Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral autoregulation is impaired in ischaemic regions. We hypothesized that pre-existing STA-MCA bypass would be superior to delayed revascularization in maintaining ipsilateral rCBF and preserving cerebral autoregulation following experimental stroke. Two series of dogs were tested to evaluate this hypothesis, but which was disproved for the chosen experimental conditions. In the first, eight dogs underwent craniotomy, STA-MCA bypass, and radiolabeled microsphere rCBF determinations. Blood pressure was manipulated with intravenous adenosine and levarterenol. Ischaemic zone rCBF was measured at MAP 60 mm Hg (97.2 ml.min-1.100 g-1) and MAP 140 mm Hg (113.6) (p = NS), in the intact arterial system with the patent bypass in place. An hemispheric ipsilateral ischaemic lesion was then created, and three further microsphere rCBF determinations were made at MAP 60 mm Hg (41.7 ml.min-1.100 g-1), MAP 100 mm Hg (52.6) and MAP 140 mm Hg (58.3). There were no significant differences between these measurements (ANOVA p = NS). In a second series of five animals the bypass was placed and the stroke lesion created first. Ischaemic zone rCBF was then measured at MAP 60 mm Hg (35 ml.min-1 . 100 g-1) and MAP 140 mm Hg (44 ml.min-1 . 100g-1) (p = NS), with the patent bypass in place. The bypass was then clamped for 15 minutes and profound ischaemia confirmed (5 ml.min-1 . 100 g-1, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral autoregulation following prophylactic and delayed experimental STA-MCA bypass. 260 72

Interactive effects between exogenous dopamine (DA) and isoflurane (I) combined with thoracic epidural blockade (TEA) were studied in dogs during chloralose anesthesia. The I-TEA intervention per se decreased heart rate (HR; 28%), mean arterial pressure (MAP; 63%), cardiac output (CO; 54%), left ventricular dP/dt (LVdP/dt; 75%) and LVdP/dt/systolic arterial pressure (SAP; 42%). Prior to the I-TEA intervention, dopamine increased MAP, CO, LVdP/dt, LVdP/dt/SAP and stroke volume (SV) already at the dose 10 micrograms.kg-1.min-1 and, additionally, increased mean pulmonary artery pressure (MPAP) at the dose 20 micrograms.kg-1.min-1. During the I-TEA intervention, the DA-induced increases in MAP and systemic vascular resistance (SVR) were significantly higher than prior to I-TEA, as indicated by significant ANOVA interactive effects. At the dose 10 micrograms.kg-1.min-1, DA restored MAP, CO, LVdP/dt, LVdP/dt/SAP and SV to levels found before the I-TEA intervention, while HR was restored first at the dose 20 micrograms.kg-1.min-1. At the dose 20 micrograms.kg-1.min-1, DA also increased MAP (39%), LVdP/dt (119%), LVdP/dt/SAP (73%), SVR (28%) and MPAP (70%) above levels prior to I-TEA. To conclude, exogenous dopamine effectively and dose-dependently counters cardiovascular depression induced by the anesthetic technique of combining I and TEA. The pressor and systemic vasoconstrictor actions of dopamine are potentiated by conjoint administration of I and TEA.
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PMID:Cardiovascular depression by isoflurane and concomitant thoracic epidural anesthesia is reversed by dopamine. 817 48

Animal studies have indicated that increased nitric oxide (NO) synthesis plays a significant role in the renal adaptation to increased sodium intake. To investigate the role of NO during increased sodium intake in humans, we studied the effect of acute, systemic injection of NG-monomethyl-L-arginine (L-NMMA) on renal hemodynamics [glomerular filtration rate and renal plasma flow (GFR and RPF, respectively)], urinary sodium excretion (FENa), systemic hemodynamics [mean arterial blood pressure and heart rate (MAP and HR)], and plasma levels of several vasoactive hormones in 12 healthy subjects during high (250 mmol/day) and low (77 mmol/day) sodium intake in a crossover design. The sodium diets were administered for 5 days before the L-NMMA treatments, in randomized order, with a washout period of 9 days between each diet and L-NMMA treatment. GFR and RPF were measured using the renal clearance of 51Cr-labeled EDTA and 125I-labeled hippuran by the constant infusion technique in clearance periods of 30-min duration. Two baseline periods were obtained, after which L-NMMA was given (3 mg/kg over 10 min), and the effect of treatment was followed over the next five clearance periods. During high sodium intake, L-NMMA induced a more pronounced relative decrease in RPF (P = 0.0417, ANOVA), a more pronounced relative decrease in FENa (P = 0.0032, ANOVA), and a more pronounced relative increase in MAP (P = 0.0231, ANOVA). During low sodium intake, the effect of L-NMMA on FENa was abolished. During low sodium intake, L-NMMA induced a sustained drop in plasma renin (31 +/- 5 vs. 25 +/- 5 microU/ml, P < 0.001), which was not seen during high sodium intake. The data indicate that increased production of NO is an important part of the adaptation to increased dietary sodium intake in healthy humans, with respect to renal hemodynamics, sodium excretion, and the secretion of renin.
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PMID:Dietary sodium affects systemic and renal hemodynamic response to NO inhibition in healthy humans. 961 29

The objective of this paper was to evaluate romifidine as a premedicant in dogs prior to propofol-halothane-N2O anesthesia, and to compare it with the other alpha2-agonists (medetomidine and xylazine). For this, ten healthy dogs were anesthetized. Each dog received 3 preanesthetic protocols: atropine (10 microg/kg BW, IM), and as a sedative, romifidine (ROM; 40 microg/kg BW, IM), xylazine (XYL; 1 microg/kg, IM), or medetomidine (MED; 20 microg/kg BW, IM). Induction of anesthesia was delivered with propofol 15 min later and maintained with halothane and N2O for one hour in all cases. The following variables were registered before preanesthesia, 10 min after the administration of preanesthesia, and at 5-minute intervals during maintenance: PR, RR, rectal temperature (RT), MAP, SAP, and DAP. During maintenance, arterial oxygen saturation (SpO2), end-tidal CO2 (EtCO2) and percentage of halothane necessary for maintaining anesthesia (%HAL) were also recorded. Induction dose of propofol (DOSE), time to extubation (TE), time to sternal recumbency (TSR) and time to standing (TS) were also registered. The statistical analysis was carried out during the anesthetic period. ANOVA for repeat measures revealed no differences between the 3 groups for PR and RR; however, MAP, SAP and DAP were higher in the MED group; SpO2 was lower in MED and EtCO2 was lower in ROM; %HAL was higher in XYL. No statistical differences were observed in DOSE, TE, TSR or TS. Percentage of halothane was lower in romifidine and medetomidine than in xylazine premedicated dogs also anesthetized with propofol. All the cardiorespiratory variables measured were within normal limits. The studied combination of romifidine, atropine, propofol, halothane and N2O appears to be a safe and effective drug combination for inducing and maintaining general anesthesia in healthy dogs.
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PMID:Romifidine, medetomidine or xylazine before propofol-halothane-N2O anesthesia in dogs. 991 31

We compared intracranial pressure (ICP) and cerebral blood flow (CBF) in dogs after inflating a subdural intracranial balloon to increase ICP to 20 mm Hg, inducing hemorrhagic shock (mean arterial pressure [MAP] of 55 mm Hg), and infusing a single bolus of fluid consisting of either 54 mL/kg of 0.8% saline (SAL), 6 mL/kg of 7.2% hypertonic saline (HS), 20% hydroxyethyl starch (HES) in 0.8% SAL, or a combination fluid (HS/HES) containing 20% HES in 7.2% saline. Twenty-six dogs were ventilated with 0.5% halothane in N2O and O2 (60:40 ratio). As ICP was maintained at 20 mm Hg, rapid hemorrhage reduced MAP to 55 mm Hg (time interval of zero [T0]) which was maintained at that level for 30 minutes (until T30). Subsequently, over a 5-minute interval (T30-T35), one of the four randomly assigned resuscitation fluids was infused. Data were collected at baseline; after subdural balloon inflation; at T0, T30, T35, and 30-minute intervals thereafter for 2 hours (T65, T95, T125, and T155). CBF and ICP were compared using repeat-measure ANOVA. Cerebral blood flow was greater at T35 in the HS and HS/HES groups than in the HES group (P = .025). In the SAL group, ICP increased significantly from T0 to T35, remaining unchanged thereafter. At T35, ICP in the HS group was significantly lower than in the SAL group (P < .05) but subsequently increased. ICP in the HS/HES group exceeded that in all other groups at T95 and T125 (P < .05). After a severe reduction in cerebral perfusion pressure (CPP), HS solutions (both HS and HS/HES) were associated with a delayed rise in ICP and did not improve global forebrain CBF in comparison with conventional saline solutions.
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PMID:Rebound intracranial hypertension in dogs after resuscitation with hypertonic solutions from hemorrhagic shock accompanied by an intracranial mass lesion. 1021 37

Six horses were randomly assigned to receive either frusemide (F) (0.5 mg/kg i.v.) or an equivalent volume of saline (S) i.v., 4 h prior to treadmill exercise. Horses were instrumented to enable measurement of heart rate (HR), systolic (SAP), mean (MAP), and diastolic (DAP) carotid arterial pressures, pulmonary artery pressure (PAP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), blood gases, and cardiac output (CO). Plasma (PV) and blood volumes (BV) were measured using 2 injections of Evan's Blue dye. Baseline parameters were recorded while the horse stood quietly. Horses were then administered F or S. Four hours later, they were warmed up for 3 min at 4 m/s and then exercised to the point of fatigue at 115% VO2max. Horses were anaesthetised immediately following exercise by administration of detomidine (0.04 mg/kg bwt i.v.) followed 5 min later by tiletamine-zolazepam (1.25 mg/kg bwt i.v.). After transporting the horse to a recovery stall, anaesthesia was maintained with isoflurane in 100% O2. Data were analysed using a 2-way ANOVA with repeated measures with post hoc differences identified using the Student-Newman-Keul's procedure. Exercise was associated with increases in HR, SAP, MAP, DAP, PAP, CVP, TEMP, PCV, and BV, and decreases in PV, pH, arterial bicarbonate and base excess. Anaesthesia was associated with marked hypercapnia, a decrease in HR following detomidine administration, and persistent pulmonary hypertension despite carotid arterial pressure which returned to baseline. No effects attributable to F were identified at any time during the study.
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PMID:Effects of pre-exercise frusemide administration and post exercise anaesthesia on cardiopulmonary and acid-base parameters and blood and plasma volumes in horses exercised supramaximally to fatigue. 1065 46

Laboratory studies of uncontrolled hemorrhage demonstrate that under resuscitation (UR) improves short-term survival, but at the expense of tissue perfusion. The long-term effects of UR have not been studied. The purpose of this study was to evaluate survival and the incidence of end-organ injury (EOI), 3 days following moderate and severe UR of uncontrolled hemorrhage. Thirty-four swine (14-24 kg) were assigned to 4 groups: Groups I, II, and III were hemorrhaged to a pulse pressure = 5 mmHg in the presence of a 4-mm aortic tear: Group I (control; n = 6) was not resuscitated; Group II (n = 11) was severely under resuscitated (MAP [mean arterial pressure] = 40 mmHg) for 75 min; Group III (n = 9) was moderately under resuscitated (MAP = 60 mmHg) for 75 min. After 75 min, the aortotomy was repaired, and animals were resuscitated to baseline physiologic parameters. Group IV (sham; n = 8) was instrumented, but not hemorrhaged. Seventy-two-hour mortality was 100%, 36%, 22%, and 0% for Groups I through IV (P = .001 Fisher's exact). Cardiac indices, serum bicarbonate, and systemic oxygen delivery were significantly lower in Group II as compared to Group III during the 75 min of UR (P < 0.05; repeated measures ANOVA). By 72 h, physiologic parameters in surviving animals had returned to baseline levels. Measures of kidney, liver, neurologic, and pulmonary function did not change from baseline. There was no histologic evidence of EOI. In this model, 75 min of UR did not result in EOI. There was a trend toward greater survival, and tissue perfusion was better preserved with moderate as compared to severe UR.
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PMID:Under-resuscitation of near-lethal uncontrolled hemorrhage: effects on mortality and end-organ function at 72 hours. 1119 52

The renin-angiotensin (RAS) and the alpha1 sympathetic nervous system (SNS) interact at different levels in cardiovascular regulation. Concurrent use of angiotensin-converting enzyme (ACE) inhibitors and alpha1 receptor antagonists result in a synergistic antihypertensive action and is of wide utility in cardiovascular therapy. We examined the impact of concurrent inhibition of RAS (captopril or losartan) and the SNS (prazosin) before and after acute nitric oxide (NO) synthase inhibition with L-nitro-L-arginine methyl ester (L-NAME) on renal cortical perfusion (RCF) and blood pressure (MAP) in healthy and acute ischemic renal failure (ARF) rats (n = 6). Captopril or losartan reduced MAP and increased RCF more in healthy (p < 0.001) and ARF rats (p < 0.02). Prazosin alone reduced both MAP and RCF (p < 0.001). The combination of prazosin with captopril or losartan caused an additive fall in MAP, and mitigated the fall in RCF. Captopril + prazosin caused a profound fall in RCF following L-NAME, in healthy but not ARF rats (p < 0.001). Acetylcholine (Ach), a vasodilator which stimulates endogenous NO production caused a profound paradoxical fall in RCF in ARF, but not in healthy rats (p < 0.001 ANOVA). These results indicate a significant interaction between angiotensin II and phenylephrine in renal vasomotion. It establishes that endogenous NO homeostatically opposes angiotensin II-alpha1-mediated renal vasoconstriction, and that the vasodilator role of NO is diminished in ARF. The paradoxical fall in RCF induced by Ach in ARF is speculated to result, at least in part, from the formation of peroxynitrite (ONOO-), which acts as a renal vasoconstrictor, following the combination of ischemia-generated super oxide anion (O-2), with endothelial NO released by Ach.
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PMID:Interactions of the renin-angiotensin system and alpha-1 adrenoceptors on renal hemodynamics in healthy and acute renal failure rats: the role of nitric oxide. 1180 63

Intraoperative radio frequency interstitial thermal ablation (RITA) may result in a reduction of the functional hepatic reserve. To assess this further, we evaluated perioperative lactate levels as a measure of hepatic dysfunction. Sixteen patients scheduled for open RITA (O-RITA) were enrolled in the study. Arterial lactate levels (mmol/L) were measured prior to tumor needle insertion (T0), after O-RITA completion (T1), after wound closure (T2) and 24 hrs after surgery (T3). Correlation between hemodynamic parameters including MAP, and CVP, at T0, T1, T2, T3 and the perioperative rate of lactate production were also analyzed. Total bilirubin, transaminases and international normalized ratio for prothrombin activity (INR) were measured preoperatively and postoperative at day 1, 2, 3 and 7. Data are expressed as mean +/- SD and analyzed with ANOVA. Additionally, the Duncan post hoc test was used for multiple comparisons of the differences in mean values. A p-value <0.05 was considered significant. Lactate levels did not increase significantly at time points specified above (P = NS). Similarly, hemodynamic parameters analyzed did not show any significant change at the different time points (P = NS). Total bilirubin and INR did not demonstrate statistically significant changes at the aforementioned time points. Serum transaminases peaked during the immediate postoperative period and normalized to preoperative values by one-week post surgery. These results demonstrate that O-RITA does not induce hyperlactatemia and does not reduce the functional residual liver parenchyma.
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PMID:Lactate levels in open interstitial thermal ablation for liver tumors. 1214 73

We examined the hypothesis that gender differences exist in platelet and vascular reactivity in type-2 diabetes mellitus, using Zucker fatty diabetic rats of both sexes and their lean littermates. Type-2 diabetes is characterized by excessive platelet production of TXA(2), which is thrombogenic. Testosterone up-regulates platelet TXA(2) receptors and the aggregation response to thromboxane mimetics. Conversely, estrogen increases vascular nitric oxide (NO) production and inhibits platelet aggregation. Hemodynamic studies were undertaken with the determination of dose-response curve for MAP and renal cortical blood flow (RCF) in response to U46619, angiotensin-II, phenylephrine and endothelin-1, as well as the systemic hemodynamic response to acetylcholine and L-NG nitro-arginine methylester (L-NAME). Platelet aggregation response was evaluated using whole blood impedance aggregometry. There were significant gender differences in the systemic blood pressure and RCF response to TXA(2)-mimetic U46619 and angiotensin-II (P<0.02, ANOVA) but not to phenylephrine or endothelin-1. Male rats exhibited a paradoxical hypotensive response to U46619 (-18+/-11 mmHg) compared with a peak pressor response of +6+/-1 mmHg in female rats (P<0.01, ANOVA). The male rats exhibited an attenuated systemic vasodilator response (P<0.001, ANOVA) to acetylcholine (fall in MAP in male diabetic rats being -24+/-8 mmHg, compared with a fall of -50+/-8 mmHg in females), but a greater rise in the renal cortical resistance in response to NO inhibition by L-NAME (P<0.03) compared with the female rats. Both the slope (46+/-2) and the peak magnitude of the U46619-induced whole blood platelet aggregation (13+/-1) ohms were significantly higher (P<0.01, ANOVA) in male (n=10) compared with female diabetic rats (n=8) (29+/-0.8 slope, 10.0+/-0.8 ohms, respectively). Thus, the male diabetic Zucker rats exhibited an impaired response to vasoconstrictors (U46619 and angiotensin-II) and to endothelial (NO)-mediated vasodilation. The male gender may therefore be associated with the greater prothrombotic activity and a worse impairment of endothelial reactivity in the type-2 diabetic state.
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PMID:Gender difference in vascular and platelet reactivity to thromboxane A(2)-mimetic U46619 and to endothelial dependent vasodilation in Zucker fatty (hypertensive, hyperinsulinemic) diabetic rats. 1248 37


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