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Biomedical subjects

J W Kiel

Publications and source records attributed to J W Kiel.

At least 19 recordsLinked to original sources
PubMed2005

Effects of a topical alpha2 adrenergic agonist on ciliary blood flow and aqueous production in rabbits.

The relationship between ciliary perfusion and aqueous production is poorly understood. It was recently reported that aqueous production decreases when ciliary blood flow is reduced by lowering the ocular perfusion pressure, and hypothesized that drug-induced reduction of ciliary blood flow would also decrease aqueous production. In the present study, we test this hypothesis with an alpha2 adrenergic agonist (brimonidine) formulated for topical application. When used acutely, brimonidine decreases intraocular pressure (IOP) by suppressing aqueous production, although its mechanism of action is unclear. The experiments were performed in four groups of anesthetized rabbits (n=33) in which the following variables were measured: ocular mean arterial pressure (OMAP), IOP, orbital venous pressure (OVP), aqueous flow, ciliary blood flow, ciliary oxygen tension (PO2), episcleral venous pressure (EVP), carotid blood flow and heart rate. The measurements were made before and after brimonidine (0.15%, 40 microl) was applied to the cornea. Brimonidine decreased IOP (-33%, p<0.01), aqueous flow (-39%, p<0.01), ciliary blood flow (-37%, p<0.01), EVP (-42%, p<0.01) and ciliary PO2 (-32%, p<0.05). We conclude that topical brimonidine is a ciliary vasoconstrictor, and that alpha2 adrenergic agonist-induced decreases in ciliary blood flow decrease aqueous production.

Administration, Topical↗
PubMed2001

Effects of nitric oxide synthase inhibition on ciliary blood flow, aqueous production and intraocular pressure.

A prior study found that inhibition of nitric oxide synthase with L-NAME causes a large, rapid decrease in IOP in anesthetized rabbits. In this follow-up study we sought to determine if this hypotensive effect was due to decreased aqueous production, possibly caused by ciliary vasoconstriction. Two protocols were performed in anesthetized rabbits. In the first protocol, mean arterial pressure (MAP) and IOP were measured by direct cannulation, and aqueous flow was measured by fluorophotometry, before and after L-NAME (5 mg kg(-1), i.v., n = 7). In the second protocol, ciliary blood flow was measured transclerally by laser Doppler flowmetry while MAP was varied mechanically over a wide range before and after L-NAME (5 mg kg(-1), i.v., n = 8). L-NAME caused a significant increase in MAP and decreases in IOP, ciliary blood flow and aqueous flow. L-NAME also caused a significant downward shift in the ciliary pressure-flow relation over the entire pressure range examined. The results indicate that L-NAME causes ciliary vasoconstriction and decreases aqueous production, suggesting that the L-NAME ocular hypotensive effect may be due in part to a blood flow-dependent decrease in aqueous production. However, assuming no uveoscleral outflow and constant episcleral venous pressure and outflow facility, the decrease in aqueous flow accounts for 66% of the drop in IOP, suggesting an additional effect of L-NAME on aqueous outflow.

Animals↗
PubMed2000

Endothelin modulation of choroidal blood flow in the rabbit.

Based on the previous finding that locally produced nitric oxide (NO) and endothelin (ET) exert competing effects on choroidal resistance vessels, the present study sought to further characterize the pharmacology of ET in the choroid. The specific goal was to quantify the choroidal blood flow responses to acute changes in perfusion pressure before and after administering endothelin 1 (ET1), a non-selective ET antagonist, and selective antagonists for the endothelin A (ETA) and endothelin B (ETB) receptor subtypes. Anesthetized rabbits were instrumented with an ear artery cannula to measure mean arterial pressure (MAP), occluders on the aorta and vena cava to control MAP, and a vitreous cannula to measure intraocular pressure (IOP). Choroidal blood flow was measured by laser Doppler flowmetry with a vitreous fiber optic probe. The protocol entailed changing the ocular perfusion pressure by varying MAP before and after ET1 (0.9 microg kg(-1), i.v., n = 14), non-selective ET blockade (A-182086, 3 mg kg(-1), i.v., n = 10), selective ETA blockade (FR-139317, 3 mg kg(-1), i.v., n = 12), and selective ETB blockade (A-192621, 3 mg kg(-1), i.v., n = 14). ET1 and ETB blockade shifted the choroidal pressure-flow relation downward, while the non-selective antagonist and the selective ETA antagonist had no effect. The choroid had a biphasic response to exogenous ET1 as seen in other tissues (i.e. initial brief dilation followed by prolonged constriction) that was blocked by the non-selective antagonist whereas the ETA antagonist enhanced the dilation and blocked the constriction, and the ETB antagonist blocked the dilation and enhanced the constriction. These results indicate that ETA and ETB receptors are present and mediate opposing effects on choroidal vascular resistance. The results also suggest that endogenous ET preferentially elicits ETB vasodilation, most likely by stimulating endothelial nitric oxide release.

Animals↗
PubMed2000

Effects of latanoprost and timolol-XE on hydrodynamics in the normal eye.

PURPOSE: To compare the effects of latanoprost and timolol-XE on ocular pressure and perfusion in healthy adults, with respect to episcleral venous pressure. METHODS: A double-masked, placebo-controlled crossover study of weeklong bedtime treatment with one drop of drug, with placebo contralaterally, followed by a 3-week washout and alternate-drug/contralateral-placebo repeat. Intraocular pressure was measured by applanation and by pneumotonometry, providing pulsatile ocular circulatory estimates. Measurements of episcleral venous pressure were obtained (Friberg method). RESULTS: Twenty subjects participated (five men, 15 women; mean age, 39 years (range, 21 to 55 years); mean baseline intraocular pressure, 13.4 mm Hg). A greater decrease in intraocular pressure was seen among these subjects the morning after initiating treatment with latanoprost (-2.0 mm Hg; P <.0001) than with timolol-XE (-0.9 mm Hg; P =.051) (latanoprost versus timolol DeltaP =.008). This ocular hypotensive effect remained significant that evening with latanoprost (-3.2 mm Hg; P <.0001) but not with timolol XE (-1.0 mm Hg; P =.2). By the morning of day 8, mean intraocular pressure remained 3.2 mm Hg below baseline with latanoprost and 2.3 mm Hg below baseline with timolol-XE (P <.0001 for both drugs). Neither drug altered episcleral venous pressure. Among a subgroup of nine subjects with comparable intraocular pressure reductions with the two drugs, latanoprost treatment was associated with a 16.7% increase in mean pulsatile ocular blood flow (P =.04) through the weeklong treatment interval, consistently higher than during timolol-XE treatment of the same subjects. CONCLUSION: Latanoprost caused an overnight decrease in intraocular pressure in normotensive normal eyes, and both drugs significantly reduced intraocular pressure within 1 week. Intraocular pressure remained higher than episcleral venous pressure throughout treatment with both drugs. Latanoprost was associated with enhanced pulsatile ocular perfusion not seen with timolol-XE treatment.

Adrenergic beta-Antagonists↗
PubMed1999

Modulation of choroidal autoregulation in the rabbit.

Previous studies show that the choroid can maintain its blood flow despite changes in perfusion pressure, behaviour possibly mediated by an autoregulatory mechanism. However, the choroid's rich autonomic innervation suggests possible neural involvement in the response. To evaluate the potential neural contribution, choroidal blood flow was measured by laser Doppler flowmetry over a wide range of perfusion pressure before and after ganglionic blockade in anaesthetized rabbits. Although an upward shift in the pressure-flow (P-F) curve was anticipated due to loss of adrenergic tone, ganglionic blockade shifted the P-F curve downward, prompting a search for a neural vasodilator to explain the response. Cholinergic blockade with atropine failed to alter the P-F curve suggesting little parasympathetic involvement. By contrast, inhibition of nitric oxide (NO) synthase with nitro-L-arginine methyl ester (L-NAME) caused a dramatic downward shift in the P-F curve, suggesting the nitridergic nerves as the source of vasodilatory tone. However, the downward shift in the P-F curve with L-NAME was greater than seen with ganglionic blockade, indicating that endothelial NO rather than neural dilator tone predominates. Moreover, calcium channel blockade after L-NAME reversed the downward shift in the P-F curve suggesting that choroidal vascular tone is modulated by an interaction between NO and an unknown vasoconstrictor. Neither hexamethonium, losartan or a vasopressin antagonist given after L-NAME reversed the downward shift in the P-F curve, ruling out a neural vasoconstrictor, angiotensin II and vasopressin as the source of constrictor tone. Phentolamine given after L-NAME caused a small but significant reversal of the downward shift in the P-F curve, suggesting a minor adrenergic contribution. By contrast, the non-selective endothelin antagonist, A-182086, given after L-NAME significantly attenuated the choroidal constriction. These results indicate that an unknown neural dilator and locally produced NO and endothelin exert competing influences on the inherent reactivity of the choroidal resistance vessels as they respond to changes in perfusion pressure, and that this local regulation is likely modulated by extrinsic neurohumoral factors that are relatively quiet in the anesthetized rabbit.

Animals↗
PubMed1998

Effects of timolol and betaxolol on choroidal blood flow in the rabbit.

This study evaluated the effects of the topical beta1-adrenergic antagonist betaxolol and the non-selective beta-adrenergic antagonist timolol on the choroidal pressure-flow relationship. Pentobarbital-anesthetized rabbits were instrumented with hydraulic occluders on the aorta and inferior vena cava to control MAP, an ear artery cannula to measure mean arterial pressure (MAP), and two vitreous cannulas to control and measure intraocular pressure (IOP). Choroidal blood flow was measured by laser Doppler flowmetry with the fiber-optic probe tip positioned over the posterior pole. Choroidal pressure-flow curves were obtained before and 30 min after topical application of 0.1 ml of betaxolol (Betoptic, 0.5%, n=10), timolol (Timoptic, 0.5%, n=10) or saline (n=8) by varying the MAP without controlling the IOP and by raising IOP while holding the MAP constant at 70 mmHg. The IOP was significantly reduced by betaxolol and timolol but not by saline. MAP was also slightly, but significantly, reduced after betaxolol but not after timolol or saline. However, the systemic hypotensive response to isoproterenol (8 microgram/kg, i.v.) was blunted after betaxolol and timolol indicating appreciable systemic absorption of both drugs. Timolol, but not betaxolol or saline, caused a significant, small increase in baseline choroidal vascular resistance. Timolol also attenuated the IOP response to MAP; however, none of the treatments had a significant effect on the choroidal pressure-flow relationship. We conclude that both drugs reach the systemic circulation after topical application, but neither betaxolol nor timolol alter the choroidal response to acute changes in perfusion pressure.

Adrenergic beta-Antagonists↗
PubMed1997

Effect of ocular perfusion pressure on retinal function in the rabbit.

The electroretinogram (ERG) vs perfusion pressure relation was studied in anesthetized rabbits during mechanically induced changes in mean arterial pressure (MAP). After 1 hr of dark adaptation, ERGs were obtained at perfusion pressures from 10 to 95 mmHg with each pressure held for 30-60 sec, and at three levels from 15 to 75 mmHg with each pressure held for 5 min. The slopes of the b-wave amplitude vs perfusion pressure data were not significantly different from zero during either the brief or longer manipulations of perfusion pressure. However, the b-wave was nearly extinguished 5 min after death. The results indicate that the rabbit ERG is maintained over a wide range of perfusion pressure.

Animals↗
PubMed1996

Adrenergic modulation of choroidal blood flow in the rabbit.

PURPOSE: To determine whether the choroidal pressure-flow is altered by the alpha-adrenergic antagonist, phentolamine, or the beta-adrenergic antagonist, propranolol. METHODS: In two groups of pentobarbital- anesthetized rabbits, the choroidal pressure-flow relationships were determined by raising the intraocular pressure (IOP) at mean arterial pressure (MAP) of 50, 60, 70, and 80 mm Hg before and after phentolamine (0.5 mg/kg, intravenously, n=7) and propranolol (0.25 mg/kg intravenously, n=7) administration. Hydraulic occluders on the thoracic aorta and inferior vena cava were used to control MAP, which was measured in the central ear artery. The eye was cannulated with two 23-gauge needles, one to manipulate the ocular volume and the other to measure the IOP. Choroidal blood flow was measured by laser Doppler flowmetry with a probe positioned over the posterior retina. The protocol consisted of setting the MAP, then infusing saline into the eye at 30 microliters/minute until the IOP increased from baseline to 100 mm Hg. RESULTS: At the MAP of 70 mm Hg, alpha-adrenergic blockade caused an upward shift in the choroidal pressure-flow relationship; beta-blockade shifted the relationship downward. CONCLUSIONS: In the pentobarbital-anesthetized rabbit, alpha- and beta- adrenergic blockade cause choroidal vasodilation and vasoconstriction, respectively. Results indicate the presence of alpha- and beta-adrenergic receptors in the rabbit choroid and a tonic level of adrenergic vascular tone in this preparation.

Adrenergic alpha-Antagonists↗
PubMed1995

The effect of arterial pressure on the ocular pressure-volume relationship in the rabbit.

The purpose of this study was to quantify the effect of mean arterial pressure (MAP) on the ocular pressure-volume relationship. The experiments were performed in pentobarbital anesthetized rabbits instrumented with occluders on the thoracic aorta and inferior vena cava to control MAP which was measured via a cannula in the central ear artery. To vary the ocular volume and measure the intraocular pressure (IOP), two 23 gauge needles were inserted through the pars plana into the vitreous: one needle was connected to a saline-filled syringe and the other needle was connected to a pressure transducer. In one group of animals (n = 5), pressure-volume curves were determined at MAPs of 100, 80, 60, 40 and 20 mmHg and post mortem by cumulative saline injections (2 microliters) every 1-1.5 sec. In a second group (n = 7), pressure-volume curves were obtained at MAPs of 80, 60 and 40 mmHg and post mortem by saline infusion at 0.5 microliter sec-1 until the IOP reached 100 mmHg. The infusion protocol was repeated in a third group (n = 11) where the choroidal flux and the concentration of moving blood cells (CMBC) were measured by a laser Doppler flowmeter as indices of choroidal blood flow and the blood volume, respectively. MAP had three primary effects on the ocular pressure-volume relationship: (1) the baseline IOP varied exponentially with MAP, (2) the steepness of the initial portion of the pressure-volume curves was MAP-dependent and (3) the curves exhibited a 'plateau' as the IOP approached the prevailing MAP at MAPs > or = 40 mmHg. All of the curves in the living eye intersected and became indistinguishable from the post mortem curve when the IOP exceeded the prevailing MAP. The flux and CMBC measurements indicated that the MAP-dependence of the initial portion of the curves was due to failure of choroidal autoregulation and diminished increases in choroidal blood volume at the lower MAPs, and that the plateau portion of the curves was due to expulsion of blood from the eye. It is concluded that MAP has a significant effect on the ocular pressure-volume relationship.

Animals↗
PubMed1995

Ocular perfusion pressure and choroidal blood flow in the rabbit.

PURPOSE: To compare choroidal blood pressure versus flow relationships obtained by three different methods of changing the ocular perfusion pressure. METHODS: Experiments were performed in pentobarbital-anesthetized rabbits with occluders on the aorta and inferior vena cava to control mean arterial pressure (MAP). The central ear artery was cannulated to measure MAP. Two 23-gauge needles were inserted through the pars plana into the vitreous: one connected to a saline-filled syringe to vary the ocular volume and the other to a pressure transducer to measure intraocular pressure (IOP). Choroidal perfusion was measured by laser-Doppler flowmetry with the probe in the vitreous over the posterior pole. In group 1 (n = 15), the MAP was varied while holding the IOP at 10, 15, 20, 25 and 30 mm Hg. In group 2 (n = 19), the IOP was increased while holding the MAP at 80, 70, 60, 50, 40, 30 and 20 mm Hg. In group 3 (n = 21), the MAP was varied without controlling the IOP. RESULTS: Group 1 baseline choroidal flows were similar at the five IOPs. When the flow was plotted against MAP, the curves diverged and extrapolated to intersect the pressure axis when the MAP equaled the set IOP. Group 2 baseline flows were similar at MAPs greater than 40 mm Hg. When the flow was plotted against the IOP, the curves diverged and intersected the pressure axis when the IOP equaled the MAP. In both groups, plotting the flow against the perfusion pressure (i.e., MAP minus IOP) collapsed the data points into single curves. Choroidal autoregulation occurred in all three groups; however, the low end of the autoregulatory perfusion pressure range was approximately 50 mm Hg in group 1, approximately 40 mm Hg in group 2, and approximately 30 mm Hg in group 3. CONCLUSIONS: The results show that the effective choroidal perfusion pressure gradient equals the MAP minus the IOP, and that choroidal autoregulation is most effective when the MAP varies and IOP is not controlled.

Animals↗
PubMed1994

Choroidal myogenic autoregulation and intraocular pressure.

This study tests the hypothesis that choroidal myogenic autoregulation participates in the intraocular pressure (IOP) response to mean arterial pressure (MAP) by minimizing arterial-pressure-dependent changes in choroidal blood volume. To test this hypothesis, the IOP response to MAP was quantified before and after impairing choroidal autoregulation. In a previous study, the efficacy of choroidal myogenic autoregulation was inversely related to IOP. Therefore, in one series of experiments (n = 6), the relationship between MAP and IOP was determined at normal and elevated baseline IOP (i.e., 15 and 25 mmHg, respectively). In a second series of experiments (n = 6), the relationship between MAP and IOP was determined at the normal IOP (15 mmHg) before and after administering hydralazine, an arterial vasodilator. In both series, the MAP manipulations were kept brief to avoid the confounding effects of aqueous compensation. The experiments were performed in pentobarbital anesthetized rabbits with hydraulic occluders placed on the thoracic descending aorta and inferior vena cava to raise and lower MAP, respectively. MAP was measured via a central ear artery catheter. The right eye was cannulated with two 23 gauge needles; one cannula was used to set the IOP by varying the ocular volume and the other was used to measure the IOP. The protocol consisted of inflating the occluders to cause brief (1-1.5 min) ramp increases and decreases in MAP over a wide pressure range. Baseline IOP was set prior to each occlusion, but was otherwise uncontrolled. In the first series, the MAP range was 30 to 95 mmHg and IOP changed by 6 mmHg at the normal baseline IOP and by 18 mmHg at the elevated baseline IOP. The corresponding volume shifts were 7.7 and 14.5 microliters, respectively. In the second series, the MAP range was 25 to 95 mmHg and IOP changed by 6 mmHg during control and by 14 mmHg after hydralazine. The corresponding volume shifts were 6.7 and 13.8 microliters, respectively. In both series, the prompt return of IOP to baseline upon restoration of normal MAP indicated that the volume changes were due to changes in ocular blood volume. Additional experiments confirmed that elevating the baseline IOP and administering hydralazine impaired choroidal autoregulation but did not alter the cranial venous pressure response to varying MAP.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

A model of countercurrent shunting of oxygen in the intestinal villus.

This report describes a mathematical model of the countercurrent shunting (CCS) of O2 in the intestinal villus. The anatomic basis for the model is the close proximity of the arteriole and venule between which O2 is free to diffuse. The model divides the villus into four segments from base to tip. Steady-state equations describe the convective and diffusive fluxes of O2 in the arteriolar, capillary, and tissue compartments within each segment. Longitudinal diffusion along the length of the villus is assumed to be negligible. Simulations with the model led to the following observations: 1) CCS shifted the VO2 vs. blood flow curve down and to the right, slightly impairing VO2 at a given blood flow; 2) the base-to-tip PO2 gradient caused by the tissue O2 consumption was reduced by CCS; 3) when blood flow was reduced, the base-to-tip PO2 gradient increased until the tip PO2 fell to zero and then fell with further flow reductions; 4) lowering blood flow initially caused slight increases in shunting but further decreases in flow reduced shunting; 5) in the blood flow range in which VO2 was flow independent, increasing the O2 demand or decreasing the intervascular distance increased shunting because of the greater arteriole-to-capillary O2 concentration gradient and the decreased diffusion distance, respectively; and 6) lowering the hemoglobin's P50 to simulate fetal blood caused slight reductions in shunting and reduced VO2 at a given flow. In summary, the model confirms the potentially deleterious effects of CCS on intestinal oxygenation, and, in contrast to assertions in the literature, it shows that a base-to-tip PO2 gradient is not prima facie evidence of counter-current shunting.

Animals↗
PubMed1992

Effect of fasting and refeeding on mesenteric autoregulation in conscious rabbits.

To determine whether feeding improves the efficacy of mesenteric autoregulation in conscious animals, rabbits were instrumented with pulsed-Doppler flow probes on the superior mesenteric artery and distal abdominal aorta to record mesenteric and hindquarters blood flow velocity. Hydraulic occluders were placed on the abdominal aorta (just below the celiac artery) and the thoracic vena cava to vary mesenteric and hindquarters arterial pressure (MAP), which was monitored via a catheter positioned in the distal abdominal aorta. Heart rate (HR) and lumbar sympathetic nerve activity (LSNA) were monitored as indexes of sympathetic nervous system activity. Pressure-velocity curves were obtained by aortic and caval occlusions on two consecutive days; first after a 24-h fast and after approximately 24 h of ad libitum refeeding. In the fed state, mesenteric velocity was significantly increased and MAP was decreased slightly; the slight decrease in MAP was counteracted by significant increases in HR and LSNA, whereas hindquarters perfusion was unchanged. The mesenteric and hindquarters pressure-velocity curves were all highly linear (r greater than or equal to 0.9) and showed no evidence of autoregulation in the fasted or fed state when pressure was changed by either the aortic or the caval occlusions. We conclude that autoregulation plays a minor role in the short-term regulation of mesenteric blood flow in the conscious rabbit.

Animals↗
PubMed1992

Autoregulation of choroidal blood flow in the rabbit.

Previous studies show that choroidal blood flow is not autoregulated when intraocular pressure (IOP) is increased to raise venous pressure and lower the perfusion pressure gradient. However, the autoregulatory response to changes in mean arterial pressure (MAP) is unclear. In the current study, the perfusion pressure gradient (MAP-IOP) was altered by (1) decreasing MAP while IOP was held at 5, 15, and 25 mmHg, and (2) increasing the IOP at the prevailing MAP in anesthetized rabbits (n = 8). An occluder on the thoracic vena cava was used to vary MAP; this was monitored through an ear artery catheter. Two catheters were inserted in the vitreous to monitor and control IOP. Choroidal blood flow was measured by laser Doppler flowmetry using a slender stainless-steel probe positioned next to the retinal surface. The efficacy of autoregulation depended on the IOP. When IOP was held constant at 5 mmHg, choroidal blood flow did not fall until the perfusion pressure gradient was less than 40 mmHg. The pressure-flow relationship became progressively more linear (ie, the efficacy of autoregulation decreased) when the IOP was held constant at 15 and 25 mmHg. When IOP was varied and MAP was held constant, the pressure-flow relationship was linear at IOPs greater than 20-25 mmHg. However, choroidal blood flow was pressure independent when the IOP was less than 20-25 mmHg. Simultations using a myogenic mathematic model of the choroid gave results similar to the experimental observations. It was concluded that a myogenic mechanism may be responsible for the autoregulation of choroidal blood flow in the rabbit.

Animals↗
PubMed1989

Gastric oxygen uptake during autoregulatory escape from sympathetic stimulation.

To assess the effects of sympathetic stimulation on gastric blood flow and oxygen utilization, the perivascular nerves were stimulated at 2, 4, 6, and 8 Hz in chambered segments of canine gastric corpus perfused at constant pressure. Spectrophotometric arteriovenous oxygen difference and electromagnetic blood flow were recorded continuously. Except at the lowest frequency of stimulation (2 Hz), total blood flow exhibited autoregulatory escape, i.e., blood flow decreased initially but then returned toward control. The fall in total blood flow at the onset of sympathetic stimulation was smaller at 2 Hz than at 4 Hz, but stimulation at 6 and 8 Hz caused no further reductions in total blood flow. However, at all frequencies, total blood flow escaped to the same steady-state value (approximately 17 ml.min-1.100 g-1). Although total blood flow was still less than control (approximately 25 ml.min-1.100 g-1), oxygen extraction increased proportionately so that oxygen consumption was not significantly less than control at any frequency of stimulation. We conclude that autoregulatory escape from sympathetic stimulation is mediated by local mechanisms acting to maintain tissue oxygenation in the stomach.

Animals↗
PubMed1989

Effects of hemodilution on gastric and intestinal oxygenation.

To determine the effects of hemodilution on gastric and intestinal oxygenation, isolated segments of canine stomach and small bowel were perfused by a pressurized reservoir with blood at hematocrits of 40 and 20%. Arteriovenous O2 difference, blood flow, and arterial and venous pressures were monitored continuously as perfusion pressure was reduced in 30-mmHg steps from 180 to 30 mmHg. O2 consumption was calculated as the product of the steady-state arteriovenous O2 difference and blood flow at each perfusion pressure. Gastric and intestinal O2 uptake were relatively well maintained over most of the pressure range when the hematocrit was set at 40%. After hemodilution, gastric O2 uptake decreased significantly only at 90 and 60 mmHg, but intestinal O2 uptake was significantly reduced except at 30 mmHg. When gastric and intestinal O2 uptake were plotted as a function of blood flow, the O2 uptake vs. blood flow relationship were shifted down and to the right by hemodilution. Hemodilution also linearized the O2 uptake vs. blood flow relationship in the intestine. However, when O2 uptake was plotted as function of O2 delivery, the gastric O2 uptake vs. delivery curves at the two hematocrits were superimposed on each other, but the O2 uptake vs. delivery curves for the intestine diverged except at low rates of O2 delivery. We conclude that by reducing the O2-carrying capacity of the blood, hemodilution adversely affects gastric and intestinal oxygenation. Our results also indicate that hemodilution lowers gastric O2 uptake by reducing O2 delivery; however, hemodilution lowers intestinal O2 uptake not only by reducing O2 delivery but also by impairing O2 extraction.

Analysis of Variance↗
PubMed1989

Optimal hematocrit for canine gastric oxygenation.

To determine whether an optimal hematocrit exists at which gastric tissue is maximally oxygenated, chambered segments of resting canine stomach were perfused at a constant pressure while hematocrit was decreased in steps from 60 to 10%. The two groups of animals used were a control group and a second group given pentagastrin to elevate metabolic activity. Total blood flow was inversely related to hematocrit in both the control and pentagastrin-treated animals, and arteriovenous oxygen difference was directly related to hematocrit. Consequently, the relationship between gastric oxygen consumption and hematocrit was parabolic in both groups. Therefore, the oxygen uptake vs. hematocrit data from each experiment were fit to a quadratic equation that was used to calculate the maximal oxygen uptake and the optimal hematocrit for each preparation. Both the maximum oxygen uptake and the optimal hematocrit in the pentagastrin-treated group (2.1 +/- 0.4 ml.min-1.100 g-1 and 45.7 +/- 1.4%, respectively) were significantly greater than in the control group (1.5 +/- 0.4 ml.min-1.100 g-1 and 38.2 +/- 0.7%, respectively). We conclude that an optimal hematocrit exists for the oxygenation of gastric tissue and that it is within the normal hematocrit range under resting conditions. However, the optimal hematocrit is slightly higher than normal during periods of increased metabolic activity.

Animals↗