PubMed Health⌕ Search

Biomedical subjects

Shailendra Joshi

Publications and source records attributed to Shailendra Joshi.

17 recordsLinked to original sources
PubMed2006

Cerebral blood flow affects dose requirements of intracarotid propofol for electrocerebral silence.

BACKGROUND: The authors hypothesized that cerebral blood flow (CBF) changes will affect the dose of intracarotid propofol required to produce electrocerebral silence. METHODS: The authors tested their hypothesis on New Zealand White rabbits. The first group of 9 animals received intracarotid propofol during (1) normoventilation, (2) hyperventilation, and (3) hypoventilation. The second group of 14 animals received intracarotid propofol with or without concurrent intraarterial verapamil, a potent cerebral vasodilator. The third group of 8 animals received bolus injection of propofol during normotension, during severe cerebral hypoperfusion, and after hemodynamic recovery. RESULTS: In the first group, there was a linear correlation between the dose of intracarotid propofol and percent change (%Delta) in CBF from the baseline due to changes in the minute ventilation, Total Dose (y) = 0.17 + 0.012 * %Delta CBF (x), n = 27, r = 0.76. In the second group, the dose of propofol was also a function of CBF change after verapamil, Total Dose (y) = 0.98 + 0.1 * %Delta CBF (x), n = 14, r = 0.75. In the third group, the duration of electrocerebral silence after intracarotid propofol (3 mg) was significantly increased with concurrent cerebral hypoperfusion compared with prehypoperfusion and posthypoperfusion values (141 +/- 38 vs. 19 +/- 24 and 16 +/- 12 s, respectively, P < 0.0001). CONCLUSIONS: The authors conclude that CBF affects the dose requirements of intracarotid propofol required to produce electrocerebral silence. Furthermore, the manipulation of CBF might be a useful tool to enhance the efficacy of intracarotid drugs.

Anesthetics, Intravenous↗
PubMed2006

Comparison of intracarotid anesthetics for EEG silence.

The goal of this study was to compare systemic and cerebrovascular effects of three anesthetic drugs (etomidate, thiopental, and propofol) when delivered by intracarotid and intravenous routes in doses that produce electrocerebral silence (electroencephalography [EEG]). EEG activity, mean arterial pressure (MAP), and laser Doppler flow as a proxy of cerebral blood flow (CBF) of 24 anesthetized New Zealand white rabbits were continuously recorded. Data were compared at three timepoints: baseline, during EEG silence, and after recovery of EEG activity. Drugs were randomly injected via the carotid artery to produce 10 minutes of EEG silence. After 30 minutes of rest, intravenous boluses of the same drug were injected to achieve 10 minutes of EEG silence. During EEG silence, transient hypotension was seen with intracarotid propofol, but there was no decrease in CBF. MAP and CBF did not decrease with either intracarotid etomidate or thiopental during EEG silence. Intracarotid/intravenous dose ratio of propofol (26%+/-22%; n=8, P<0.02) was much higher than that of etomidate and thiopental (14%+/-2% and 19%+/-11%, respectively; NS). Collectively, these results suggest intracarotid etomidate and thiopental are more useful than propofol in producing EEG silence because they offer better dose advantage and are less likely to impair cerebral or systemic hemodynamics.

Anesthetics, Intravenous↗
PubMed2006

Bolus configuration affects dose requirements of intracarotid propofol for electroencephalographic silence.

We hypothesized that an intracarotid bolus injection of propofol to produce electroencephalographic (EEG) silence would require a smaller dose of the drug compared with the continuous infusion of the drug. Furthermore, the bolus propofol dose will be a function of the bolus characteristics in each bolus (mass/volume). We compared the dose requirements of intracarotid propofol needed to maintain EEG silence when delivered as bolus injections to continuous infusions in rabbits. Subsequently, we compared whether four different bolus characteristics (concentration and volume) of propofol (0.33% x 0.1 mL, 0.33% x 0.3 mL, 1% x 0.1 mL, and 1% x 0.3 mL) affected the dose required to produce EEG silence. We found that the infusion rate of propofol required to sustain EEG silence was three-fold larger than the dose required by bolus injections, 22.8 +/- 11.9 vs 6.2 +/- 2.9 mL/h for infusion versus bolus, respectively (n = 7, P < 0.004). Furthermore, during bolus injection, the doses of propofol required to produce EEG silence were a direct function of the bolus volume and the mass of drug in each bolus, total dose = 3.6 + 29 x mg/bolus, n = 32, r = 0.85. For maximum regional effects of the bolus intracarotid drug injection, the bolus characteristics (volume and drug concentration) have to be optimized.

Anesthetics, Intravenous↗
PubMed2005

Pial arterial response to topical verapamil in acute closed cranial windows in rabbits.

We have previously observed that intraarterial verapamil increases cerebral blood flow, whereas nitric oxide donors, such as nitroglycerin, do not. Clinically, both verapamil and nitroglycerin dilate large cerebral arteries. Therefore, we hypothesized that topical verapamil would dilate both the large proximal and the small distal cerebral arteries, whereas nitroglycerin would preferentially dilate only the large proximal arteries. We tested our hypothesis in acute cranial windows implanted in 10 New Zealand White rabbits. After predrug measurements, we superfused 4 increasing concentrations of verapamil or nitroglycerin (10(-8), 10(-6), 10(-4), and 10(-3) M) in the cranial windows for 5 min each. The maximum increase in diameter was expressed as a percentage change from predrug diameters. There was a 30-min period of rest between the two drug challenges. Topical verapamil increased the arterial diameter of the larger proximal arterioles (>60 microm) by 32% +/- 18% and that of the smaller distal arterioles (<60 microm) by 62% +/- 42%. A modest increase in arterial diameters of 11% +/- 11% was observed after topical nitroglycerin that was significant only for the large-proximal arterioles. Within the 10(-8) to 10(-3) M range, topical verapamil, compared with nitroglycerin, proved to be a more potent cerebral vasodilator and had a more robust vasodilator effect on the distal small pial arteries.

Administration, Topical↗
PubMed2005

Reducing cerebral blood flow increases the duration of electroencephalographic silence by intracarotid thiopental.

The effects of IV anesthetics are enhanced by increased cerebral blood flow (CBF) because of a greater delivery of drugs to the brain. In contrast, mathematical simulations suggest that a decrease in CBF, by increasing regional drug uptake and decreasing drug washout, enhances the efficacy of intraarterial drugs. We hypothesized that administrating intracarotid anesthetics during cerebral hypoperfusion will significantly prolong the duration of electroencephalographic (EEG) silence. We tested our hypothesis on New Zealand White rabbits. In the first group of 7 animals, we observed that decreasing CBF by approximately 70% attenuated, but did not abolish, EEG activity. Subsequently, 9 animals received 3 intracarotid injections of 3 mg of thiopental (thiopental-1, thiopental + hypoperfusion, and thiopental-2). The first and third injections were made under physiological conditions. The second drug injection was made during cerebral hypoperfusion. Compared with injection of thiopental-1 and -2, thiopental + hypoperfusion resulted in a profound increase in EEG silence (from 45 +/- 5 and 67 +/- 27 s, to 206 +/- 46 s, respectively, n = 9, P < 0.0001). The EEG recovery profile was similar during all three thiopental challenges. The study suggests that modulation of CBF is an important tool for enhancing intraarterial drug delivery to the brain.

Adenosine↗
PubMed2004

Intracarotid verapamil decreases both proximal and distal human cerebrovascular resistance.

BACKGROUND: The authors determined the segmental effects of intracarotid verapamil in human subjects by using a novel method of measuring proximal and distal cerebrovascular resistance. Their hypothesis was that intracarotid verapamil, a calcium channel-blocking drug that augments cerebral blood flow and reverses arterial spasm, would decrease both the proximal-conductance and the distal-arteriolar resistance. METHODS: Coaxial catheters were transfemorally floated into internal carotid and middle cerebral arteries during cerebral angiography. Pressures were recorded in the femoral, internal carotid, and middle cerebral arteries. Hemispheric cerebral blood flow was measured by the intracarotid Xe injection technique. Cerebrovascular resistance was measured for the proximal and distal arteries. Cerebral blood flow and hemodynamic data were recorded during intracarotid infusion of saline and verapamil (1 mg/min) for 5 min. Transcranial Doppler blood flow velocity in the middle cerebral artery was also recorded. RESULTS: Intracarotid verapamil increased in 133Xe cerebral blood flow from 43 +/- 11 to 59 +/- 11 ml.100 g(-1).min(-1) (P = 0.001; n = 9). The cerebrovascular resistance measured for the proximal and distal arteries decreased from 0.17 +/- 0.95 to 0.12 +/- 0.75 and from 1.63 +/- 0.78 to 1.03 +/- 0.33 mmHg.ml(-1).100 g(-1).min(-1) (P < 0.01), respectively. The calculated proximal-conductive and distal-arteriolar (pial plus parenchymal) resistances showed a similar decrease. Transcranial Doppler measurements (n = 5) underestimated the effects of intracarotid verapamil that were consistent with an increase in middle cerebral artery diameter. CONCLUSIONS: Intracarotid verapamil decreases both the proximal-conductance and the distal-arteriolar resistance. Furthermore, it is feasible to investigate segmental effects of drugs in human subjects by measuring changes in pressure gradients within the cerebral arteries and simultaneous Xe cerebral blood flow measurements.

Adult↗
PubMed2004

Retinal discoloration test.

There are considerable variations in the size and the origin of internal carotid arteries (ICAs) of New Zealand white rabbits. A simple test that could correctly identify the ICA could facilitate intracarotid delivery of drugs and embolic material for research in these animals. Five conventional methods for identifying the ICA proved inferior to a novel retinal discoloration test (RDT). A positive RDT implies a change in color of the retinal reflex after injection of 0.2 mL of indigo-carmine blue (ICB). We conclude that RDT is a useful test for correctly identifying and isolating the ICA in this animal species.

Animals↗
PubMed2004

Electrocerebral silence by intracarotid anesthetics does not affect early hyperemia after transient cerebral ischemia in rabbits.

UNLABELLED: Evidence suggests that early postischemic hyperemia is mediated by both neurological and vascular mechanisms. We hypothesized that if neuronal activity were primarily responsible for reperfusion hyperemia, then electrocerebral silence induced by intracarotid anesthetics (propofol and pentothal) would attenuate the hyperemic response. New Zealand white rabbits were subjected to 10 min of cerebral ischemia using bilateral carotid occlusion and systemic hypotension. Subsequently, carotid occlusion was released, and the mean arterial blood pressure was increased to baseline values. In the control group, intracarotid saline was periodically injected during reperfusion. In the treatment groups, intracarotid propofol or thiopental was administered to maintain electrocerebral silence for 10 min. Physiological data were measured at baseline, during ischemia, and at reperfusion. Satisfactory data were available for 16 of 19 rabbits. Mean arterial blood pressure, end-tidal CO(2), and cerebral blood flows decreased significantly in both groups during carotid occlusion. During early reperfusion, a similar percent increase in cerebral blood flow from baseline values was observed in all 3 groups (192% +/- 76%, 218% +/- 84%, and 185% +/- 101% for saline, propofol, and pentothal, respectively). These results suggest that suppression of neuronal activity during reperfusion does not affect early hyperemia after transient cerebral ischemia. IMPLICATIONS: Intracarotid injection of anesthetic drugs in doses that are sufficient to produce electrocerebral silence do not obtund early cerebral hyperemia after transient cerebral ischemia. This suggests that vascular, not neuronal mechanisms, are primarily responsible for early postischemic cerebral hyperperfusion.

Anesthetics, Intravenous↗
PubMed2003

Despite in vitro increase in cyclic guanosine monophosphate concentrations, intracarotid nitroprusside fails to augment cerebral blood flow of healthy baboons.

BACKGROUND: During cerebral angiography, intracarotid infusion of sodium nitroprusside (SNP), an endothelium-independent nitric oxide donor, fails to increase cerebral blood flow (CBF) of human subjects. A confounding effect of intracranial pathology or that of radiocontrast could not be ruled out in these experiments. The authors hypothesized that, if nitric oxide was a significant regulator of CBF of primates, then intracarotid SNP will augment CBF of baboons. METHODS: In studies, CBF (intraarterial (133)Xe technique) was measured in healthy baboons during isoflurane anesthesia at (1) baseline and during (2) induced hypertension with intravenous phenylephrine, (3) concurrent infusions of intravenous phenylephrine and intracarotid SNP, and (4) intracarotid verapamil (positive control drug). In studies, the authors measured tissue cyclic guanosine monophosphate (cGMP) by radioimmunoassay after incubating vascular rings obtained from freshly killed baboons (1) with increasing concentrations of SNP and (2) after SNP exposure following preincubation with the radiocontrast agent, iohexhol. RESULTS: In the studies, coinfusion of intravenous phenylephrine and intracarotid SNP did not increase CBF. However, intracarotid verapamil significantly increased CBF (from 26 +/- 7 to 43 +/- 11 ml x 100 g(-1) x min(-1); P < 0.0001) without a change in mean arterial pressure. In the studies, incubation of intracranial arterial rings in SNP resulted in dose-dependent increases in cGMP concentrations. A similar increase in cGMP content was evident despite iohexhol preincubation. CONCLUSIONS: Collectively, these results suggest that, in healthy baboons, intracarotid SNP does not decrease arteriolar resistance, although SNP could affect proximal arterial tone, as demonstrated by the increase in cGMP content of these vessels.

Animals↗
PubMed2003

Comparison of intracarotid and intravenous propofol for electrocerebral silence in rabbits.

BACKGROUND: The high lipid solubility that permits rapid transfer across the blood-brain barrier makes propofol attractive for intracarotid injection. The authors hypothesized that intracarotid injection produces electrocerebral silence at a fraction of the intravenous dose and with less adverse systemic and cerebrovascular side effects. METHODS: The authors compared the systemic and cerebrovascular effects of intracarotid and intravenous propofol during transient (10 s) and sustained (1 h) electrocerebral silence in anesthetized New Zealand White rabbits. Hemispheric electrocerebral activity, mean arterial blood pressure, ipsilateral and contralateral cerebral blood flow, tympanic temperature, and end-tidal carbon dioxide were continuously monitored in these animals. Changes in outcome variables were analyzed at four time points: at baseline, during electrical silence, during burst suppression, and after recovery of electrocerebral activity. Propofol (1%) was injected as intracarotid (0.1 ml) or intravenous (0.5 ml) boluses. RESULTS: Intracarotid propofol produced electrocerebral silence at one fifth (sustained silence) to one tenth (transient silence) of the intravenous dose. Compared with baseline values, the mean arterial pressure and ipsilateral cerebral blood flow remained unchanged or decreased transiently during electrocerebral silence with intracarotid propofol. In contrast, intravenous propofol resulted in systemic hypotension and a decrease in ipsilateral cerebral blood flow. CONCLUSIONS: Intracarotid propofol resulted in electrocerebral silence at a fraction of the intravenous dose that was not associated with systemic hypotension or a sustained decrease in the cerebral blood flow. Intracarotid propofol could be potentially useful for providing electrocerebral silence when cerebral perfusion is at risk.

Action Potentials↗
PubMed2003

The acute cerebrovascular effects of intracarotid adenosine in nonhuman primates.

UNLABELLED: In this study we sought to determine the acute cerebrovascular effects of intracarotid adenosine by using real-time cerebral blood flow (CBF) measurements in nonhuman primates. The internal carotid arteries of healthy anesthetized baboons were transfemorally cannulated. Changes in CBF were continuously measured at baseline and with 6 increasing doses of adenosine (0.002 to 1.5 mg/min) by use of an intraparenchymal thermal diffusion (TD) probe. Each infusion lasted 5 min. At baseline and at the largest dose of adenosine, CBF was also determined by the intraarterial (133)Xe technique. TD measurements revealed a dose-dependent increase in CBF from 32 +/- 6 mL x l00 g(-1) x min(-1) at baseline to 90 +/- 38 mL x l00 g(-1) x min(-1) with the largest dose of adenosine (n = 5; P < 0.0001). A similar magnitude of increase in CBF was also observed with (133)Xe CBF measurements. No significant increases in intracranial pressure or adverse systemic hemodynamic side effects were observed during adenosine infusion. The increase in CBF after adenosine lasted only for the duration of drug infusion. In conclusion, the transient cerebrovascular effects of intracarotid adenosine make it suitable for a trial of intraarterial vasodilator therapy and for controlled manipulation of cerebrovascular resistance. IMPLICATIONS: Using a real-time cerebral blood flow (CBF) measurement technique, we evaluated the acute cerebrovascular effects of intracarotid adenosine in anesthetized baboons. The increase in CBF lasted only for the duration of the adenosine infusion. Adenosine might be a suitable drug for trial as an intraarterial vasodilator for the treatment of cerebral vasospasm.

Adenosine↗
PubMed2002

In nonhuman primates intracarotid adenosine, but not sodium nitroprusside, increases cerebral blood flow.

UNLABELLED: Intracarotid infusion of short-acting vasodilators, such as adenosine and nitroprusside, in doses that lack significant systemic side effects, may permit controlled manipulation of cerebrovascular resistance. In this experiment we assessed changes in cerebral blood flow (CBF) after intracarotid infusion of nitroprusside and adenosine. The study was conducted on six adult baboons under isoflurane anesthesia and controlled ventilation. Intracarotid drug infusion protocol avoided hypotension during nitroprusside infusion and tested for autoregulatory vasoconstriction. CBF (intraarterial (133)Xe technique) was measured four times during infusions of 1) intracarotid saline, 2) IV phenylephrine (0.2 microg x kg(-1) x min(-1)) aimed to increase mean arterial pressure by 10-15 mm Hg, 3) IV phenylephrine and intracarotid nitroprusside (0.5 microg x kg(-1) x min(-1)), and 4) intracarotid adenosine (1 mg/min). IV phenylephrine increased mean arterial pressure (69 +/- 8 to 91 +/- 9 mm Hg, P < 0.0001, n = 6), and concurrent infusion of intracarotid nitroprusside reversed this effect. However, compared with baseline, CBF did not change with IV phenylephrine or with concurrent infusion of IV phenylephrine and intracarotid nitroprusside. Intracarotid adenosine profoundly increased CBF (from 29 +/- 8 to 75 +/- 32 mL x 100 g(-1) x min(-1); P < 0.0001). In nonhuman primates, intracarotid adenosine increases CBF in doses that lack significant systemic side effects, whereas intracarotid nitroprusside has no effect. Intracarotid adenosine may be useful for manipulating cerebrovascular resistance and augmenting CBF during cerebral ischemia. IMPLICATIONS: Intraarterial (133)Xe cerebral blood flow (CBF) measurements suggest that intracarotid adenosine, in a dose that lacks significant systemic side effects, profoundly increases CBF, whereas nitroprusside has no effect.(5-12)

Adenosine↗
PubMed2002

Intracarotid nitroprusside does not augment cerebral blood flow in human subjects.

BACKGROUND: The recent resurgence of interest in the cerebrovascular effects of nitroprusside can be attributed to the possibility of using nitric oxide donors in treating cerebrovascular insufficiency. However, limited human data suggest that intracarotid nitroprusside does not directly affect cerebrovascular resistance. In previous studies, physiologic or pharmacologic reactivity of the preparation was not tested at the time of nitroprusside challenge. The authors hypothesized that if nitric oxide is a potent modulator of human cerebral blood flow (CBF), then intracarotid infusion of nitroprusside will augment CBF. METHODS: Cerebral blood flow was measured (intraarterial (133)Xe technique) in sedated human subjects undergoing cerebral angiography during sequential infusions of (1) intracarotid saline, (2) intravenous phenylephrine to induce systemic hypertension, (3) intravenous phenylephrine with intracarotid nitroprusside (0.5 microg x kg(-1) x min(-1)), and (4) intracarotid verapamil (0.013 mg x kg(-1) x min(-1)). Data (mean +/- SD) were analyzed by repeated-measures analysis of variance and post hoc Bonferroni-Dunn test. RESULTS: Intravenous phenylephrine increased systemic mean arterial pressure (from 83 +/- 12 to 98 +/- 6 mmHg; n = 8; P < 0.001), and concurrent infusion of intravenous phenylephrine and intracarotid nitroprusside reversed this effect. However, compared with baseline, CBF did not change with intravenous phenylephrine or with concurrent infusions of intravenous phenylephrine and intracarotid nitroprusside. Intracarotid verapamil increased CBF (43 +/- 9 to 65 +/- 11 ml x 100 g(-1) x min(-1); P < 0.05). CONCLUSIONS: The authors conclude that, in humans, intracarotid nitroprusside sufficient to decrease mean arterial pressure during recirculation, does not augment CBF. Failure of intracarotid nitroprusside to augment CBF despite demonstrable autoregulatory vasoconstriction and pharmacologic vasodilation questions the significance of nitric oxide-mediated vasodilation in human cerebral circulation.

Adult↗
PubMed2002

Clinical utility of quantitative cerebral blood flow measurements during internal carotid artery test occlusions.

OBJECTIVE: Internal carotid artery (ICA) balloon test occlusions (BTOs) are performed in the angiography suite to predict whether the patient has adequate collateral circulation to prevent stroke when permanent ICA occlusion (PCO) is required for treatment. Although many criteria have been proposed to facilitate predictions of stroke risk after PCO, no BTO techniques have been subjected to predictive validity testing in outcome studies. We describe a prospective case series study that tests the predictive validity of quantitative cerebral blood flow (CBF) measurements during ICA BTO. METHODS: Thirty-three patients with clinical indications for PCO underwent ICA BTO and then PCO. During BTO, standard neurological examinations, sustained-attention testing, and quantitative CBF measurements were performed. Two scalp scintillation detectors recorded washout data after ipsilateral intracarotid injection of xenon-133 through a port at the tip of the ICA-occluding balloon. Patients were monitored for the outcome measure of ipsilateral stroke for a mean of 34 months. The variables of quantitative CBF values, neurological examination results, sustained-attention test results, age, sex, and side of occlusion were examined with Kaplan-Meier log-rank tests, predictive validity analyses, and logistic regression analyses. RESULTS: CBF of less than 30 ml/100 g/min during BTO was the only variable that predicted stroke after PCO (log rank = 5.87, P = 0.015). The negative and positive predictive values for CBF findings were superior to those for standard neurological examination findings and sustained-attention test results. Age, sex, and side of occlusion did not predict stroke. CONCLUSION: Quantitative CBF testing, via the intracarotid injection technique, during BTO seems to be an important predictor of stroke after PCO.

Adult↗
PubMed2002

Intra-arterial 133Xe measurements suggest a dose-dependent increase in cerebral blood flow during intracarotid infusion of adenosine in nonhuman primates.

Intra-arterial vasodilators, such as papaverine, have been used to treat cerebrovascular insufficiency. The short biologic half-life, and the vasodilating and neuroprotective properties of adenosine could be useful during the treatment of cerebral ischemia. However, in human subjects a proposed intracarotid dose of 1 mg/min adenosine was ineffective in augmenting cerebral blood flow (CBF). The object of this experiment was to determine the dose-CBF response characteristics of intracarotid adenosine in nonhuman primates. Studies were conducted on five male baboons under isoflurane anesthesia. After transfemoral internal carotid artery cannulation, changes in CBF (intra-arterial 133Xe technique) were determined after intracarotid infusion of saline and three increasing doses of adenosine (0.5, 1.0, and 1.5 mg/min). Each infusion lasted 5 minutes. Data (mean +/- standard deviation) were analyzed by repeated-measure analysis of variance and the post hoc Tukey test. Intracarotid adenosine (0.5, 1.0, and 1.5 mg/min) resulted in a dose-dependent increase in CBF from 22.6 +/- 4 mL/100 g/min at baseline to 50 +/- 15, 65 +/- 22, and 83 +/- 31 mL/100 g/min respectively (n = 5, P < .05 each). No adverse hemodynamic side effects were noted, and animals recovered promptly from anesthesia. The authors conclude that intracarotid adenosine in the range of 0.5 to 1.5 mg/min results in a robust increase in CBF. Based on body weight, intracarotid adenosine in a dose range of 2.5 to 7.5 mg/min may be required to augment CBF in human subjects.

Adenosine↗
PubMed2002

Characterization of the cerebral blood flow response to balloon deflation after temporary internal carotid artery test occlusion.

The authors tested the hypothesis that cerebral blood flow (CBF) would increase after acute and relatively brief internal carotid artery (ICA) test occlusion, and examined the relationship of the postdeflation CBF to the development of neurologic symptoms. In 16 patients undergoing ICA test occlusion with deliberate hypotension, the authors measured intracarotid 133Xe CBF at baseline, occlusion, and deflation. Four patients developed neurologic symptoms during occlusion. As positive controls, 11 other patients received intracarotid verapamil or papaverine before deflation as part of another protocol. Balloon occlusion was 23.1 +/- 10.5 minutes (mean +/- standard deviation) in duration. At 1.3 +/- 1.6 minutes after balloon deflation, there was a trend (12 +/- 31%) for CBF to increase (48 +/- 9 mL/100 g/min versus 53 +/- 17 mL/100 g/min, P =.15), and a 16 +/- 27% decrease in cerebrovascular resistance (CVR; 2.1 +/- 0.6 mm Hg/100 g/min/mL versus 1.7 +/- 0.6 mm Hg/100 g/min/mL, P =.03) compared with baseline values. By comparison, patients who received a intracarotid dilator demonstrated a 53 +/- 55% increase in CBF (48 +/- 10 mL/100/min versus 70 +/- 23 mL/100 g/min, P = .007) and a 33 +/- 31% decrease in CVR (2.2 +/- 0.6 mm Hg/100 g/min/mL versus 1.4 +/- 0.6 mm Hg/100 g/min/mL, P = .0007) compared with baseline. Analysis of variance and regression analysis showed no other relationships between postocclusion CBF and balloon occlusion duration, distal internal carotid occlusion ("stump") pressure, or the development of neurologic symptoms. Acute, temporary interruption of ICA blood flow resulted in minimal postocclusive changes in cerebrovascular hemodynamics, even in those patients who developed neurologic symptoms during the period of test occlusion.

Adult↗