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Biomedical subjects

C H Baker

Publications and source records attributed to C H Baker.

At least 73 records · Page 4Linked to original sources

Frequency-dependent control of nutritional and nonnutritional circuits in the dog paw.

The neural control of blood flow and volume distribution between parallel nutritional and nonnutritional circuits has been investigated in 13 vascularly and neurally isolated dog hindpaws. The superficial and deep fibular nerves and the tibial nerve were cut and individually stimulated at frequencies of 0.1, 1, 5, 10 and 15 Hz. Increasing stimulation rates to each nerve progressively increased blood flow resistance. Vascular volume changes were determined by indicator dilution and tissue volume changes by plethysmography. The permeability surface area product of 86Rb (PS) and the capillary filtration coefficient (CFC) were determined. Superficial fibular nerve and deep fibular nerve stimulations caused progressively increased nonnutritional circuit constriction with increasing stimulation frequencies resulting in blood flow redistribution to the nutritional circuit as evidenced by increasing PS and CFC values. Tibial nerve stimulation at 0.1 Hz caused nonnutritional circuit constriction and blood flow redistribution to the nutritional circuit (PS and CFC increased). As the stimulation frequency was increased, there was progressive increase of the nutritional circuit constriction and altered blood flow distribution; i.e., CFC and PS decreased with increasing frequency of stimulation, presumably due to predominantly arterial segment resistance increase.

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Microvascular plasma velocity and indicator dispersion with hemorrhage.

The effects of stepwise hemorrhages on plasma flow velocity and indicator (FITC-Dextran) dispersion in series and parallel coupled microvascular vessels has been studied. The mesentery of cats (0.6 kg) anesthetized with Dial-Urethane was exposed and studied with a microscope equipped for fluorescense microscopy. Indicator was injected as a bolus (0.1 ml in 0.5 seconds) in a small branch of the mesenteric artery. Indicator curves were recorded from a video tape recording of the passage of the indicator by a video sampler with intensity sensitive windows. The mean transit time (t), appearance time (t(a)), peak time (t(p)), curve duration (t(E)), plasma velocity and vessel diameter changes were determined. Arterioles 68 +/- 8 micron and 35 +/- 3 micron and venules 55 +/- 6 micron constricted gradually with hemorrhage. Arterioles 20 +/- 2 micron constricted with mild hemorrhage and remained constricted with further hemorrhage. Arteriolar and venular plasma velocities decreased abruptly with mild hemorrhage and then continued to decrease gradually with further hemorrhage. Capillary flow ceased after moderate hemorrhage and was not reestablished until at least an hour after reinfusion. Arteriole t increased with hemorrhage but t increased much more in capillaries and venules. t(E) changes paralled t changes. The ratio t(a)/t was lower for venules than arterioles and both decreased with hemorrhage but the venular ratio decreased significantly more. Venular t(p)-t(a) and t(E)-t(p) increased more than arteriolar values. Hemorrhage increased indicator dispersion with the greatest effect occurring between the arteriolar and venular vessels.

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Nonhemodynamic effects of histamine on gracilis muscle capillary permeability.

The effects of histamine were studied in the maximally vasodilated gracilis muscle. Dog gracilis muscles were isolated in a plethysmograph and perfused at constant inflow pressure (102 +/- 2 mm Hg). Maximal vasodilation was produced with constant infusion of papaverine (0.2 mg/ml). Constant infusion of blood labeled with albumin-131l or red blood cells (RBC)-51Cr was made throughout the duration of the experiment. Tissue radioactivity and tissue volume changes were continuously measured. Papaverine did not increase transcapillary movement of protein, Histamine (5 microgram/kg/min) was added to the blood and 10 to 15 min later the dose level was increased to 60 microgram/kg/min. Since the vasculature was maximally dilated, changes in tissue radioactivity and tissue volume would be due to transcapillary movement rather than to vascular volume effects. The low dose of histamine significantly steepened the slopes of tissue volume and tissue albumin-s131l increase. The highest dose of histamine significantly further increased these rates. The tissue red cells-51Cr slope was not significantly increased with either dose of histamine. The capillary filtration coefficient was significantly increased above the papaverine vasodilation value by the histamine. The data would support increased transcapillary movement of proteins by other than hemodynamic mechanisms.

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Neural control of nutritional and nonnutritional circuits in the dog hindpaw.

The neural control of blood flow and volume distribution between parallel nutritional and nonnutritional circuits has been investigated in the vascularly and neurally isolated dog hindpaw. Twelve paws were perfused by controlled pressure and ten paws were perfused by controlled flow via the cranial tibial artery. Venous outflow was measured and collected from the lateral saphenous vein. The superficial and deep fibular nerves and the tibial nerve were cut and individually stimulated, resulting in rates which at least doubled the blood flow resistance. Vascular volume changes were measured by injections of 51Cr-labeled red cells and 131I-labeled albumin. Tissue volume changes were measured by plethysmography. Capillary diffusion capacity was calculated from 86Rb extractions, and capillary filtration coefficients were determined. Superficial fibular nerve and deep fibular nerve stimulations apparently resulted in nonnutritional circuit constriction with resulting blood flow redistribution to nutritional circuits, possibly located in tissues other than the skin, e.g., adipose tissue. Tibial nerve stimulation caused no redistribution of blood flow between the two circuits presumably due to a uniform constriction of arteries and small vessel segments.

Animals↗

Hypothalamic and brachial nerve effects on circulation of isolated canine forelimb,.

Canine forelimbs were vascularly isolated and perfused at either constant inflow or constant inflow pressure. A comparison of the effects of electrical stimulation of hypothalamic pressor areas and brachial nerves was made on several vascular parameters. During constant pressure perfusion, forelimb resistance increased and total forelimb volume decreased. Additionally active vascular volumes measured with 131I-labeled albumin and 51Cr-labeled red cells decreased significantly. Capillary diffusion capacity product calculated from extraction of 86RbCl also decreased significantly as did the capillary filtration coefficient (CFC). The only significant differences between hypothalamic and brachial nerve stimulation were noted in the larger decreases in active volumes and CFC during the latter stimulations.

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Forelimb blood flow distribution during hypothalamic dilator response.

An attempt is made to determine whether hypothalamically induced forelimb vascular dilation in the dog affects primarily exchange beds or shunt circuits. Slug injections of [131I] albumin and 86RbCl were used to measure the active vascular volume of the forelimbs and permeability surface area product (PS), respectively. Changes in total vascular volume (TVV), filtration, and capillary filtration coefficient (CFD) were measured by plethysmography. During stimulation, forelimb blood flow increased 25% and TVV increased an average 1.5 ml. There was no plethysmographic evidence of outward capillary filtration. Active vascular volume decreased 11%. PS decreased 11%, and CFC decreased 20%. These results point to a redistribution of blood flow from exchange circuits to faster flow channels. During constant-inflow perfusion, there was evidence from CFC and PS measurements that the capillary surface area was increased while active vascular volume decreased. The results observed with hypothalamic stimulation are different from those obtained with pharmacologic dilators and denervation. It is suggested that the former method has a more selective effect in lowering resistance in the faster shuntlike vessels.

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Skeletal muscle vascular volume changes with increased venous pressure.

Dog gracilis muscles were removed, enclosed in a plethysmograph and perfused at constant inflow pressure or constant inflow. Circulating blood volumes were measured by the constant infusion technique using RBC-51Cr or albumin-131I. Control venous pressure averaged 3 mm Hg and elevations (delta PV) over the range of 5-40 mm Hg were produced. Volume changes were determined during and following delta PV by plethysmography and by changes in total muscle radioactivity. Changes in total (amount of blood in the tissue), active (circulating), and mobilized vascular volumes were calculated. Active vascular volumes and total vascular volumes increased with venous pressure increments up to 25 mm Hg and then plateaued. Active vascular volumes (indicators) increased by amounts significantly greater than the increases in total vascular volume (plethysmography). Volume changes in the constant flow groups were double those in the constant pressure groups. The mobilized active vascular volume (active vascular volume change minus total vascular volume change) consists of a volume of blood contained in vessels unattainable by the indicators during the control period but which were made available to the indicator by the delta PV. Mobilized vascular volume averaged 45% of the active vascular volume change. With venous pressure elevation there was an increase in the RBC-51Cr volume to albumin-131I volume ratio. This suggests a redistribution of red cells with respect to plasma, possibly resulting from reduced plasma skimming.

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Vascular and extravascular volume changes due to elevated venous pressure.

Abrupt elevation of venous pressure causes an initial rapid and a secondary slow increase in total tissue volume (plethysmography). Changes in total tissue volume and blood conductivity from the isovolumetric state were determined to assess what factors determined the two components of the tissue volume change. The initial component of the plethysmograph record would appear to be 90% vascular volume change and 10% extra-vascular volume change. Since the two techniques measured identical amounts of capillary filtration during the second component of the recording there would seem to be no slow component of vascular volume increase following venous pressure elevation. Evidence that elevation of venous pressure causes myogenic closure of precapillary vessels isolating a segment of the microvasculature is presented.

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