Combined indocyanine green and quantitative perfusion assessment with hyperspectral imaging during colorectal resections.

Anastomotic insufficiencies still represent one of the most severe complications in colorectal surgery. Since tissue perfusion highly affects anastomotic healing, its objective assessment is an unmet clinical need. Indocyanine green-based fluorescence angiography (ICG-FA) and hyperspectral imaging (HSI) have received great interest in recent years but surgeons have to decide between both techniques. For the first time, two data processing pipelines capable of reconstructing an ICG-FA correlating signal from hyperspectral data were developed. Results were technically evaluated and compared to ground truth data obtained during colorectal resections. In 87% of 46 data sets, the reconstructed images resembled the ground truth data. The combined applicability of ICG-FA and HSI within one imaging system might provide supportive and complementary information about tissue vascularization, shorten surgery time, and reduce perioperative mortality.

[Possibilities and perspectives of hyperspectral imaging in visceral surgery]. / Möglichkeiten und Perspektiven der Hyperspektralbildgebung in der Viszeralchirurgie.

HyperSpectral Imaging (HSI) technology enables quantitative tissue analyses beyond the limitations of the human eye. Thus, it serves as a new diagnostic tool for optical properties of diverse tissues. In contrast to other intraoperative imaging methods, HSI is contactless, noninvasive, and the administration of a contrast medium is not necessary. The duration of measurements takes only a few seconds and the surgical procedure is only marginally disturbed. Preliminary HSI applications in visceral surgery are promising with the potential of optimized outcomes. Current concepts, possibilities and new perspectives regarding HSI technology together with its limitations are discussed in this article.

[Hyperspectral imaging of gastrointestinal anastomoses]. / Hyperspektral-Imaging bei gastrointestinalen Anastomosen.

INTRODUCTION: Anastomotic insufficiency (AI) remains the most feared surgical complication in gastrointestinal surgery, which is closely associated with a prolonged inpatient hospital stay and significant postoperative mortality. Hyperspectral imaging (HSI) is a relatively new medical imaging procedure which has proven to be promising in tissue identification as well as in the analysis of tissue oxygenation and water content. Until now, no data exist on the in vivo HSI analysis of gastrointestinal anastomoses. METHODS: Intraoperative images were obtained using the TIVITA™ tissue system HSI camera from Diaspective Vision GmbH (Pepelow, Germany). In 47 patients who underwent gastrointestinal surgery with esophageal, gastric, pancreatic, small bowel or colorectal anastomoses, 97 assessable recordings were generated. Parameters obtained at the sites of the anastomoses included tissue oxygenation (StO2), the tissue hemoglobin index (THI), near-infrared (NIR) perfusion index, and tissue water index (TWI). RESULTS: Obtaining and analyzing the intraoperative images with this non-invasive imaging system proved practicable and delivered good results on a consistent basis. A NIR gradient along and across the anastomosis was observed and, furthermore, analysis of the tissue water and oxygenation content showed specific changes at the site of anastomosis. CONCLUSION: The HSI method provides a non-contact, non-invasive, intraoperative imaging procedure without the use of a contrast medium, which enables a real-time analysis of physiological anastomotic parameters, which may contribute to determine the "ideal" anastomotic region. In light of this, the establishment of this methodology in the field of visceral surgery, enabling the generation of normal or cut off values for different gastrointestinal anastomotic types, is an obvious necessity.

Online time and resource management based on surgical workflow time series analysis.

PURPOSE: Hospitals' effectiveness and efficiency can be enhanced by automating the resource and time management of the most cost-intensive unit in the hospital: the operating room (OR). The key elements required for the ideal organization of hospital staff and technical resources (such as instruments in the OR) are an exact online forecast of both the surgeon's resource usage and the remaining intervention time. METHODS: This paper presents a novel online approach relying on time series analysis and the application of a linear time-variant system. We calculated the power spectral density and the spectrogram of surgical perspectives (e.g., used instrument) of interest to compare several surgical workflows. RESULTS: Considering only the use of the surgeon's right hand during an intervention, we were able to predict the remaining intervention time online with an error of 21 min 45 s ±9 min 59 s for lumbar discectomy. Furthermore, the performance of forecasting of technical resource usage in the next 20 min was calculated for a combination of spectral analysis and the application of a linear time-variant system (sensitivity: 74 %; specificity: 75 %) focusing on just the use of surgeon's instrument in question. CONCLUSION: The outstanding benefit of these methods is that the automated recording of surgical workflows has minimal impact during interventions since the whole set of surgical perspectives need not be recorded. The resulting predictions can help various stakeholders such as OR staff and hospital technicians. Moreover, reducing resource conflicts could well improve patient care.

Effects of sugammadex on incidence of postoperative residual neuromuscular blockade: a randomized, controlled study.

BACKGROUND: This study aimed to investigate whether reversal of rocuronium-induced neuromuscular blockade with sugammadex reduced the incidence of residual blockade and facilitated operating room discharge readiness. METHODS: Adult patients undergoing abdominal surgery received rocuronium, followed by randomized allocation to sugammadex (2 or 4 mg kg(-1)) or usual care (neostigmine/glycopyrrolate, dosing per usual care practice) for reversal of neuromuscular blockade. Timing of reversal agent administration was based on the providers' clinical judgement. Primary endpoint was the presence of residual neuromuscular blockade at PACU admission, defined as a train-of-four (TOF) ratio <0.9, using TOF-Watch® SX. Key secondary endpoint was time between reversal agent administration and operating room discharge-readiness; analysed with analysis of covariance. RESULTS: Of 154 patients randomized, 150 had a TOF value measured at PACU entry. Zero out of 74 sugammadex patients and 33 out of 76 (43.4%) usual care patients had TOF-Watch SX-assessed residual neuromuscular blockade at PACU admission (odds ratio 0.0, 95% CI [0-0.06], P<0.0001). Of these 33 usual care patients, 2 also had clinical evidence of partial paralysis. Time between reversal agent administration and operating room discharge-readiness was shorter for sugammadex vs usual care (14.7 vs. 18.6 min respectively; P=0.02). CONCLUSIONS: After abdominal surgery, sugammadex reversal eliminated residual neuromuscular blockade in the PACU, and shortened the time from start of study medication administration to the time the patient was ready for discharge from the operating room. CLINICAL TRIAL REGISTRATION: Clinicaltrials.gov:NCT01479764.

Procalcitonin as a predictor of severe appendicitis in children.

The aim of this study was to assess the diagnostic value of procalcitonin (PCT) in 212 children with appendicitis and compare it with that of the standard diagnostic modalities, C-reactive protein (CRP) level, leukocyte count, and abdominal ultrasound findings, in relation to the surgical and histological findings of the appendix. A PCT value of >0.5 ng/ml was found to be indicative of perforation or gangrene with 73.4% sensitivity and 94.6% specificity, a CRP level of >50 mg/l and a leukocyte count of >10(4)/mm3 were useful diagnostic markers for perforation, while abdominal ultrasonography had a sensitivity of 82.8% and a specificity of 91.2% for detecting appendicitis with imaging findings. PCT measurement seems to be a useful adjunctive tool for diagnosing acute necrotizing appendicitis or perforation, and surgical exploration will probably be required in patients with PCT values >0.5 ng/ml.

Comparison of remifentanil and fentanyl in patients undergoing craniotomy for supratentorial space-occupying lesions.

BACKGROUND: Remifentanil hydrochloride is an ultra-short-acting, esterase-metabolized mu-opioid receptor agonist. This study compared the use of remifentanil or fentanyl during elective supratentorial craniotomy for space-occupying lesions. METHODS: Sixty-three adults gave written informed consent for this prospective, randomized, double-blind, multiple-center trial. Anesthesia was induced with thiopental, pancuronium, nitrous oxide/oxygen, and fentanyl (n = 32; 2 micrograms.kg.-1. min-1) or remifentanil (n = 31; 1 mu.kg-1.min-1). After tracheal intubation, infusion rates were reduced to 0.03 microgram.kg-1.min-1 (fentanyl) or 0.2 microgram.kg-1.min-1 (remifentanil) and then adjusted to maintain anesthesia and stable hemodynamics. Isoflurane was given only after specified infusion rate increases had occurred. At the time of the first burr hole, intracranial pressure was measured in a subset of patients. At bone flap replacement either saline (fentanyl group) or remifentanil (approximately 0.2 microgram.kg-1.min-1) were infused until dressing completion. Hemodynamics and time to recovery were monitored for 60 min. Analgesic requirements and nausea and vomiting were observed for 24 h. Neurological examinations were performed before operation and on postoperative days 1 and 7. RESULTS: Induction hemodynamics were similar. Systolic blood pressure was greater in the patients receiving fentanyl after tracheal intubation (fentanyl = 127 +/- 18 mmHg; remifentanil = 113 +/- 18 mmHg; P = 0.004). Intracranial pressure (fentanyl = 14 +/- 13 mmHg; remifentanil = 13 +/- 10 mmHg) and cerebral perfusion pressure (fentanyl = 76 +/- 19 mmHg; remifentanil = 78 +/- 14 mmHg) were similar. Isoflurane use was greater in the patients who received fentanyl. Median time to tracheal extubation was similar (fentanyl = 4 min: range = -1 to 40 min; remifentanil = 5 min: range = 1 to 15 min). Seven patients receiving fentanyl and none receiving remifentanil required naloxone. Postoperative systolic blood pressure was greater (fentanyl = 134 +/- 16 mmHg; remifentanil = 147 +/- 15 mmHg; P = 0.001) and analgesics were required earlier in patients receiving remifentanil. Incidences of nausea and vomiting were similar. CONCLUSIONS: Remifentanil appears to be a reasonable alternative to fentanyl during elective supratentorial craniotomy.

Angiotensin II contributes to cerebral vasodilatation during hypoxia in the rabbit.

BACKGROUND: and Purpose Hypoxia increases cerebral blood flow (CBF). Hypoxia also exerts a major influence on the renin-angiotensin system. In addition to the circulating renin-angiotensin system, a local renin-angiotensin system appears to be present in the brain, and angiotensin II receptors have been identified in cerebral blood vessels. In this study we tested the hypothesis that endogenous angiotensin II attenuates dilatation of the cerebral vessels during hypoxia. METHODS: Pentobarbital-anesthetized rabbits were prepared for measurement of blood flow (microspheres) and assigned to one of two groups: in group 1 (n = 11), rabbits were subjected to 30 minutes of stable hypoxia (PaO2 = 34 +/- 1 mm Hg, mean +/- SD) followed by 15 minutes of reoxygenation (PaO2 = 177 to 200 mm Hg). Blood flow was measured four times: under control conditions, after 15 and 30 minutes of hypoxia, and after 15 minutes of reoxygenation. This was a control group to characterize changes in CBF during hypoxia. In group 2 (n = 11), blood flow was measured as in the previous group except that an infusion of the angiotensin II receptor antagonist saralasin (1 microgram.kg-1.min-1 IV) was started with the onset of hypoxia and continued through reoxygenation to the end of the experiment. The goal of this group was to examine whether endogenous activation of receptors for angiotensin II influences increases in CBF during hypoxia. In a separate series of experiments we examined the influence of the angiotensin-converting enzyme (ACE) inhibitor captopril on the hypoxic response. Thus, in one group of rabbits we measured CBF in the same manner as in group 1 (n = 13). In another group of rabbits we also measured blood flow as in group 1 except that rabbits received 10 mg/kg of the ACE inhibitor captopril before the control measurement (n = 11). We tested for significant differences between groups using two-way ANOVA. RESULTS: Under control conditions, CBF was similar in all groups and averaged 53 +/- 15 mL.min-1.100 g-1. During hypoxia, CBF increased to a greater extent in the absence versus the presence of saralasin (95 +/- 31 and 104 +/- 30 mL.min-1.100 g-1 versus 72 +/- 24 and 71 +/- 25 mL.min-1.100 g-1, respectively; P = .003). Increase in CBF during hypoxia was also significantly greater in the animals that did not receive captopril versus those that were treated with captopril (100 +/- 24 and 89 +/- 16 mL.min-1.100 g-1 versus 72 +/- 16 and 73 +/- 17 mL.min-1.100 g-1). To rule out the possibility that saralasin produced non-specific attenuation of cerebral vasodilatation, we tested the influence of hypercapnia on CBF in the absence and presence of saralasin. During normocapnia, CBF values were not significantly different in the absence and presence of saralasin (57 +/- 17 and 64 +/- 6 mL.min-1.100 g-1, respectively; P > .05). Hypercapnia increased CBF similarly in the absence and presence of saralasin (81 +/- 22 and 91 +/- 19 mL.min-1.100 g-1; PaCO2 = 61 +/- 2 and 60 +/- 2 mm Hg, respectively; P > .05). CONCLUSIONS: Because the ACE inhibitor captopril and the angiotensin II receptor blocker saralasin attenuated increased in CBF during hypoxia, the findings suggest that endogenous release of angiotensin II contributes to the increase in CBF during hypoxia.

Cerebral blood flow and oxygen delivery during hypoxemia and hemodilution: role of arterial oxygen content.

To determine the role of arterial O2 content (CaO2) in the cerebral blood flow (CBF) responses to hypoxemia and hemodilution, CaO2 was progressively reduced from approximately 18 to approximately 6 ml O2/dl in normocapnic, normothermic, pentobarbital-anesthetized rabbits. This was done either by reducing PaO2 (hypoxemia, minimum PaO2 approximately 26 mmHg) or arterial hematocrit (isovolemic hemodilution with hetastarch, minimum hematocrit approximately 14%) while CBF was measured with radioactive microspheres. As CaO2 decreased, CBF increased in both groups but was greater in hypoxemic animals at CaO2 values < or = 9 ml O2/dl. For example, at a CaO2 approximately 6 ml O2/dl, CBF in hypoxemic animals was 110 +/- 38 ml.100 g-1.min-1 (means +/- SD) compared with 82 +/- 22 ml.100 g-1.min-1 in hemodiluted animals (means +/- SD). While calculated cerebral O2 delivery (cerebral DO2) was well maintained in hypoxemic animals, it decreased significantly during hemodilution (from 7.95 +/- 2.92 baseline to 5.08 +/- 1.10 ml O2/dl.100 g-1.min-1 at the lowest CaO2 value). This decrease in cerebral DO2 was offset by an increase in oxygen extraction ratio during hemodilution. By contrast, the small increase in oxygen extraction ratio seen with hypoxemia did not achieve significance. These results suggest that there are different adaptive responses to acute hypoxemia or hemodilution . They also imply that at similar CBF and CaO2 values, tissue O2 availability may be greater during hemodilution than during hypoxemia.

Endogenous angiotensin II inhibits production of cerebrospinal fluid during posthypoxemic reoxygenation in the rabbit.

BACKGROUND AND PURPOSE: The choroid plexus, the major source of cerebrospinal fluid (CSF), contains receptors for angiotensin II and a very high concentration of angiotensin converting enzyme. Circulating angiotensin II decreases blood flow to the choroid plexus and the production of CSF. During recovery from hypoxia, marked increases in circulating angiotensin II have been described in some studies. We tested the hypothesis that CSF production decreases during posthypoxemic reoxygenation and examined related changes in plasma concentrations of angiotensin II. We also determined whether effect of posthypoxic reoxygenation on production of CSF is due to endogenous release of angiotensin II. METHODS: We measured production of CSF in chloralose-anesthetized rabbits using ventriculocisternal perfusion of artificial CSF containing blue dextran. After control measurements, rabbits were subjected to one of the following interventions: (1) 30 minutes of hypoxia (PaO2 = 36 +/- 1 mmHg [mean +/- SE]) followed by 90 minutes of reoxygenation; (2) 30 minutes of hypoxia (PaO2 = 37 +/- 2 mmHg) followed by 90 minutes of reoxygenation in the presence of the angiotensin II antagonist saralasin; (3) hypoxia for 120 minutes (PaO2 = 35 +/- 1 mmHg); and (4) infusion of vehicle under normoxic conditions for 120 minutes (time control). Plasma concentrations of angiotensin II were also measured (radioimmunoassay) under control conditions, during hypoxia, and during posthypoxic reoxygenation (first intervention) and at corresponding time intervals in time control animals (fourth intervention). RESULTS: Under control conditions, the rate of production of CSF averaged 6.7 +/- 0.1 microL.min-1. During posthypoxemic reoxygenation, production of CSF decreased by 31 +/- 4% (P < .05). In the presence of sarlasin, CSF production did not change significantly during posthypoxemic reoxygenation (-12 +/- 6%, P > .05). In time control animals and during prolonged hypoxia, CSF production did not change significantly (-12 +/- 5% [P > .05] and 9 +/- 7% [P > .05], respectively). Plasma concentrations of angiotensin were below the threshold of sensitivity of the assay under control conditions and during interventions in animals that were made hypoxic and then reoxygenated and in time control animals. CONCLUSIONS: CSF production decreases during posthpoxemic reoxygenation. Since plasma concentrations of angiotensin II did not change during posthypoxic reoxygenation, this effect does not appear to be mediated by increases in circulating angiotensin II. We speculate that endogenous release of angiotensin II, perhaps in the choroid plexus epithelium, decreases production of CSF after hypoxic brain injury.

The dose-related effects of nitric oxide synthase inhibition on cerebral blood flow during isoflurane and pentobarbital anesthesia.

BACKGROUND: Recent work in animals suggests that nitric oxide may play a role in the cerebral blood flow (CBF) changes produced by anesthetics, particularly the vasodilation seen with volatile anesthetics. It is not clear, however, whether nitric oxide causes the flow increase or simply plays some constitutive role. To distinguish between these possibilities, we studied the dose-related effects of nitric oxide synthase inhibition in rabbits with varying baseline CBFs, produced by anesthesia with isoflurane, low-dose pentobarbital, or high-dose pentobarbital. METHODS: New Zealand White rabbits were anesthetized with 1 MAC isoflurane, low-dose pentobarbital (50-mg/kg load, 7.5-mg.kg-1.h-1 infusion), or high-dose pentobarbital (50-mg/kg load, 20-mg.kg-1.h-1, deep burst-suppression on the electroencephalogram), and prepared for the measurement of CBF using radioactive microspheres. The confluence of sinuses was also exposed to permit sampling of cerebral venous blood and the determination of cerebral metabolic rate for O2 (CMRO2). Normocapnia and normothermia were maintained throughout. After baseline measurements, animals were sequentially given a cumulative total of 3, 13, and 43 mg/kg intravenous N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase. CBF and CMRO2 were recorded approximately 10 min after each dose. RESULTS: L-NAME produced a dose-related reduction in CBF in all three anesthetic groups. Statistical examination indicated that the dose response curves were parallel. For example, in isoflurane-anesthetized rabbits, CBF decreased from 77 +/- 19 to 47 +/- 11 ml.100 g-1.min-1 after the 43 mg/kg L-NAME, whereas in high-dose pentobarbital animals, CBF decreased from 42 +/- 15 to 26 +/- 8 ml.100 g-1.min-1 (all values mean +/- SD). Decreases in CMRO2 did not quite achieve significance (P = 0.08), and the CBF/CMRO2 ratio decreased in all animals, suggesting that the CBF reductions were due primarily to direct vasoconstriction. There were no electroencephalographic changes. In separate groups of isoflurane-anesthetized rabbits given 3 mg/kg L-NAME, treatment with 300 mg/kg L-arginine partially reversed the decreases in CBF. By contrast, the effects of 43 mg/kg L-NAME were not reversible with 430 mg/kg L-arginine. CONCLUSIONS: Although L-NAME reduced CBF in all three anesthetic conditions, it did not alter the relative differences among them: CBF in the presence of isoflurane remained much higher than that seen with the barbiturates. This suggests that nitric oxide may not the primary mediator of anesthetic CBF effects, but rather acts to influence background vascular tone in these anesthetized animals.

A prospective, comparative trial of three anesthetics for elective supratentorial craniotomy. Propofol/fentanyl, isoflurane/nitrous oxide, and fentanyl/nitrous oxide.

BACKGROUND: Different anesthetic agents have different effects on cerebrovascular physiology. However, the importance of these differences in neuroanesthetic practice are unclear. In an effort to determine whether important clinical differences are present, the authors compared three anesthetic techniques in 121 adults undergoing elective surgical removal of a supratentorial, intracranial mass lesion. METHODS: Patients were assigned randomly to one of three groups. In group 1 (n = 40), anesthesia was induced with propofol and maintained with fentanyl (approximately 10 micrograms/kg load, 2-3 micrograms.kg-1.h-1 infusion) and propofol (50-300 micrograms.kg-1.min-1). In group 2 (n = 40), anesthesia was induced with thiopental and maintained with isoflurane and nitrous oxide. Up to 2 micrograms/kg fentanyl was given after replacement of the bone flap. In group 3 (n = 41), anesthesia was induced with thiopental and maintained with fentanyl (approximately 10 micrograms/kg load, 2-3 micrograms.kg-1.h-1 infusion), nitrous oxide, and low-dose isoflurane, if required. Blood pressure, heart rate, expired gas concentrations, and ventilatory parameters were recorded automatically in all patients. Epidural intracranial pressure (ICP) was measured via the first burr hole, brain swelling was rated at the time of dural opening, and emergence was monitored closely. Preoperative computed tomography or magnetic resonance imaging scans were evaluated, and pre- and postoperative neurologic exams were performed by a neurosurgeon unaware of group assignments. Total hospital stay (days) and total hospital cost (exclusive of physician charges) also were reviewed. RESULTS: During induction, higher heart rates were seen in isoflurane/nitrous oxide patients, whereas mean arterial pressure was approximately 10 mmHg less during the maintenance phase (compared with both other groups). Otherwise, there were few intergroup hemodynamic differences. While there were no clinically important intergroup differences in mean ICP (+/- SD)-group 1, ICP = 12 +/- 7 mmHg; group 2, 15 +/- 12 mmHg; group 3, ICP = 11 +/- 8 mmHg-more isoflurane/nitrous oxide patients (nine, group 2) had an ICP > or = 24 mmHg than in the other groups (two each). Emergence was, overall, more rapid with fentanyl/nitrous oxide. For example, the median time until the patient could be awakened by quiet verbal command, e.g., "Open your eye," was 5 min, versus 10 min in the other groups. There were no relationships between ICP and any measurement of emergence (e.g., time to response to commands). Seven of 41 (17%) fentanyl/nitrous oxide patients vomited in the early postoperative period, compared with only 1 of 40 (2.5%) of those given propofol/fentanyl and 2 of 40 (5%) receiving isoflurane/nitrous oxide (P = 0.03). There were no differences in the incidence of new postoperative deficits, total hospital stay, or cost. CONCLUSIONS: Although there are modest differences among the three tested anesthetics, short-term outcome was not affected. These results indicate that, despite their respective cerebrovascular effects, all of the anesthetic regimens used were acceptable in these patients undergoing elective surgery.

Angiotensin II decreases the rate of production of cerebrospinal fluid.

The choroid plexus, which produces cerebrospinal fluid (CSF), contains receptors for angiotensin II and a very high concentration of angiotensin-converting enzyme. Circulating angiotensin II decreases blood flow to the choroid plexus. The first goal of this study was to examine the hypothesis that angiotensin II decreases the production of CSF. The second goal was to determine whether effects of angiotensin II on the production of CSF were receptor-mediated. Production of CSF was measured in chloralose-anesthetized rabbits using ventriculocisternal perfusion of artificial CSF containing blue dextran. Rabbits received either vehicle, angiotensin II, angiotensin II in the presence of an angiotensin II antagonist (saralasin), or saralasin intravenously. Increases in blood pressure, during administration of angiotensin II, were prevented by withdrawal of blood. Under control conditions, CSF production averaged 7.2 +/- 0.2 microliters/min (mean +/- S.E.). Angiotensin II (100 ng/kg/min i.v.) decreased CSF production by 24 +/- 3% (P < 0.05, n = 8). In the presence of saralasin (1 microgram/kg/min i.v.), angiotensin II had no significant effect on CSF production (-4 +/- 6%, P > 0.05, n = 7). Vehicle did not affect CSF production significantly (-2 +/- 6%, P > 0.05, n = 7). Saralasin alone decreased production of CSF (-21 +/- 5%, P < 0.05, n = 7). To test the specificity of saralasin in blocking effects of angiotensin II receptor stimulation on CSF production, the carbonic anhydrase inhibitor acetazolamide was administered in the presence and absence of saralasin.(ABSTRACT TRUNCATED AT 250 WORDS)

Halothane decreases the rate of production of cerebrospinal fluid. Possible role of vasopressin V1 receptors.

BACKGROUND: Circulating vasoactive hormones (e.g., vasopressin) play an important role in the regulation of blood flow to the choroid plexus and the rate of cerebrospinal fluid (CSF) production. We tested the hypothesis that halothane decreases CSF production through a vasopressin-related mechanism and examined the related changes in blood flow to the choroid plexus. METHODS: Using ventriculocisternal perfusion, CSF production was measured in chloralose anesthetized, normothermic rabbits whose lungs were mechanically ventilated. Rabbits received either 0.5 minimum alveolar concentration (MAC; end-tidal) of halothane (added to a preestablished chloralose anesthetic), 0.5 MAC of halothane in the presence of a vasopressin V1 antagonist (iv), or the V1 antagonist alone. In addition, we examined animals in which no intervention was made (time control) and animals subjected to a 25% decrease in mean blood pressure produced by hemorrhage, with and without the V1-antagonist. In a separate series of rabbits, regional and total blood flows to the brain and the choroid plexus were measured using radioactive microspheres. These studies were carried out under similar conditions, except that the effects of end-tidal 0.25, 0.5, and 1 MAC of halothane were examined in each rabbit (each added to a preestablished chloralose anesthetic). RESULTS: Under control conditions, blood flow to the choroid plexus averaged 351 +/- 198 ml.min-1.100 g-1 (mean +/- SD) and CSF production averaged 10.1 +/- 1.9 microliters.min.-1. Halothane (0.25, 0.5, and 1 MAC) did not alter choroid plexus blood flow but decreased CSF production by 28 +/- 6% at 0.5 MAC (P < .05). In contrast, 1 MAC of halothane increased total blood flow to the brain by 20 +/- 25% (P < .05). The V1 antagonist, which did not affect production of CSF when given alone, prevented the decrease in CSF production in response to halothane. Hemorrhage decreased blood flow to the choroid plexus but not to the brain, and the V1 antagonist attenuated the decrease in the rate of CSF production by hemorrhage (34 +/- 11% vs. 48 +/- 18%, P < .05). CONCLUSIONS: Halothane decreases CSF production with no net change in the blood flow to the choroid plexus. Decrease in CSF production appears to be mediated through a vasopressin-related mechanism and not to the blood pressure decrease seen during halothane anesthesia.

Effects of central and intravascular angiotensin I and II on the choroid plexus.

The choroid plexus contains receptors for angiotensin II (ANG II) and a very high concentration of angiotensin-converting enzyme. The goal of this study was to test the hypothesis that central, as well as circulating, ANG I and II decrease blood flow to the choroid plexus. Under control conditions in anesthetized rabbits, blood flow (microspheres) to the choroid plexus was 449 +/- 21 (mean +/- SE) ml.min-1.100 g(-1). Intravascular ANG I (30 and 100 ng.kg-1.min-1) decreased blood flow to the choroid plexus by 19 +/- 14 and 28 +/- 18%, respectively. Intravascular ANG II (30 and 100 ng.kg-1.min-1) also produced a decrease in blood flow by 28 +/- 9 and 47 +/- 7%, respectively. When administered into the lateral ventricle, ANG I and II (10 and 100 ng.kg-1.min-1) decreased blood flow to a similar degree: 22 +/- 11 and 31 +/- 10% and 12 +/- 10 and 27 +/- 8%, respectively. Cerebral blood flow was not decreased by intravascular or central ANG I or II. The angiotensin-converting enzyme inhibitor quinaprilat prevented the decrease in blood flow to the choroid plexus in response to ANG I without affecting responses to ANG II. Thus 1) circulating ANG I and II are potent constrictors of blood vessels of the choroid plexus, 2) the constrictor effect of ANG I on the blood vessels of the choroid plexus appears mediated primarily by generation of ANG II, and 3) intracerebroventricular ANG I produces large reductions in the blood flow to the choroid plexus, which suggests that there is an effective central system that converts ANG I to ANG II.(ABSTRACT TRUNCATED AT 250 WORDS)

Tongue skills and clearance of toffee in two age-groups and in children with problems of speech articulation.

If children use the same tongue skills in swallowing and clearing remnants of sticky foods from the mouth as they do in articulating during speech, it could then be hypothesized that those with impaired articulation might have poorer tongue skills and, consequently, slower rates of food clearance. Does age alter these skills and rates of clearance? Measurements were made of oral stereognosis, tongue-tip manipulation skill, control of tongue protrusion, and the time taken to chew and swallow a standardized piece of toffee and to clear it from the mouth. A statistically significant improvement in tongue skills with age was observed when results for twenty-three 19- to 23-year-old students were compared with those for twenty-nine 6 to 11-year-old children, but no distant differences in clearance rates were noted. Results for thirty-nine 5- to 8-year old children with impaired articulation and forty normal age-matched children showed the former group to have delayed chewing times and clearance rates, and poorer oral stereognosis and tongue protrusion control. Although these tests have shown significant differences between relatively large groups, the value of such tests on individuals is limited.

Effects of angiotensin II on blood flow to choroid plexus.

The choroid plexus contains receptors for angiotensin II and a very high concentration of angiotensin-converting enzyme. The goal of this study was to test the hypothesis that angiotensin II decreases blood flow to the choroid plexus. In rabbits anesthetized with chloralose, blood flow (microspheres) to the choroid plexus was 438 +/- 46 (mean +/- SE) ml.min-1.100 g-1 under control conditions. Angiotensin II (10, 30, and 100 ng.kg-1.min-1 iv) decreased blood flow to the choroid plexus by 12 +/- 8, 39 +/- 7, and 57 +/- 5%, respectively, with aortic pressure maintained at control levels. Cerebral blood flow was not affected by angiotensin II. Blood flow to the kidney decreased by 15 +/- 7, 30 +/- 3, and 49 +/- 5%, respectively, during infusion of the three doses of angiotensin II. The angiotensin II antagonist saralasin (1 micrograms.kg-1.min-1 iv) did not affect blood flow to the cerebrum or the choroid plexus under control conditions. Saralasin blocked the vasoconstrictor effect of angiotensin II on the choroid plexus and the kidney. Thus circulating angiotensin II has important and parallel effects on blood flow to the choroid plexus and kidney that are mediated by angiotensin II receptors. We speculate that circulating and perhaps locally produced angiotensin II may play an important role in regulation of blood flow to the choroid plexus.

Nicardipine HCl: clinical experience in patients undergoing anaesthesia for intracranial aneurysm clipping.

Previous studies have reported haemodynamic interactions between dihydropyridine calcium antagonists and general anaesthesia. During anaesthesia for intracranial aneurysm surgery, we prospectively compared haemodynamic values obtained from 13 patients being treated with nicardipine HCl (0.15 mg.kg-1.hr-1 IV) for cerebral vasospasm against values obtained from 11 untreated controls. Prior to induction of anaesthesia, nicardipine-treated patients had significantly elevated mean +/- SD cardiac index (5.67 +/- 1.30 vs 3.99 +/- 0.73 L.min-1.m-2) while MAP (86 +/- 10 vs 99 +/- 14 mmHg) and systemic vascular resistance (647 +/- 227 vs 1141 +/- 404 dynes.sec-1.cm-5) were reduced. Heart rate, CVP, and PACWP were similar between groups. Anaesthesia induction and tracheal intubation resulted in similar haemodynamic values between groups with the exception of CVP (10 +/- 5 vs 5 +/- 2 mmHg) and PACWP (15 +/- 5 vs 8 +/- 3 mmHg) which were elevated in the nicardipine group (P less than 0.01). Mannitol infusion and deliberate hypotension resulted in nearly identical haemodynamic responses in both groups. Nicardipine-treated patients required more intravenous fluids during the operative procedure (2.4 +/- 0.3 L vs 1.5 +/- 0.4 L, P less than 0.05) and were less likely to require isoflurane supplementation to morphine sulphate/nitrous oxide anaesthesia (P less than 0.01). In summary, our experience with nicardipine HCl revealed no major untoward effects with respect to maintenance of intraoperative haemodynamic stability despite continuous antivasospasm therapy with this vasodilator.

Comparison of nitroprusside, nitroglycerin, and deep isoflurane anesthesia for induced hypotension.

Three methods of inducing hypotension were studied for their effects on the cardiovascular system and intrapulmonary shunting. Thirty patients were anesthetized with isoflurane in 70% N2O to a total of 1.25 to 1.3 MAC. Patients were divided into three groups of 10 each on the basis of the drug used to induce hypotension; sodium nitroprusside (SNP), nitroglycerin (NTG), or deep isoflurane anesthesia (ISF). Cardiac index was significantly decreased by NTG and ISF at a mean arterial blood pressure of 40 mm Hg compared to SNP (P less than 0.05). Systemic vascular resistance was decreased in all groups. Mixed venous oxygen content was significantly decreased from control in the NTG and ISF groups. There was no difference between the groups in arterial and mixed venous O2 content. Intrapulmonary shunting decreased with induction and, in the NTG and SNP groups, increased slightly but not significantly with induction of hypotension. Our data do not show a clear superiority of any agent over the other to induce hypotension, although SNP and perhaps ISF appear to be better than NTG to induce hypotension.