from supine to upright posture. Nonintrusive technology providing indicators sensitive to acute changes in blood pressure could act as an early warning system to identify risk for hypotension that place astronauts, or people on Earth, at risk of impaired cognitive performance, fainting, and falls.


1994 ◽  
Vol 80 (5) ◽  
pp. 857-864 ◽  
Author(s):  
Joseph M. Darby ◽  
Howard Yonas ◽  
Elizabeth C. Marks ◽  
Susan Durham ◽  
Robert W. Snyder ◽  
...  

✓ The effects of dopamine-induced hypertension on local cerebral blood flow (CBF) were investigated in 13 patients suspected of suffering clinical vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. A territorial local CBF of 25 ml/100 gm/min or less was used to define ischemia and was identified in nine of the 13 patients. Raising mean arterial blood pressure from 90 ± 11 mm Hg to 111 ± 13 mm Hg (p < 0.05) via dopamine administration increased territorial local CBF above the ischemic range in more than 90% of the uninfarcted territories identified on CT while decreasing local CBF in one-third of the nonischemic territories. Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. Of the 13 patients initially suspected of suffering clinical vasospasm, only 54% had identifiable reversible ischemia. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. However, flow changes associated with dopamine-induced hypertension may not be entirely dependent on changes in systemic blood pressure. The direct cerebrovascular effects of dopamine may have important, yet unpredictable, effects on CBF under clinical pathological conditions. Because there is a potential risk of dopamine-induced ischemia, treatment may be best guided by local CBF measurements.


1976 ◽  
Vol 45 (6) ◽  
pp. 609-616 ◽  
Author(s):  
Delbert E. Evans ◽  
William A. Alter ◽  
Stanley A. Shatsky ◽  
E. Neal Gunby

✓ The cardiovascular events resulting from experimental head injury were studied to determine the incidence of cardiac arrhythmias and to define the autonomic mechanisms responsible for these changes. Electrocardiograms and arterial blood pressure were recorded in anesthetized monkeys before and after the animals were subjected to temporoparietal head impact. Cardiac arrhythmias and hypotension occurred immediately following impact in every animal studied. Various atrioventricular nodal and ventricular arrhythmias were seen. Cholinergic blockade was found to prevent arrhythmias induced by head injury whereas adrenergic blockade was found to be ineffective.


1989 ◽  
Vol 257 (3) ◽  
pp. R595-R598 ◽  
Author(s):  
K. G. Cornish ◽  
M. W. Barazanji ◽  
T. Yong ◽  
J. P. Gilmore

We examined the effect of intravascular volume expansion (VE) on the arterial baroreflex control of pulse rate (PR) in conscious, chronically instrumented monkeys tethered in their cages. A total of five monkeys was studied after surgical implantation of catheters in the descending aorta, the left atrium, and the internal jugular vein. Mean arterial blood pressure (MABP)-PR stimulus response curves were constructed by decreasing and increasing blood pressure with nitroprusside and phenylephrine, respectively. The data were analyzed with a regression analysis that generated a sigmoid curve and the maximum sensitivity (slope) of the curve. The data were obtained before and after VE with an isotonic isoncotic dextran solution equal to 20% of the estimated blood volume. After VE, the MABP-PR curve shifted to the right at the high blood pressures, and there was a significant decrease in the maximum sensitivity from 5.65 +/- 1.44 for control to 2.14 +/- 0.63 after VE (P less than 0.05). We concluded that VE attenuates the baroreflex control of heart rate in the conscious nonhuman primate.


1983 ◽  
Vol 58 (5) ◽  
pp. 771-773 ◽  
Author(s):  
Henryk Majchrzak ◽  
Tadeusz Wencel ◽  
Tadeusz Dragan ◽  
Joanna Bialas

✓ The authors present the case of a patient with a pituitary tumor, who manifested signs of subarachnoid hemorrhage (SHA) and loss of consciousness. After he had regained consciousness, massive left-sided paralysis was noted. Angiography and computerized tomography showed hemorrhage into the tumor, SAH, and ischemia of the right frontal lobe as a result of occlusion of the anterior cerebral artery. Removal of the tumor 3 weeks after the SAH did not lead to resumption of the anterior cerebral artery blood flow.


1995 ◽  
Vol 83 (3) ◽  
pp. 430-434 ◽  
Author(s):  
William McAuliffe ◽  
Murphy Townsend ◽  
Joseph M. Eskridge ◽  
David W. Newell ◽  
M. Sean Grady ◽  
...  

✓ The authors reviewed the cases of 21 patients who received intraarterial infusions of papaverine to determine the drug's effects on intracranial pressure (ICP), mean arterial blood pressure, pulse rate, and cerebral perfusion pressure (CPP). The study focused on patients with aneurysmal subarachnoid hemorrhage who developed clinical signs and symptoms of vasospasm, which was documented by cerebral angiography. In 18 patients, an average dose of 300 mg papaverine was administered over 20 to 35 minutes using a No. 5 French catheter inserted into the high cervical internal carotid artery or vertebral artery. Two other patients received superselective infusions via a microcatheter placed in the anterior cerebral artery. Sixteen patients (76%) experienced good angiographic results, and 11 (52%) obtained objective clinical improvement within 48 hours. Significant elevations in ICP, blood pressure, and pulse rate were noted during papaverine infusion. In contrast, no statistically significant sustained change in CPP was observed, although it tended to decrease during papaverine infusion. In one elderly patient, infusion of the common carotid artery resulted in profound bradycardia and hypotension with a subsequent significant increase in ICP and a marked decrease in CPP. The increase in ICP in these patients correlates well with changes seen in animal models and is probably related to increased cerebral blood flow. A careful, titrated infusion of papaverine, with constant reference to the patient's ICP, blood pressure, and pulse rate, minimizes the transient increase in ICP while maintaining adequate blood pressure and CPP. Failure to monitor these parameters during the infusion, with appropriate modification of the rate of titration, could potentially produce an uncontrolled change in ICP or CPP.


2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Osman Çelikay ◽  
Sinan Çalışkan ◽  
Tolga Biçer ◽  
Naciye Kabataş ◽  
Canan Gürdal

Objective. To determine the effect of hemodialysis (HD) on choroidal thickness (CT).Methods. The right eyes of 41 patients with end-stage renal disease (ESRD) undergoing HD were included. All patients underwent an ophthalmic examination, including CT measurement via optical coherence tomography, intraocular pressure (IOP), blood pressure, and body weight measurement immediately before and after a HD session.Results. Mean subfoveal choroidal thickness (SFCT) after HD decreased significantly from 254.59 ± 84.66 µm to 229.34 ± 77.79 µm(p<0.001). CT at the temporal and nasal regions also decreased significantly after HD (bothp<0.001). IOP changes after HD were insignificant(p=0.958). CT difference was insignificant in patients with diabetes mellitus (DM) and without DM before and after HD, respectively (p=0.285andp=0.707). Stepwise multivariate linear regression analysis showed that diastolic blood pressure was the best fitted factor to explain the changes in CT (r=0.327andp=0.040).  Conclusion. CT was decreased in the patients with ESRD following a HD session. This study suggested that the changes in CT may be related to the changes in systemic blood pressure.


2005 ◽  
Vol 99 (5) ◽  
pp. 2028-2035 ◽  
Author(s):  
M. J. Campen ◽  
L. A. Shimoda ◽  
C. P. O’Donnell

We investigated the effects of 1) acute hypoxia and 2) 5 wk of chronic intermittent hypoxia (IH) on the systemic and pulmonary circulations of C57BL/6J mice. Mice were chronically instrumented with either femoral artery or right ventricular catheters. In response to acute hypoxia (4 min of 10% O2; n = 6), systemic arterial blood pressure fell ( P < 0.005) from 107.7 ± 2.5 to 84.7 ± 6.5 mmHg, whereas right ventricular pressure increased ( P < 0.005) from 11.7 ± 0.8 to 14.9 ± 1.3 mmHg. Another cohort of mice was then exposed to IH for 5 wk (O2 nadir = 5%, 60-s cycles, 12 h/day) and then implanted with catheters. In response to 5 wk of chronic IH, mice ( n = 8) increased systemic blood pressure by 7.5 mmHg, left ventricle + septum weight by 32.2 ± 7.5 × 10−2 g/100 g body wt ( P < 0.015), and right ventricle weight by 19.3 ± 3.2 × 10−2 g/100 g body wt ( P < 0.001), resulting in a 14% increase in the right ventricle/left ventricle + septum weight ( P < 0.005). We conclude that in C57BL/6J mice 1) acute hypoxia causes opposite effects on the pulmonary and systemic circulations, leading to preferential loading of the right heart; and 2) chronic IH in mice results in mild to moderate systemic and pulmonary hypertension, with resultant left- and right-sided ventricular hypertrophy.


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