scholarly journals The Effects of Dipyridamole and Theophylline on Rat Pial Vessels during Hypocarbia

1988 ◽  
Vol 8 (6) ◽  
pp. 829-833 ◽  
Author(s):  
Setsuro Ibayashi ◽  
Al C. Ngai ◽  
Joseph R. Meno ◽  
H. Richard Winn
Keyword(s):  
Adenosine Receptors ◽  
The Other ◽  
Monitor System ◽  
Video Monitor ◽  
Mechanically Ventilated ◽  
Cranial Window ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Before And After ◽  
Pial Arterioles

Hypocarbia results in an increase in brain adenosine concentrations, presumably because of brain hypoxia associated with hypocarbic vasoconstriction. It was hypothesized that adenosine limits the degree of hypocarbic vasoconstriction. To test this hypothesis, the effects of dipyridamole and theophylline on CO2 reactivity during hypocarbia were investigated in anesthetized rats. Dipyridamole should reduce the vasoconstriction by potentiating adenosine action, whereas theophylline should increase the vasoconstriction by blocking adenosine receptors. Cortical pial arterioles of mechanically ventilated and anesthetized rats were displayed on a video monitor system through a closed cranial window. Arterial blood pressure and oxygen tension were stable. CO2 reactivity, formulated as 100 x [Δ diameter (μm)/resting diameter (μm)]/Δ PaCO2 (mmHg), in the hypocarbic phase was calculated before and after topical superfusion of dipyridamole (10−6 M; n = 7) and theophylline (5 × 10−5 M; n = 6). CO2 reactivity was significantly decreased after superfusion of dipyridamole (0.57 ± 0.08; mean ± SEM) as compared with mock cerebrospinal fluid (CSF) (0.97 ± 0.17, p < 0.05, n = 7). On the other hand, CO2 reactivity after superfusion of theophylline was increased (1.63 ± 0.28) as compared with mock CSF (1.00 ± 0.20, p < 0.05, n = 6), indicating that adenosine is involved in hypocarbic vasoconstriction.

scholarly journals Safety in intrahospital transportation: evaluation of respiratory and hemodynamic parameters. A prospective cohort study

2008 ◽  
Vol 126 (6) ◽  
pp. 319-322 ◽  
Author(s):  
Bruno Franco Mazza ◽  
José Luiz Gomes do Amaral ◽  
Heloisa Rosseti ◽  
Rosana Borges Carvalho ◽  
Ana Paula Resque Senna ◽  
...  
Keyword(s):  
Cohort Study ◽  
Prospective Cohort Study ◽  
Prospective Cohort ◽  
Mechanically Ventilated ◽  
Mechanically Ventilated Patients ◽  
Arterial Blood ◽  
Before And After ◽  
High Risk Situation ◽  
Change In Mean ◽  
Ventilated Patients

CONTEXT AND OBJECTIVE: Intrahospital transportation of mechanically ventilated patients is a high-risk situation. We aimed to determine whether transfers could be safely performed by using a transportation routine. DESIGN AND SETTING: Prospective cohort study with "before and after" evaluation. METHODS: Mechanically ventilated patients who needed transportation were included. Hemodynamic and respiratory parameters were measured before and after transportation. Statistical analysis consisted of variance analysis and paired Student's t test. Results were considered significant if P < 0.05. RESULTS: We studied 37 transfers of 26 patients (12 female) of mean age 46.6 ± 15.7. Patients with pulmonary diseases, positive end expiratory pressure > 5, FiO2 > 0.4 and vasoactive drug use comprised 42.4%, 24.3%, 21.6% and 33.0% of cases, respectively. Mean duration of transportation was 43.4 ± 18.9 minutes. Complications occurred in 32.4%. There was a significant increase in CO2 (before transportation, 29.6 ± 7.3 and after transportation, 34.9 ± 7.0; P = 0.000); a trend towards improved PO2/FiO2 ratio (before transportation, 318.0 ± 137.0 and after transportation, 356.8 ± 119.9; P = 0.053); increased heart rate (before transportation, 80.9 ± 18.7 and after transportation, 85.5 ± 17.6; P = 0.08); and no significant change in mean arterial blood pressure (P = 0.93). CONCLUSION: These results suggest that intrahospital transportation can be safely performed. Our low incidence of complications was possibly related to both the presence of a multidisciplinary transportation team and proper equipment.

scholarly journals Role of nitric oxide-containing factors in the ventilatory and cardiovascular responses elicited by hypoxic challenge in isoflurane-anesthetized rats

2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vital Role ◽  
Initial Increase ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Before And After

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.

Hemodilution causes size-dependent constriction of pial arterioles in the cat

1989 ◽  
Vol 257 (3) ◽  
pp. H912-H917 ◽  
Author(s):  
M. L. Hudak ◽  
M. D. Jones ◽  
A. S. Popel ◽  
R. C. Koehler ◽  
R. J. Traystman ◽  
...  
Keyword(s):  
Blood Gases ◽  
Base Line ◽  
Isovolemic Hemodilution ◽  
Size Dependent ◽  
Cranial Window ◽  
Arterial Blood ◽  
Equal Importance ◽  
Pial Arterioles ◽  
Cerebral Arterioles ◽  
Cerebral Vasodilation

Cerebral blood flow (CBF) rises as hematocrit (Hct) falls. We previously attributed this rise in CBF to two independent factors of equal importance, decreased arterial O2 content and decreased blood viscosity. We hypothesized that decreased arterial O2 content would dilate cerebral arterioles and that the magnitude of the vasodilation would depend on the magnitude of the passive fall in vascular resistance attributable to decreased viscosity. The present study was designed to test the hypothesis that anemia is accompanied by cerebral vasodilation. Using a closed cranial window, we measured the diameters of 42 pial arterioles (35-305 microns) in 7 cats as serial isovolemic hemodilution lowered Hct by 44% from 31 +/- 4 to 17 +/- 3%. Hemodilution increased CBF (microsphere technique) but did not change mean arterial blood pressure or arterial blood gases. Anticipated vasodilation did not occur; instead, pial arterioles constricted as Hct fell. Maximum vasoconstriction was observed when Hct reached 65-70% of the initial value. Vasoconstriction lessened as Hct was lowered further, but arteriolar diameters at the lowest Hcts remained less than base-line levels. Constriction was greater in small (less than 100 microns) than in large (greater than or equal to 100 microns) arterioles. The initial constriction of pial arterioles may represent myogenic vasoconstriction in response to flow-induced vasodilation of more proximal portions of the cerebrovascular bed and/or to washout of an endogenous vasodilator. Arteriolar relaxation with more profound hemodilution may reflect superimposed metabolic vasodilation.

Effect of Thoracentesis on Intubated Patients with Acute Lung Injury

2016 ◽  
Vol 82 (3) ◽  
pp. 266-270
Author(s):  
Matthew B. Bloom ◽  
Derek Serna-Gallegos ◽  
Mark Ault ◽  
Ahsan Khan ◽  
Rex Chung ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Blood Gases ◽  
Surgical Intensive Care Unit ◽  
Surgical Intensive Care ◽  
Mechanically Ventilated ◽  
Arterial Blood ◽  
Tertiary Center ◽  
Before And After ◽  
The Impact

Pleural effusions occur frequently in mechanically ventilated patients, but no consensus exists regarding the clinical benefit of effusion drainage. We sought to determine the impact of thoracentesis on gas exchange in patients with differing severities of acute lung injury (ALI). A retrospective analysis was conducted on therapeutic thoracenteses performed on intubated patients in an adult surgical intensive care unit of a tertiary center. Effusions judged by ultrasound to be 400 mL or larger were drained. Subjects were divided into groups based on their initial P:F ratios: normal >300, ALI 200 to 300, and acute respiratory distress syndrome (ARDS) <200. Baseline characteristics, physiologic variables, arterial blood gases, and ventilator settings before and after the intervention were analyzed. The primary end point was the change in measures of oxygenation. Significant improvements in P:F ratios (mean ± SD) were seen only in patients with ARDS (50.4 ± 38.5, P = 0.001) and ALI (90.6 ± 161.7, P = 0.022). Statistically significant improvement was observed in the pO2 (31.1, P = 0.005) and O2 saturation (4.1, P < 0.001) of the ARDS group. The volume of effusion removed did not correlate with changes in individual patient's oxygenation. These data support the role of therapeutic thoracentesis for intubated patients with abnormal P:F ratios.

Potentiation of hypoxic pulmonary vasoconstriction by ethyl alcohol in dogs

1978 ◽  
Vol 44 (1) ◽  
pp. 76-80 ◽  
Author(s):  
R. C. Doekel ◽  
E. K. Weir ◽  
R. Looga ◽  
R. F. Grover ◽  
J. T. Reeves
Keyword(s):  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Blood Gases ◽  
Adrenergic Blockade ◽  
Mechanically Ventilated ◽  
Pulmonary Vasoconstriction ◽  
Arterial Blood ◽  
Before And After ◽  
Pressor Activity ◽  
Inhibition Of Prostaglandin Synthesis

Pulmonary and systemic hemodynamics and arterial blood gases were measured in anesthetized and mechanically ventilated dogs before and after oral or intravenous administration of ethanol. Increases in mean pulmonary artery pressure and pulmonary vascular resistance occurred. Platelet antiserum-induced thrombocytopenia inhibition of prostaglandin synthesis with meclofenamate, or alpha-adrenergic blockade did not alter the pulmonary pressor response to ethanol. However, the increase in resistance following ethanol was abolished by hyperoxia and potentiated by hypoxia. Thus, it appears that the effect of ethanol is to augment hypoxic pulmonary vasoconstriction, whereas ethanol per se has no independent pulmonary pressor activity.

Ouabain prevents loss of autoregulation in rat pial arterioles caused by reoxygenation after a brief hypoxic episode

1989 ◽  
Vol 67 (5) ◽  
pp. 423-427 ◽  
Author(s):  
J. Kettler ◽  
B. Y. Ong ◽  
D. Bose
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Protective Effects ◽  
Cranial Window ◽  
Arterial Blood ◽  
Hypoxic Episode ◽  
Electrogenic Sodium Pump ◽  
Before And After ◽  
Pressure Changes ◽  
Arteriolar Diameter

Pial arteriolar diameter changes inversely with changes in systemic arterial blood pressure. Such changes are consistent with autoregulatory functions. These responses are reduced by a brief period of hypoxia followed by reoxygenation. By using an open cranial window preparation we assessed the changes in pial arteriolar diameters during blood pressure changes in rats induced by hemorrhage and reinfusion of blood, before and after a brief period of hypoxia. The slopes of the changes in pial arteriolar diameter as a function of mean arterial blood pressure were −0.47 ± 0.26 μm/mmHg (mean ± SD; 1 mmHg = 133.3 Pa) before hypoxia and −0.11 ± 0.23 μm/mmHg after hypoxia in the untreated rats. In ouabain-treated rats, corresponding slopes were −0.42 ± 0.24 and −0.46 ± 0.22 μm/mmHg. The observed protective effects of ouabain might be a blockade of the Na–K pump in the sarcolemma of the vascular smooth muscle.Key words: vascular smooth muscle, electrogenic sodium pump, metabolic inhibition.

Mechanism of cerebral arteriolar abnormalities after acute hypertension

1981 ◽  
Vol 240 (4) ◽  
pp. H511-H527 ◽  
Author(s):  
H. A. Kontos ◽  
E. P. Wei ◽  
W. D. Dietrich ◽  
R. M. Navari ◽  
J. T. Povlishock ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Oxygen Radicals ◽  
Sudden Increase ◽  
Free Oxygen Radicals ◽  
Acute Hypertension ◽  
Free Oxygen ◽  
Cranial Window ◽  
Brain Surface ◽  
Arterial Blood ◽  
Pial Arterioles

Acute severe hypertension induced by intravenous norepinephrine or angiotensin in anesthetized cats equipped with a cranial window caused prolonged arteriolar vasodilation associated with reduced responsiveness to arterial hypercapnia or hypocapnia and passive response to changes in arterial blood pressure. Scanning and transmission electron microscopy of such pial arterioles showed discrete destructive endothelial lesions the density of which correlated with the degree of vasodilation. Abnormalities of the vascular smooth muscle were seen in all dilated arterioles but affected only a small number of smooth muscle cells. The oxygen consumption of pial arterioles from cats subjected to hypertension was significantly reduced in comparison to that of vessels from normal animals. The arteriolar abnormalities induced by hypertension were inhibited by pretreatment with inhibitors of cyclooxygenase (indomethacin or AHR-5850) or by topical application on the brain surface of scavengers of free oxygen radicals (mannitol or superoxide dismutase). The results suggest that the mechanism of the arteriolar abnormalities from acute hypertension involves a sudden increase in prostaglandin synthesis that leads to generation of free oxygen radicals.

Direct Effects of Ropivacaine and Bupivacaine on Spinal Pial Vessels in Canine 

1997 ◽  
Vol 87 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Hiroki Iida ◽  
Yukinaga Watanabe ◽  
Shuji Dohi ◽  
Tadahiko Ishiyama
Keyword(s):  
Topical Application ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Beta Adrenoceptor ◽  
Pial Vessels ◽  
Arterial Blood ◽  
Before And After ◽  
Pial Arterioles ◽  
Anesthetized Dogs ◽  
Pial Vessel

Background Ropivacaine produces a vasoconstriction of cutaneous vessels in contrast to vasodilation produced by bupivacaine. To evaluate direct spinal microvascular actions of these local anesthetics, the authors investigated the concentration-related effects of ropivacaine and bupivacaine on spinal pial vascular diameters using the spinal window technique. Methods Anesthetized dogs (n = 14) divided into two groups (ropivacaine, n = 7; bupivacaine, n = 7) were prepared for measurement of spinal pial vessel diameters by intravital microscopy in a spinal window preparation. The authors administered six concentrations of each drug (10(-8)-10(-3) M) under the window and directly measured the spinal pial arteriolar and venular diameters at sequential times. Physiologic data including mean arterial blood pressure (MAP) and heart rate (HR) were determined before and after topical application of each concentration of the drugs. In additional experiments (n = 18), the action of topical ropivacaine and bupivacaine solution on spinal vessels was evaluated in the presence of yohimbine, prazosin, and propranolol. Results Ropivacaine significantly constricted whereas bupivacaine dilated pial arterioles and venules, both in a concentration-dependent manner. Microvascular alteration was not blocked with any of the adrenoceptor antagonists tested (yohimbine, prazosin, propranolol), each of which per se did not affect pial vessel diameters. Topical application of ropivacaine or bupivacaine did not induce any change in MAP or HR. Conclusions The present results indicate that ropivacaine constricts and bupivacaine dilates the pial vessels of the spinal cord in a concentration-dependent fashion, and the mechanisms involved in such actions do not seem to be mediated via alpha- or beta-adrenoceptor of spinal vasculature.

Pial arteriolar vessel diameter and CO2 reactivity during prolonged hyperventilation in the rabbit

1988 ◽  
Vol 69 (6) ◽  
pp. 923-927 ◽  
Author(s):  
J. Paul Muizelaar ◽  
Henk G. van der Poel ◽  
Zhongchao Li ◽  
Hermes A. Kontos ◽  
Joseph E. Levasseur
Keyword(s):  
Cerebral Blood Volume ◽  
Vessel Diameter ◽  
Endotracheal Suctioning ◽  
Content Type ◽  
Cranial Window ◽  
Arterial Blood ◽  
Long Term Effect ◽  
Pial Arterioles ◽  
Injured Patients ◽  
Fine Print

✓ Hyperventilation reduces intracranial pressure (ICP) acutely through vasoconstriction, but its long-term effect on vessel diameter is unknown. In seven rabbits with a cranial window implanted 3 weeks earlier, the effect of prolonged hyperventilation on vessel diameter was studied. Anesthesia was maintained for 54 hours with a pentobarbital drip (1 mg/kg/hr). The pH, CO2, and HCO3− levels were measured in arterial blood and cisterna magna cerebrospinal fluid (CSF). The diameter of 31 pial arterioles was measured with an image splitter. After baseline measurements, pCO2 was reduced from 38 to 25 mm Hg and allowed to return to 38 mm Hg for 10 minutes every 4 hours. There was an initial vasoconstriction of 13%, which progressively diminished by 3% every 4 hours. Thus, by the 20th hour, vessel diameters at a pCO2 of 25 mm Hg had returned to slightly above baseline values obtained at a pCO2 of 38 mm Hg. The temporary return of pCO2 to 38 mm Hg every 4 hours caused vasodilation: 12% at 4 hours, gradually increasing to 16% at 52 hours. Thus, at 52 hours, the vessel diameters were 105% of baseline at a pCO2 of 25 mm Hg and increased to 122% at a pCO2 of 38 mm Hg. Arterial pH had returned to baseline at 20 hours, and CSF pH had returned at 24 hours. Bicarbonate in blood and CSF remained decreased throughout the experiments. In three control experiments during which normocapnia was maintained, vessel diameter and pH and bicarbonate levels remained unaltered over the same period. The CO2 reactivity, tested by brief periods of hyperventilation every 4 hours, also did not change. These results indicate that hyperventilation is effective in reducing cerebral blood volume for less than 24 hours and that it should be used only during actual ICP elevations. If used preventively, its effect may have worn off by the time ICP starts to rise for other reasons, and further decreases in pCO2 cannot be obtained. Moreover, the reduction in buffer capacity with lower bicarbonate renders the vessels more sensitive to changes in PaCO2. This could lead to more pronounced elevations in ICP during transient rises in PaCO2, such as during endotracheal suctioning in head-injured patients.

Magnesium is a cerebrovasodilator in newborn piglets

1997 ◽  
Vol 272 (1) ◽  
pp. H511-H516
Author(s):  
C. R. Kim ◽  
W. Oh ◽  
B. S. Stonestreet
Keyword(s):  
Parietal Cortex ◽  
Hydrolysis Product ◽  
Vessel Diameter ◽  
Magnesium Concentration ◽  
Cyclooxygenase Inhibition ◽  
Cranial Window ◽  
Newborn Piglets ◽  
Before And After ◽  
Pial Arterioles ◽  
Dose Dependent

We tested the hypothesis that, in newborn piglets, magnesium results in a dose-dependent prostanoid-mediated cerebrovasodilation. Pial arterioles (50-200 microns in diameter) were serially measured, and cortical subarachnoid cerebrospinal fluid (CSF) was collected for radioimmunoassay of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha, hydrolysis product of prostacyclin) and thromboxane B2 (TxB2, metabolite of thromboxane A2) before and after CSF containing 1.2, 2.4, 4.8, and 9.6 mM MgCl2 was suffused over the parietal cortex under a closed cranial window in twelve 2- to 4-day-old piglets. Magnesium suffusion resulted (P < 0.05) in a dose-dependent pial arteriolar vasodilation. The increase in vessel diameter was greater (P < 0.001) with 2.4, 4.8, and 9.6 mM than with 1.2 mM concentration of magnesium. The increase in vessel diameter with 9.6 mM was also greater (P < 0.001) than with the 2.4 mM concentration of magnesium. Magnesium suffusion did not result in changes in cortical CSF prostanoid concentrations. The effect of intravenous indomethacin (5 mg/kg) on cyclooxygenase inhibition in the pial arterioles was confirmed by a 24 +/- 3% decrease in vessel diameter at the baseline (1.2 mM) magnesium concentration. In contrast, cyclooxygenase inhibition with intravenous indomethacin did not attenuate the magnesium-induced cerebrovasodilation. We conclude that in new born piglets magnesium suffusion over the parietal cortex results in a dose-dependent cerebrovasodilation that is most likely not mediated by prostanoids.

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