Search PubMed⌕ Search

Biomedical subjects

G J Crystal

Publications and source records attributed to G J Crystal.

At least 73 records · Page 4Linked to original sources
PubMed1988

Myocardial blood flow and oxygen consumption during isovolemic hemodilution alone and in combination with adenosine-induced controlled hypotension.

Recent reports have proposed combining isovolemic hemodilution and controlled hypotension to limit blood loss during surgery. Before such a technique can be considered for clinical use, it must be demonstrated that it does not endanger maintenance of adequate myocardial oxygenation. Accordingly, measurements of left ventricular myocardial blood flow and oxygen consumption were obtained during isovolemic hemodilution alone and in combination with adenosine-induced controlled hypotension in ten pentobarbital-anesthetized, open chest dogs with normal coronary circulation. Hemodilution to a hematocrit of 21.7% was produced by isovolemic exchange of whole blood for 5% dextran. In the presence of hemodilution, adenosine was infused intravenously at a rate sufficient to decrease mean aortic pressure to 51 mm Hg. Myocardial blood flow was measured with radioactive microspheres and used to calculate global left ventricular myocardial oxygen consumption and oxygen supply. Hemodilution alone increased aortic blood flow (+43%) but had no effect on aortic pressure, left atrial pressure, heart rate, or left ventricular dP/dtmax; an increase in myocardial blood flow (+130%) maintained oxygen supply and consumption at the baseline level. Adenosine-induced hypotension during hemodilution decreased heart rate (-35%), left ventricular dP/dt max (-28%), and aortic blood flow (-14%). These systemic responses were accompanied by reduced myocardial oxygen consumption (-29%) and increased myocardial blood flow (+54%) and myocardial oxygen supply (+72%). These latter effects resulted in reduction in the coronary arteriovenous oxygen content difference and in an attendant rise in coronary sinus Po2 (+66%), which are signs of luxuriant myocardial perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1987

Validation of local venous sampling within the at risk left anterior descending artery vascular bed in the canine left ventricle.

The validity of using blood sampled from the anterior interventricular vein (AIV), anatomically located within the myocardium perfused by the left anterior descending (LAD) coronary artery, to represent venous drainage originating from the LAD vascular territory was studied in eight anaesthetised, open chest dogs. The LAD was cannulated and perfused from a blood reservoir isolated from the systemic circulation. To determine the presence of blood from non-LAD sources that appears in the AIV sample, 51Cr-labelled red blood cells were injected into the left atrium and distributed in the systemic circulation while the LAD was perfused by non-radioactive blood. The percentage spillover of red blood cells from non-LAD sources into the AIV drainage was determined under control, reduced LAD flow, ischaemia, and reperfusion conditions as 100 X (AIV chromium content/arterial chromium content). Spillover of red blood cells into AIV blood samples averaged only 1.5(1.3)% under control conditions and increased insignificantly to 8.6(3.5)% during reduced LAD flow. During ischaemia red blood cells in AIV blood increased insignificantly to 98.3(5.0)% but decreased to 1.9(1.3)% after reperfusion. Studies in five dogs with microspheres showed that a portion of this admixture from non-LAD sources originated from precapillary nutritional collateral or overlapping blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Effect of controlled ventilation on renal and splanchnic blood flows during severe arterial hypoxia.

The present study was undertaken to evaluate the extent that the lung inflation reflex attenuates vasoconstrictor responses in renal cortex and splanchnic beds during severe arterial hypoxia. Hypoxia was induced by inspiration of a 3-5% oxygen gas mixture in three groups of chloralose-anesthetized dogs: Group I, free breathing; Group II, controlled ventilation; Group III, free breathing with arterial PCO2 held constant. Regional vascular conductances (VC) were calculated from regional blood flows measured with 15-microns radioactive microspheres. In Group I, hypoxia caused marked hyperventilation, which was accompanied by no significant change in VC in renal cortex, and by reductions in VC in spleen (-36%), pancreas (-56%), and duodenum (-28%). In Group II, hypoxia caused reduction in VC in renal cortex (-70%), and reductions in VC in spleen, pancreas, and duodenum similar to those in Group I. In Group III, hypoxia again caused marked hyperventilation, but reductions in VC in renal cortex, spleen, pancreas, and duodenum were similar to those in Group II. Results indicate that during severe arterial hypoxia activation of lung inflation reflex does not attenuate or reverse vasoconstriction in renal cortex, spleen, pancreas, and duodenum.

Animals↗
PubMed1985

Effect of controlled ventilation on renal and splanchnic blood flows during nicotine.

The present study was undertaken to evaluate the influence of respiratory condition [free breathing (FB) vs. controlled ventilation (CV)] and of anesthetic [pentobarbital (PA) vs. chloralose (CA)] on nicotine-induced vasomotor responses in the renal cortex and splanchnic beds. Nicotine (36 micrograms . kg-1 . min-1 iv) was infused in four groups of dogs: group I, PA and CV; group II, PA and FB; group III, CA and CV; group IV, CA and FB. Regional vascular conductances (VC) were calculated from regional blood flows measured with 15-microns radioactive microspheres. In group I, VC fell in renal cortex (-22%) and pancreas (-52%), increased in liver (hepatic arterial bed +130%), and did not change significantly in duodenum and spleen. In group III, VC fell to a greater extent in renal cortex, pancreas, duodenum, and spleen than in group I; VC in hepatic arterial bed did not change. In FB dogs (groups II and IV), nicotine caused marked hyperventilation, but decreases in VC in renal cortex, pancreas, and duodenum were similar to those in CV dogs. Results indicate that during intravenous infusion of nicotine 1) hyperventilation does not attenuate or reverse vasoconstriction in renal cortex, pancreas, or duodenum under either PA or CA, although it does in spleen under CA; 2) vasodilator mechanisms predominate over vasoconstrictor mechanisms in the hepatic arterial bed; and 3) vasoconstrictor responses in renal cortex, pancreas, duodenum, spleen, and liver are more pronounced under CA than under PA.

Anesthesia, General↗
PubMed1984

Persistent coronary vasodilation during long-term, supramaximal doses of adenosine.

Active and reactive hyperemias have been observed in the skeletal muscle circulation tachyphylactic to exogenous adenosine following 3-h supramaximal doses of the vasodilator. These findings failed to support a need for adenosine in metabolic control of skeletal muscle blood flow. The present study was conducted to determine if the coronary circulation also develops tachyphylaxis to adenosine while remaining sensitive to other metabolically linked vasodilator mechanisms. Experiments were conducted in eight pentobarbital-anesthetized, open-chest dogs whose blood flow in the left anterior descending coronary artery (LAD) was measured electromagnetically during 3-h infusion of adenosine into the LAD. Measurements of regional myocardial blood flow (radioactive microspheres), myocardial O2 consumption (Fick principle), and percent segment shortening (ultrasonic crystals) were also obtained. Adenosine was infused into the LAD at a rate of 27.0-72.0 mumol/min, depending on blood flow rate. Calculated concentration of adenosine in LAD blood averaged 0.484 +/- 0.111 mumol/ml, which was well in excess of that required for maximal coronary vasodilation. LAD blood flow averaged 21.5 +/- 2.2 ml/min during the preadenosine control condition. LAD blood flow after 3 h adenosine (123.3 +/- 23.0 ml/min) was not significantly different from that after 1-3 min adenosine (105.8 +/- 17.9 ml/min). There was no significant transmural variation in LAD blood flow during adenosine infusion. Adenosine had no significant effect on myocardial O2 consumption or percent segment shortening. Our results demonstrate persistent transmural vasodilation in the canine coronary circulation during long-term, supramaximal doses of adenosine and are consistent with a role for endogenous adenosine in maintenance of coronary vasodilation during sustained elevations in myocardial energy demands.

Adenosine↗
PubMed1983

Asynchronous transmural perfusion during coronary reactive hyperaemia.

Dynamic variation in the transmural distribution of myocardial blood flow was studied in 36 anaesthetised open-chest dogs during the course of the reactive hyperaemia following a 90 s occlusion of the left anterior descending coronary artery. Myocardial blood flow was estimated from tissue uptake of radioactive microspheres, 9 to 10 micrometers in diameter. Endo/epi flow ratios indicated asynchronous reactive hyperaemic responses across the free wall of the left ventricle; flow was preferentially to subepicardium during the initial (pre-peak) phase, whereas flow was preferentially to subendocardium during the prolonged recovery phase. The mean of endo/epi flow ratios obtained during the peak plateau of coronary artery reactive hyperaemia indicated essentially uniform transmural distribution. However, further analysis indicated that this was result of ratios less than 1 early in the peak plateau and ratios greater than 1 late in the peak plateau. Reversal of the endo/epi flow ratios due to regionally asynchronous maximum flows is responsible for the prolonged plateau at peak flow observed in measurements of coronary artery reactive hyperaemia. Transmural asynchrony of peak reactive hyperaemic flow may also account for underestimates in vasodilator capability of ischaemia based on measurements of either coronary artery or myocardial blood flow.

Animals↗
PubMed1982

Nonischemic myocardial hypoxia: coronary dilation without increased tissue adenosine.

Experiments were performed in 23 open-chest, anesthetized dogs to evaluate 1) the extent of coronary vasodilation during nonischemic hypoxia and 2) whether this dilation is associated with changes in cardiac concentrations of adenosine, inosine, and hypoxanthine. Three minutes of nonischemic myocardial hypoxia caused by selective perfusion of the left anterior descending coronary artery (LAD) with hypoxic blood (PO2 = 11.7 Torr) increased coronary flow 623%, an increase that was not significantly different from that at the peak hyperemic response following 3 min of ischemic hypoxia secondary to LAD occlusion (+534%). Concentrations for adenosine and inosine (nmol/g) in myocardium sampled during nonischemic hypoxia [0.8 +/- 0.2 (SE) and 0.8 +/- 0.2, respectively] were significantly less than values during control conditions (1.7 +/- 0.3 and 1.4 +/- 0.2). Hypoxanthine concentrations did not differ for nonischemic hypoxia and control conditions. During ischemic hypoxia concentrations for adenosine (31.2 +/- 4.9), inosine (91.0 +/- 13.6), and hypoxanthine (44.0 +/- 15.3) were considerably greater than values during nonischemic hypoxia and during control conditions. The results indicate that nonischemic hypoxia induced pronounced coronary vasodilation similar to that during ischemic hypoxia, with reduced rather than with increased tissue concentrations of adenosine and inosine. These findings suggest that reduced myocardial oxygen tension may cause dilation of coronary resistance vessels by a direct relaxant effect on arteriolar vascular smooth muscle.

Adenosine↗
PubMed1982

Regional renal and splanchnic blood flows during nicotine infusion: effects of alpha and of combined alpha and beta adrenergic blockade.

Renal (cortex and medulla) and splanchnic (duodenum, liver, pancreas and spleen) blood flows were measured with 25-mu radioactive microspheres in anesthetized, open-chest dogs. The effects of nicotine (36 micrograms/kg/min i.v.) before and after selective alpha adrenergic blockade (phenoxybenzamine, 1 mg/kg i.v.) and before and after combined alpha and beta adrenergic blockade (phenoxybenzamine, 1 mg/kg i.v. and propranolol, 1 mg/kg i.v.) were evaluated. Before adrenergic blockade, nicotine increased arterial pressure (+82%) but had heterogeneous directional effects on regional blood flows: pancreas (-64%), duodenum (-33%), kidney cortex (-31%), kidney medulla (-17%), liver (+5%) and spleen (+71%). Vascular conductance was reduced in kidney cortex (-61%), kidney medulla (-57%), duodenum (-59%), liver (-46%) and pancreas (-79%) and was not altered in spleen. Selective alpha adrenergic blockade prevented the hypertensive response to nicotine, but heterogeneous changes in regional flows persisted: pancreas (-40%), spleen (-40%), kidney medulla (-35%), kidney cortex (-31%), liver (+50%) and duodenum (+74%). After combined alpha and beta adrenergic blockade, nicotine increased systemic arterial pressure (+75%) and decreased vascular conductance in all tissues. Results indicate: 1) a heterogeneous influence of nicotine in renal and splanchnic circulations associated with regional differences in activities of alpha and beta adrenergic receptors and 2) a potent nonadrenergic vasoconstrictor response in these circulations to nicotine after blockade of alpha and beta adrenergic receptors.

Adrenergic alpha-Antagonists↗
PubMed1981

Evaluation of noncoronary sources of left ventricular perfusion to intercoronary collateral-dependent myocardium due to chronic major vessel occlusion: absent contribution of luminal and extracardiac channels.

Liminal contribution to perfusion of collateral-dependent left ventricular (LV) myocardium was evaluated in six dogs. A portion of LV free wall was rendered collateral-dependent by gradual occlusion of left circumflex artery with Ameroid constrictor. Eight to 10 weeks after implantation of constrictor, measurements of LV myocardial flow were made by left atrial injections of 9-10 micro radioactive microspheres. To measure total collateral flow, microspheres were injected under control conditions, and to measure luminal contribution to collateral flow, microspheres were injected after ligation of right coronary artery during extracorporeal perfusion of left common coronary artery (LCCA) with microsphere-free arterial blood, and during stoppage of flow through LCCA. Under control conditions, myocardial blood flow in collateral-dependent region, 1.01 +/- 0.31 ml/min/gm, was not significantly different from that in normal region, 1.06 +/- 0.32 ml/min/gm. Flow from luminal collateral vessels was negligible (less than 0.005 ml/min/gm) in both collateral-dependent and normal myocardium, and was not affected by stoppage of flow through LCCA. These results indicate that luminal collateral vessels, as well as collateral vessels originating from other noncoronary sources, do not contribute significantly to perfusion of normal or collateral-dependent LV myocardium.

Animals↗
PubMed1981

Small vessel and total coronary blood volume during intracoronary adenosine.

The effect of a maximally dilating dose of intracoronary adenosine on total (CBV) and small-vessel blood volume (MSVBV, an index of open-capillary density), hematocrit (MSVHct), and related parameters of O2 supply-demand ratio was examined in left ventricular myocardium of anesthetized open-chest dogs. CBV was measured from washout of 51Cr-labeled red blood cells (RBC) and MSVBV and MSVHct from contents of 51Cr-RBC and plasma label, either 131I-serum albumin or 59Fe-siderophilin, in samples of myocardium and blood. Coronary blood flow (CBF) was measured by electromagnetic flowmeter. Myocardial oxygen consumption (MVO2) was computed with the Fick equation. Myocardial oxygen tension (MPO2) was measured with bare-tipped platinum electrodes. Adenosine raised CBV 75%, CBF, 574%, and MPO2 122%, but did not affect significantly MSVBV, MSVHct, or MVO2. These results indicate that infusion of adenosine into a coronary artery perfused at constant pressure causes relaxation of smooth muscle of arteriolar resistance vessels and of other vessels larger than 100 micrometers diam, but not that of the precapillary sphincters. This may be explained by the opposing action of increased MPO2 on the sphincters when flow increases. MSVHct was consistently much less than large-vessel Hct. This warrants combined use of red blood cell and plasma labels for accurate measurements of MSVBV.

Adenosine↗
PubMed1979

Shunting of microspheres across the canine coronary circulation.

Coronary shunting of 9 +/-1 micrometer and 25 +/- 5 micrometer radiolabeled microspheres was examined in anesthetized, open-chest dogs, whose left common coronary arteries were perfused at controlled pressures. Shunting was estimated from the difference in radioactivity between perfusion line and coronary sinus blood samples during selective elevations of coronary perfusion pressure (CPP), left ventricular afterload, and inspired oxygen. A linear relationship was found between coronary shunting of 9-micrometer microspheres and CPP over the range 100-200 mmHg. According to regression analysis, percent shunt flow was 4.0% at control CPP (100 mmHg) and 10.0% at CPP of 200 mmHg. No shunting of 25-micrometer microspheres occurred at any CPP. Raising afterload did not affect shunting at control CPP but attenuated the increase in shunting at elevated CPP. Changing inspired gas from room air to 100% oxygen did not influence shunting at control or elevated CPP. Raising CPP to 150 and 200 mmHg also released 2.5% and 5.9% of pretrapped 9-micrometer microspheres, respectively. This study demonstrates that vessels permitting passage of microspheres across coronary circulation are sensitive to elevated perfusion pressure.

Animals↗
PubMedDate not supplied

Myocardial oxygen consumption and blood flow during nicotine infusion: effect of combined alpha- and beta-adrenergic blockade.

The effect of combined alpha- and beta-adrenergic blockade with phenoxybenzamine and propranolol, respectively, on changes in left ventricular myocardial oxygen consumption and blood flow during nicotine administrations (36 micrograms/kg/min, i.v.) was evaluated in anesthetized, open-chest dogs. Myocardial blood flow was estimated by injection of 8 to 10 micrometers diameter radioactive microspheres into the left atrium, and myocardial oxygen consumption was computed from the Fick principle. Before adrenergic blockade, nicotine caused a market (+151%) elevation in myocardial oxygen consumption and a parallel increase in myocardial blood flow. The increase in myocardial blood flow was uniform transmurally. These cardiac changes were accompanied by elevations in systemic arterial and left atrial pressures, peripheral vascular resistance, and heart rate, but by no change in aortic flow or in myocardial contractility. After adrenergic blockade, nicotine caused somewhat lesser, though still marked, elevations in myocardial oxygen consumption (+60%) and blood flow (+43%). Again, myocardial blood flow increases were uniform transmurally. Also, nicotine-induced increases in systemic arterial and left atrial pressure and in peripheral vascular resistance persisted after adrenergic blockade, whereas heart rate remained constant and aortic flow and myocardial contractility declined. The results indicate that nonadrenergic mechanisms contribute significantly to the increase in myocardial oxygen demand during nicotine infusion.

Animals↗
PubMedDate not supplied

Regional myocardial blood flow during nicotine infusion after chronic coronary artery occlusion: effect of beta-adrenergic blockade.

In eight dogs a portion of the left ventricular free wall (LVFW) was rendered collateral-dependent (CD) by gradual occlusion of the left anterior descending coronary artery with a surgically implanted Ameroid constrictor. Six to 8 weeks later, the dogs were anesthetized and regional myocardial blood flow was measured with 7-10-micron radioactive microspheres during (a) control conditions, (b) nicotine alone (24 micrograms/kg/min i.v.), and (c) nicotine (24 micrograms/kg/min i.v.) after beta-adrenergic blockade with propranolol. During control conditions, mean transmural flow was similar in CD, border, and normal regions of the LVFW. Nicotine alone increased flow in all regions of the LVFW, with normal (+ 104%) greater than CD (+ 56%). These changes in flow were accompanied by increases in mean arterial pressure (+ 34%) and mean aortic flow (+ 54%). Nicotine after beta-adrenergic blockade appreciably raised mean arterial pressure (+ 83%) and mean left atrial pressure (+ 307%), but caused no increase in flow to any region of the LVFW. The results indicate (a) that the nicotine-induced increase in flow is blunted in a CD region, and that (b) beta-adrenergic blockade unmasks coronary vasoconstrictor mechanisms during nicotine infusion which prevent increases in flow to either normal or CD regions despite increased perfusion pressure and augmented myocardial oxygen demands.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Pressure-induced changes in coronary flow and volume during reperfusion in canine hearts.

1. The effects of coronary artery occlusion and reperfusion on pressure-induced changes in coronary blood flow and blood volume were investigated. 2. The left anterior descending coronary artery (LAD) of canine hearts was cannulated and perfused independently with arterial blood by a controlled pressure system. LAD flow was measured continuously with an electromagnetic flowmeter and LAD volume was measured in the steady-state by indicator dilution. Measurements were made with perfusion pressure at 100 mmHg (control), 50 mmHg, and 150 mmHg before and after 2 h of LAD occlusion followed by 2 h of reperfusion. 3. With perfusion pressure at control, occlusion-reperfusion reduced LAD flow 19%, but had no significant effect on LAD volume. 4. Steady-state LAD flow and volume always varied directly with changes in perfusion pressure; after occlusion-reperfusion these variations were accentuated. 5. Analysis of transient and steady-state flow responses indicated diminished capability of arteriolar resistance vessels for active, autoregulatory adjustments in lumenal calibre following changes in perfusion pressure. 6. The results of this study demonstrate that occlusion-reperfusion causes derangement to pressure-volume and pressure-flow control mechanisms in the coronary circulation.

Animals↗