Search PubMed⌕ Search

Biomedical subjects

C H Baker

Publications and source records attributed to C H Baker.

At least 55 records · Page 3Linked to original sources
PubMed1986

Dependence of the length-tension relationship on agonist concentration in vascular smooth muscle.

This study examines the dependence of the length-tension (L-T) relationship in vascular smooth muscle on its level of activation. A horizontal shift of the L-T relationship with a change in activation level has been shown in striated muscle when L-T curves could not be superimposed. Active force at each length was normalized to the maximum active force in each curve. Indices of a horizontal shift of a L-T curve include the initial length for an active response (Li) and the length for maximum active force (Lmax). In this study normalized L-T curves were obtained from rings of the dog anterior tibial artery at low (approximately ED50) and high (maximal activation) concentrations of potassium (K+), norepinephrine (NE), and calcium (Ca2+). The normalized curve with a low concentration of K+ or NE was shifted to the right of the curve obtained with a high concentration. Li and Lmax were significantly longer for a low concentration of K+ or NE than a high concentration. With the same concentration of NE (10(-5) M) no difference in the normalized L-T curves, in Li, or in Lmax were found when low (0.085 mM) Ca2+ experiments were compared to normal (1.7 mM) Ca2+ experiments. It may be concluded that the length-tension relationship in vascular smooth muscle is shifted to longer lengths with a decrease in the concentration of a chemical agonist but not by a decrease in external calcium. We suggest that a concentration dependent shift in the length-tension relationship may have a role in the regulation of blood flow.

Animals↗
PubMed1986

Reduced RBC versus plasma microvascular flow due to endotoxin.

The microvascular circuits traversed by red blood cells (RBCs) and plasma from first-order arterioles to first-order venules are complicated by variations in hemodynamic, rheologic, and dimensional parameters. Escherichia coli endotoxin causes microcirculatory derangements expected to alter RBC and plasma transport through these circuits. Wistar male rats were anesthetized with pentobarbital; the left cremaster muscle was spread over an optical port in a Krebs solution bath and administered endotoxin (6 mg/kg) iv over a 1-h period. The right femoral artery was cannulated for measurement of aortic pressure (Pm) and ia bolus injections of fluorescent DTAF-RBC and FITC-dextran. Fluorescence epi-illumination videomicroscopy and densitometry were used to obtained time-concentration curves (TCCs) in arterioles and venules. Control Pm averaged 106 +/- 8 mm Hg and progressively decreased during the 150-min observation period following endotoxin infusion. Arteriolar and venular diameters decreased approximately 50% during the 150-min observation period. At control DTAF-RBC flow velocity exceeded FITC-dextran velocities but by 90 min postendotoxin, even though both velocities were greatly reduced, plasma velocity, significantly exceeded red cell velocity. The control mean transit times for FITC-dextran exceeded the DTAF-RBC times in all vessels; 90 min postendotoxin the DTAF-RBC mean transit times significantly exceeded the FITC times and cell aggregates were in venous blood. The data suggest that cell aggregation, vasoconstriction and use of longer alternate parallel vascular circuits occur in endotoxin shock, restricting red cell flow. Plasma bypasses RBCs, flowing more rapidly than red cells in terminal shock.

Animals↗
PubMed1986

Norepinephrine effects on SHR muscle vessel diameters, RBC and plasma flow.

The distribution of blood flow through the cremaster microcirculation of pentobarbital anesthetized WKY and SHR rats was studied using fluorescence videomicroscopy and videodensitometry. The left cremaster muscle was spread over an optical port in a bath filled with modified krebs solution (pH = 7.4, 34 degrees C). The right femoral artery was cannulated with PE-10 tubing for the measurement of mean arterial blood pressure and bolus injections of indicators (DTAF-RBC's and FITC-dextran) into the aorta. The passage of indicators through the microvessels and vessel diameters were recorded on video tape during the topical application of norepinephrine (10(-10) M to 10(-6) M). Mean arterial blood pressure was 95 +/- 4 mmHg for WKY rats and 146 +/- 6 for SHR. Venular diameters were greater in WKY than in SHR. Norepinephrine decreased vessel diameters and blood flow velocity in a dose dependent manner. Mean transit time (t) for DTAF-RBC's was less than for FITC-dextran in first order arterioles for both normotensive and hypertensive animals. At high concentrations of norepinephrine differences in t for the two indicators disappeared. The t of both indicators were not different between normotensive and hypertensive animals in arterioles. However, t for both indicators were significantly increased in venules at all concentrations of norepinephrine in SHR but significantly less than in WKY. t for both indicators were increased in a dose dependent manner in both arterioles and venules. Arterioles of SHR appear to be constricted reducing the number of parallel circuits available for flow which allows passage of both RBC and plasma more directly and rapidly through shorter routes than in WKY, but restricts flow of RBC through the terminal arterioles.

Animals↗
PubMed1984

Microvascular responses to E. coli endotoxin with altered adrenergic activity.

The cremaster muscle microcirculation of pentobarbital-anesthetized Wistar rats was studied using videomicroscopy. The left cremaster muscle was spread over an optical port in a bath filled with modified Krebs solution (pH 7.4, 34 degrees C). The right femoral artery was cannulated for determination of mean arterial pressure (Pm). Following control measurements of Pm and arteriolar and venular dimensions, dose-response curves of arteriolar and venular dimensions to topical norepinephrine (10(-10) M to 10(-3) M) was obtained. The rats were then administered E. coli endotoxin (6 mg/kg, iv, LD100) over a 1-hr period. The dose response curves were than repeated at intervals of 30 min. Before endotoxin the threshold dose for norepinephrine was consistently 10(-9) M or 0(-8) M. Pm decreased progressively with time postendotoxin. After endotoxin infusion, there was a gradual and progressive constriction of both arterioles and venules. The threshold dosage for norepinephrine to produce constriction of both arterioles and venules increased progressively with time. At 3 hr postendotoxin the threshold dose had increased to 10(-6) M to 10(-4) M. This is the dose that produces maximum constriction of arterioles in the preendotoxin control period. The study was terminated when the animal died or the field was obscured by petechiae. The microvessel sensitivity to norepinephrine is markedly reduced during endotoxin shock possibly due to increase in the active state of the vascular smooth muscle or to change in length of the muscle fibers or to changes in sympathetic alpha-adrenergic activity. The response was not prevented by H1 and H2 receptor blockade, but was prevented by alpha-adrenergic blockade with phentolamine.

Animals↗
PubMed1983

Temperature effects on dog hindpaw series and parallel vascular circuits.

The effect of environmental temperature (skin surface) on distribution of blood flow between the parallel vascular circuits has been assessed in vascularly and neurally isolated hindpaws perfused at constant pressure. The paw was sealed in a chamber filled with water at 10, 20, 30, or 40 degrees C. Peripheral resistance increased as the temperature decreased in both innervated and denervated paws. Resistance in the denervated paws was less than in the innervated paws at all temperatures. Recovery of 85Sr microspheres was less at 40 degrees C than at 10, 20, or 30 degrees C in the denervated paws but did not change in innervated paws. Capillary availability (diffusion capacity and filtration coefficient) increased with each elevation in temperature in both groups. At 10 degrees C both arteriovenous (AV) shunt and capillary flows were low in innervated paws with low capillary and high shunt flow in denervated paws. At 20 and 30 degrees C capillary flow increased with temperature and arteriovenous anastomosis (AVA) flow was unchanged in denervated paws. In innervated paws AV shunt flow fraction slightly increased, with capillary perfusion markedly increased as temperature was elevated. The increased capillary flow in both groups passed through an enlarged capillary bed, whereas the number and/or diameter of AVAs remained essentially unchanged.

Animals↗
PubMed1983

Innervation sites of dog hindpaw series and parallel vascular circuits.

The neural control of the distribution of blood flow between the parallel nutritional and nonnutritional vascular circuits in the dog hindpaw has been assessed. The right hindpaw of anesthetized dogs was vascularly and neurally isolated and placed in a volume recorder sealed by the skin flap. The animals were heparinized. The autoperfused preparation was isovolumetric during the control period. The inflow tubing had side arms for measurement of perfusion pressure and for injections of indicators (131I-albumin, 86Rb and 85Sr-microspheres). Vascular volume changes were determined from venous time-concentration curves and by plethysmography. The peripheral cut ends of the superficial and deep fibular nerves and the tibial nerve were individually stimulated at 5 and 11 Hz. The permeability surface area product of 86Rb and the capillary filtration coefficient were determined and A-V shunt patency was assessed by the venous recovery of 85Sr 15 microns microspheres. Each nerve stimulation increased blood flow resistance. Superficial fibular nerve innervation included essentially uniform effects on the arterioles and A-V shunts, the upstream arteries and also the veins. Deep fibular nerve stimulation indicated that its innervation included the arteries and the A-V shunt nonexchange vessels. Tibial nerve stimulations indicated that its innervation included the A-V shunt vessels and veins with minimal influences on the arteries and arterioles.

Animals↗
PubMed1982

Red blood cell and plasma distribution in SHR cremaster muscle microvessels.

Distribution of blood in the cremaster muscle microvasculature of spontaneously hypertensive (SHR) and Wistar-Kyoto normotensive (WKY) rats was determined by fluorescence videomicroscopy and densitometry. Bolus intra-arterial injections of fluorescein isothiocyanate (FITC)-dextran or dichlorotriazenylaminofluorescein-treated red blood cells (DTAF-RBC) produced time-concentration curves in the series-coupled segments. WKY and SHR mean arterial pressure averaged 89 +/- 6 and 125 +/- 5 mmHg, respectively. Arteriolar diameters were not different between the two groups. The smallest SHR venules (V4) and larger diameters than those of WKY (P less than 0.05), whereas V3 and V2 were not different. WKY diameters for V1 were significantly greater than those of SHR. The mean transit (t) and appearance times (ta) of both indicators were equal at the largest arteriole (A1) in both groups. In A2, A3, and A4 the t for both indicators were generally lower in SHR than in WKY rats but not significantly. The venular t were significantly greater in SHR than in WKY rats with DTAF-RBC consistently less than FITC-dextran values. The greater cross-sectional area of V4 in SHR than WKY rats would reduce flow velocity and elevate t. Dispersion (ta/t = 1.0 indicates no dispersion) of both indicators was less in WKY than in SHR. The ratios for both groups increased at V4 because ta increased more than t. Shorter circuits for red blood cells than for plasma and less plasma skimming exists in WKY than in SHR.

Animals↗
PubMed1982

Length-tension properties of the anterior tibial artery in normotensive and perinephritic hypertensive dogs.

The length-active tension relation has been previously reported to be decreased or unchanged in hypertensive vessels whereas resting distensibility was unchanged or increased. We found the maximum active stress and the internal ring circumference, in millimeters, at which it occurs (Lmax) to be lower in arterial rings from perinephritic hypertensive dogs than in rings from normotensive dogs. The internal circumferences (length) at which resting force and active force became zero (L0 and Lmin, respectively) were unchanged. Lmax, L0 and Lmin were used to normalize length-tension diagrams. Active stress was significantly lower in hypertensive vessels at most of the lengths tested with the diagram normalized to Lmax. When the length-tension diagram was normalized to Lmin there was no difference in the active stress at any of the lengths tested. The length-resting stress curves were identical when rhe diagram was normalized to Lmax but the curve for hypertensive vessels was higher when the diagram was normalized to L0. An important characteristic of these length-tension curves is that normalized lengths correspond to the same absolute length in each group of vessels when the reference length has the same absolute value (L0 and Lmin in this study). This separates differences due to absolute length from differences associated with hypertension. We conclude that perinephritic hypertension in the dog is accompanied by a decrease in resting distensibility of the arterial wall. The results indicate that the choice of reference length may affect the values of stress and tension that are obtained for comparison of length-tension relationships in hypertensive and normotensive blood vessels.

Animals↗
PubMed1982

Arteriolar to venular red cell and plasma dispersion in hemorrhage- and endotoxin-shocked cats.

The passage of red cells is more rapid than for plasma through the microcirculation of most tissues. The effects of hemorrhage (13 ml/kg) and endotoxin (3 mg/kg) on this phenomenon were studied in the exposed mesentery of cats anesthetized with Dial-urethane using epi-illumination fluorescence or transillumination television microscopy. Femoral artery pressure, arteriolar pressure, and arteriolar and venular diameters were measured. FITC-dextran, the plasma label, and DTAF-labeled red cells (DTAF-RBCs) or sulphemoglobin-labeled RBCs (SH-RBCs) were injected as a bolus (0.005 ml in 0.5 seconds) into a small branch of the mesenteric artery at control and after the experimental procedure. Animals were hemorrhaged from the left femoral artery (13 ml/kg) or injected IV with endotoxin. Time-concentration curves were recorded from video tape recordings of the passage of the indicator by videodensitometry for determination of the mean transit times (t). During hemorrhage and endotoxin the arterial pressure decreased significantly as did the arteriolar flow velocity. Following hemorrhage arteriolar and venular diameters and arteriolar pressures decreased significantly. Postendotoxin, arteriolar and venular diameters increased and arteriolar pressures did not decrease significantly. During control the t of labeled red cells was exceeded significantly by those of FITC-dextran in all microvascular segments. Following hemorrhage the t of the two indicators were increased significantly but were not significantly different in the arterioles. However, they were different in the venules. One hour after endotoxin t was significantly increased in all segments and further increased at three hours. However, the labeled red cell values were still exceeded by the FITC-dextran values at both times. It would appear that the differences in t would be abolished by vasoconstriction reducing axial streaming and plasma skimming whereas vasodilation does not change these phenomena.

Animals↗
PubMed1982

RBC and plasma distribution changes in cat mesenteric microvessels after hemorrhage and reinfusion.

The mesenteries of ten cats (0.6 kg) anesthetized with Dial-urethane were exposed and studied using fluorescence television microscopy. Femoral artery pressure was determined. FITC-dextran, the plasma label, or DTAF-labeled red cells (DTAF-RBCs) were injected as a bolus (0.005 ml in 0.5 sec) into a small branch of the mesenteric artery. Animals were hemorrhaged from the left femoral artery into a reservoir. Control mean arterial pressure averaged 100 +/- 2 mmHg and decreased to 84 +/- 1 mmHg subsequent to an average bled volume of 13 ml/kg. Time-concentration curves were recorded from videotape recordings of the passage of indicator by videodensitometry. Following hemorrhage, arteriolar (N = 134) FITC-dextran mean transit time (t) was increased significantly to 194 +/- 10% of control, while t for DTAF-RBCs increased significantly to 211 +/- 10% of the control value. In the venules (N = 180) hemorrhage significantly increased FITC-dextran t to 197 +/- 9% of control while venular DTAF-RBC t was significantly increased to 182 +/- 5% of control. Arteriolar t was significantly lower for DTAF-RBC than for FITC-dextran during the control period and following reinfusion. Following hemorrhage, arteriolar t for DTAF-RBCs was not different from that for FITC-dextran. Venular values were significantly lower for DTAF-RBCs than FITC-dextran during all three periods. Dispersion was increased (reduced ta/t) by hemorrhage in arterioles and venules. The elevated t after hemorrhage would appear to be the result of increased peripheral resistance and resulting reduced flow velocity through the circuits. The absence of a difference in arteriolar t between the two indicators post-hemorrhage would indicate reduced Fahraeus effects owing to reduced blood flow velocity and perfusion pressure.

Animals↗
PubMed1980

Microvessel mean transit time and blood flow velocity of sulfhemoglobin-RBC.

An indicator dilution technique is described for obtaining time-concentration curves subsequent to bolus injections of sulfhemoglobin red blood cells (SH-RBC), which have a deep greenish-brown color (absorption peak 620 nm vs. 542 and 564 nm for normal red cells). The series- and parallel-coupled microvessels of cat mesentery were studied. This is accomplished by means of video microscopy with a two-window intensity-sensitive video sampler system. The relationship between SH-RBC concentration in blood and optical measurement is linear. Blood flow velocities were calculated from the difference in mean transit times between two points along a vessel. When this technique is used in association with the previously reported method for determining time-concentration curves for the plasma indicator FITC-dextran the mean transit time (t) for red blood cells was less than for plasma in arterioles. The reproducibility of t and flow velocity for both SH-RBC and FITC-dextran from successive injections were reported. The mean transit time ratio of arteriolar SH-RBC to FITC-dextran averages 0.89. Blood flow velocity calculated from SH-RBC is greater than that calculated from FITC-dextran in these same arterioles. The ratio of the velocities averages 1.29.

Animals↗
PubMed1980

Effects of endotoxin on microvascular flow velocity and indicator dispersion.

The effects of endotoxin (3mg/kgLD100) on the microcirculation of exposed mesentery were studied in anesthetized cats (0.7 kg). A femoral artery and vein were cannulated for arterial pressure determination and injections. Successive bolus injections (0.05 ml) of blood containing sulphhemoglobin red blood cells (SH-RBC) and fluorescein isothiocyanate-labeled dextran (FITC-Dextran) were made into a mesenteric artery branch. The indicator passage through the microvessels was recorded on videotape. Upon replay, the outputs of an injection signal and two video sampler (VS) intensity-sensitive windows (placed at each end of the vessel) were monitored for obtaining indicator time-concentration curves. The arteriolar flow velocity was calculated as the distance between windows (millimeters) divided by the difference in mean transit time (t) of the two curves. Vessel dimensions were determined as the calibrated distance between the windows. During the first hour postendotoxin, the arterial pressure decreased while arterioles (35 micrometer and larger) and venular diameters increased. Terminal arteriole (20-micrometer)diameters decreased. SH-RBC and FITC-Dextran velocities decreased 50%, t increased, and indicator dispersion increased. Arterial pressure increased to above control levels during the next two hours and 55-micrometers and 35-micrometers arteriolar and venular diameters decreased, and 20 micrometers arterioles increased; SH-RBC and FITC-Dextran flow velocities gradually decreased; arteriolar t increased markedly; and indicator dispersion increased. During the terminal phase, arterial pressure decreased rapidly, all vessel diameters increased, velocities decreased, t markedly increased, and indicator dispersion increased. Control SH-RBC velocities were greater and t were less than for FITC-Dextran.

Animals↗