Biomedical subjects

E T Sutton

Publications and source records attributed to E T Sutton.

At least 37 records · Page 2Linked to original sources

PubMed1995

Maintenance of dynamic microvascular function and structure in a rat model of endotoxic shock by blockade of the interleukin-1 receptor.

The microvascular and macrovascular effects of IL-1 receptor antagonist (IL-1ra) were examined in rat cremaster muscle A1, A2, and A3 arterioles by videomicroscopy to better define its protective effects during endotoxemia. Mean arterial pressure (MAP), arteriolar diameters, and responses to norepinephrine (NE) and acetylcholine (ACh) were examined hourly after the administration of Escherichia coli endotoxin (6 mg/kg intravenously). Animals received saline (Control) or IL-1ra (.2 mg/kg/min intravenously) beginning 1 h prior to endotoxin. Serum tumor necrosis factor-alpha (TNF-alpha) and nitrate/nitrite (NO) were determined terminally. Aortic endothelium was examined by electron microscopy (EM). All Control animals, but no IL-1ra animals, died within 6 h (p < .01).IL-1ra significantly attenuated endotoxin-induced vasoconstriction of A1 and A2 arterioles (p < .01), while MAP and NE threshold remained at baseline (p < .01 vs. Control). Serum TNF and NO were elevated following endotoxin (p < .001), but only TNF was decreased (p < .005) in animals receiving IL-1ra. Aortic endothelium was damaged in all Control animals but was spared with IL-1 antagonism. IL-1ra increases survival during endotoxic shock and attenuates production of TNF but not NO. IL-1ra maintains MAP, arteriolar diameters, reactivity of arterioles to NE and ACh, and the integrity of the aortic endothelium.

Acetylcholine↗

PubMed1995

Arteriolar reactivity of endotoxin-tolerant rats after hemorrhage and reinfusion.

Adrenergic and endothelium-dependent arteriolar reactivity are greatly reduced in hemorrhagic shock. However, development of tolerance to endotoxin may prevent the decrease. The reactivity of cremaster muscle arterioles was tested in pentobarbital-anesthetized endotoxin-tolerant (ENDT-T) and nontolerant control rats. Tolerance was developed by sublethal intraperitoneal injections of Escherichia coli endotoxin for 4 days (n = 9). Controls received saline (n = 9). Mean arterial pressure (MAP), arteriolar diameter-response curves to topical norepinephrine (NE) (10-9M to 10-3M) and responses to 10-3M acetylcholine (ACh) were obtained as follows 1) at control, 2) following hemorrhage to 40 mmHg. 3) after uptake of 25% of bled volume with the remainder infused, and 4) at 240 min post-hemorrhage. The A1, A2, and A3 arterioles were constricted following hemorrhage in the ENDT-T group and in the saline group. After reinfusion and in late shock, vessel diameters remained constricted. MAP increased to control levels (106 +/- 5 and 101 +/- 4 mmHg, respectively) following re-infusion in both groups but in late shock it decreased until death in the nontolerant group and decreased only minimally (96 +/- 4 mmHg) in the ENDT-T group. The nontolerant group NE ED50 increased from pre-hemorrhage to late shock (p < .05). The ENDT-T group ED50 was unchanged. The bleeding volumes of the two groups were not different. The survival time of the nontolerant group was 234 +/- 36 min, whereas the ENDT-T group all survived and were sacrificed at 427 +/- 30 min. The response to endothelium-dependent ACH vasodilation in late shock was significantly reduced in the saline group but was unchanged in the ENDT-T group. Alpha 1 receptor activity was maintained in both groups. Alpha 2 receptor activity was attenuated pre-hemorrhage and at 240 min post-hemorrhage in ENDT-T rats. In late shock, alpha 2 receptor activity was attenuated in nontolerant rats. The development of endotoxin tolerance prevents the loss of arteriolar responsiveness to NE and ACh. ENDT-T rats have attenuated alpha 2 receptor activity but not alpha 1 receptor activity.

Acetylcholine↗

PubMed1994

In vitro femoral arterial responses to vasoconstrictor and vasodilator agents in endotoxin shock.

The hypothesis for this study is that the decreased arterial response to catecholamines may be due to the effect of endotoxemia on vessel tone. One control ring was taken from one femoral artery of a Wistar rat and after endotoxin (ENDT) infusion (i.v. 6 mg/kg-1 hr.), one ring was removed from the contralateral artery. The post-ENDT rings were tested in four groups which were determined by the mean arterial pressure (MAP) levels at the time of dissection: 100 mmHg (120 min), 80 mmHg (270 min), 60 mmHg (300 min) or 40 mmHg (330 min). KCl, phenylephrine (PHE) and arginine-vasopressin (AVP) dose-response curves (DR) were obtained at a preload of 500 mg which allowed the maximum response in control rings. When compared at 500 mg preload the maximal active response to all agonists post-ENDT was decreased by about 50%. By increasing the preload on the ENDT rings to 800 mg, the active tension became 2.49 times the active tension of the control rings. Length-tension experiments also showed a greater response for post-ENDT rings and a greater preload at maximum response but the ring circumference was the same. In contrast the in vivo femoral artery diameters at 90 min post-ENDT (100 mmHg) were 82.6% of control. Endothelium-dependent relaxation by acetylcholine (ACh) was abolished by ENDT but endothelium-independent relaxation to nitroprusside (NP) was not affected. It is concluded that the resting tone and active tension of femoral artery smooth muscle is increased by ENDT and the decreased in vivo responsiveness to vasoconstrictor agonists may be the result of vessel constriction due to loss of endothelium. The results also suggest that in vitro comparison of vessels in studies of endotoxin shock be done at the same muscle length rather than at the same preload.

Acetylcholine↗

PubMed1994

Attenuation of arteriolar alpha 2-adrenoceptor sensitivity during endotoxemia.

It is well documented that adrenergic responses after endotoxin (ENDT) administration are greatly reduced. The hypothesis of this study is that either alpha 1- or alpha 2-receptor activity is attenuated and the other receptor type is minimally affected during ENDT shock. Reactivity of the arterioles of left cremaster muscles of male Wistar rats anesthetized with pentobarbital sodium was studied using videomicroscopy. Femoral mean arterial pressure and first-, second-, third-, and fourth-order arteriolar diameters were measured. In group I, the decreases in arteriolar diameter and half-maximal effective dose (ED50) values with increasing phenylephrine concentration (alpha 1-adrenergic receptor agonist) were similar in all four branching orders before and after ENDT. In group II, the decreases in arteriolar diameter with increasing clonidine concentrations (alpha 2-adrenergic receptor agonist) were effectively attenuated by ENDT, and ED50 values were increased above control in all four branching orders. In group III, idazoxan (alpha 2-receptor antagonist) effectively blocked the vasoconstrictor effects of clonidine but did not affect the responses to phenylephrine before or after ENDT in all four arteriolar orders. In group IV, prazosin (alpha 1-adrenergic receptor antagonist) blocked the vasoconstrictor effects of phenylephrine before and after the administration of ENDT. However, vasoconstriction due to clonidine post-ENDT even at maximal dosage (10(-3) M), was greatly attenuated in all four branching orders as in group II. It is concluded that during endotoxemia the reduced adrenergic vasoconstrictor response of cremaster muscle arterioles is the result of attenuated activity of alpha 2-adrenergic receptors with minimal if any effects on alpha 1-adrenergic receptor activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Modification of vasopressin microvascular responses by endotoxin, endothelin, and nitric oxide.

The sensitivity of rat cremaster muscle arterioles to topically applied arginine vasopressin (AVP) is greatly increased by endotoxin (ENDT) [1]. The hypothesis is that the increase in vasoconstrictor sensitivity is in part due to modification of the AVP responses by endothelial compounds such as nitric oxide (NO) and endothelin. Reactivity of left cremaster muscle microvessels of pentobarbital anesthetized Sprague-Dawley rats was measured using videomicroscopy. Femoral arterial pressure as well as second and third order arteriolar (A2 and A3) vasoconstrictor threshold responses were determined for topical AVP (10(-15)-10(-6) M). These measurements were repeated in the presence of ENDT (6 mg/kg) alone and in the presence of the NO synthase inhibitor L-NAME (N omega-nitro-L-arginine methyl ester; 1 mg/kg) and ENDT (group 1). The control threshold (M)(-log) for arteriolar constriction by AVP was 9.4 +/- 0.7. After ENDT the threshold decreased significantly (P < 0.05) to 13.8 +/- 0.5, but returned to 9.0 +/- 0.5 after i.v. injected L-NAME. Acetylcholine (ACh) injected i.a. during AVP constriction significantly increased diameters at control and after ENDT, but not after L-NAME. In group 2 the AVP threshold was determined at control, after L-NAME plus hydroquinone (HQ), and at 30, 90, and 120 min post-ENDT in the presence of L-NAME + HQ. The AVP threshold at control was 9.0 +/- 0.3, after L-NAME 9.0 +/- 0.6, and after HQ 8.0 +/- 0.7. After L-NAME + HQ, the threshold was significantly increased to 7.3 +/- 0.2. After ENDT, in the presence of both antagonists, the threshold remained elevated at 7.4 +/- 0.2.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1993

Arteriolar endothelium-dependent vasodilation occurs during endotoxin shock.

Endotoxin shock has been reported to alter endothelial structure as well as function of large arteries from in vitro experiments. Cremaster muscle arteriolar dilator reactivity of pentobarbital-anesthetized rats was determined by videomicroscopy at control and 30, 90, 150, and 210 min after intravenous infusion of Escherichia coli endotoxin (6 mg/kg, 1-h period). The dilator response was tested by intra-arterial injections of 90 ng acetylcholine (ACh). At control A1, A2, and A3 arterioles dilated 45, 21, and 34%, respectively. Postendotoxin arterial pressure decreased progressively, the A1 arterioles constricted (P < 0.05), A2 diameters were unchanged and A3 diameters increased. Postendotoxin ACh dilations averaged 28, 23, and 25%. A1 dilation was significantly (P < 0.05) less than at control. Methylene blue (2.5 mg ia) attenuated the ACh response at control, but after endotoxin an intense downstream vasoconstriction resulted in stasis and reduced survival time occurred. Hydroquinone (HQ) partially blocked the responses to ACh postendotoxin. HQ significantly increased the survival time postendotoxin. It is evident postendotoxin that the endothelia of arterioles are functional and able to release nitric oxide (NO) throughout the entire survival period. The microvascular release of NO and the dilation response to ACh were substantially attenuated by methylene blue and HQ. The latter may block the more lethal effects of the inducible NO synthase.

Acetylcholine↗

PubMed1993

Effect of muscle length on the in vitro comparison of femoral arteries before and after endotoxin shock.

Control and endotoxin-treated femoral arteries were compared in vitro for the effect of muscle length. Rats were anesthetized with pentobarbital, and endotoxin (6 mg/kg) was infused for 1 h. A control ring before endotoxin treatment and a ring after endotoxin treatment (blood pressure = 40 mmHg) were excised from the contralateral artery for length-tension and dose-response experiments with phenylephrine. The initial length for resting tension (Li) was shorter for endotoxic rings (1.23 +/- 0.01 vs. 1.41 +/- 0.02 mm in control), but the length of maximum active tension (Lmax) was the same. In length-tension experiments the values for active tension (6.36 +/- 0.61 vs. 4.06 +/- 0.60 x 10(3) dyn/cm), preload at Lmax (1,333 +/- 204 vs. 733 +/- 146 mg), and passive stiffness were increased after endotoxin. In dose-response experiments at the same preload, the endotoxic rings had a lower active tension (3.28 +/- 0.28 vs. 6.55 +/- 0.27 x 10(3) dyn/cm) but the same sensitivity. At Lmax, active tension (12.45 +/- 0.48 vs. 5.01 +/- 0.89 x 10(3) dyn/cm in control vessels) and sensitivity (half-maximum effective dose = 0.68 +/- 0.8 x 10(-6) vs. 1.39 +/- 0.29 x 10(-6) M in control vessels) were greater for endotoxic rings. These experiments show that phenylephrine sensitivity and active tension in the rat femoral artery are increased by endotoxin shock, and the importance of muscle length is implied.

Animals↗

PubMed1993

Differences in arterial and arteriolar endothelial structure during endotoxin shock.

Previous studies of physiological and ultrastructural assessment changes in the walls of the femoral artery and A1, A2, and A3 arterioles in the rat cremaster muscle after infusion of Escherichia coli endotoxin (ENDT) (6 mg/kg-1 hr. period) indicate there may be a difference in the alteration of the endothelial structure of arteries and arterioles. Functionally, ENDT has been shown to abolish acetylcholine (ACh)-induced relaxation in the femoral artery [Zhou, PhD dissertation, University of South Florida, Tampa, 1992]. Dilations of A1 arterioles were shown to be reduced, but dilations of A2 and A3 arterioles were not significantly changed from control [Baker and Sutton, Am J Physiol, 264:H 1118-H 1123, 1993]. In the current study, ultrastructural evaluation of femoral arterial tissue post-ENDT at the mean arterial pressure (MAP) of 100 mm Hg revealed partially destroyed endothelial cells. The MAP decreased as the animal progressed into shock. At 80 mm Hg, 60 mm Hg and 40 mm Hg, essentially all endothelial cells were destroyed, with the internal elastic lamina denuded. In contrast, endotoxin damage in the A1, A2, and A3 arterioles was minimal even at a MAP of 40 mm Hg. Endothelial cells of A1 arterioles post-ENDT had more vacuoles than at control. Therefore, arteriolar endothelium was functionally and anatomically relatively undamaged, consequent to endotoxin administration, in contrast to femoral arteries where the endothelium was destroyed in a short time.

Animals↗

PubMed1993

Antagonism of acetylcholine and adenosine rat cremaster arteriolar vasodilation by combination of NO antagonists.

It has become evident that complete elimination of the vasodilator response to agonists that require the release of nitric oxide (NO) is necessary for certain studies of the microcirculation. The A2 and A3 arterioles of the rat cremaster muscle microcirculation were studied by video-microscopy. At control, arterioles at rest or constricted by arginine vasopressin (AVP) were dilated by intra-arterially injected acetylcholine (ACh), intra-arterially injected adenosine (ADO) and topical adenosine. The NO antagonists, Nw-nitro-L-arginine methyl ester (L-NAME) and hydroquinone (HQ), which acts as an antagonist by generating free radicals, in maximal doses, individually partially blocked the vasodilator actions of intra-arterial ACh and intra-arterial ADO. Combining L-NAME and HQ eliminated the vasodilation by intra-arterial ACh and intra-arterial ADO. Sodium nitroprusside dilated the arterioles to the resting level or above at control and in the presence of the antagonists either individually or when combined. However, the NO antagonists did not block the arteriolar vasodilator responses to topical ADO. The reduction of the production of NO and enhancement of its destruction by superoxide radicals results in the total absence of the vasodilator response due to intra-arterially injected acetylcholine and adenosine. The data suggest that luminal ADO receptors cause arteriolar dilation by endothelial-dependent mechanisms and abluminal receptors cause dilation by another mechanism.

Acetylcholine↗

PubMed1992

Endotoxin alteration of muscle microvascular renin-angiotensin responses.

Endotoxin decreases arteriolar sensitivity to norepinephrine and sympathetic neural activity, but vasopressin sensitivity is increased. Vascular responses to the renin-angiotensin system may also be altered by endotoxin (ENDT). Reactivity of cremaster muscle microvessels of pentobarbital anesthetized Wistar rats was studied using videomicroscopy. Escherichia coli endotoxin (6 mg/kg) was infused i.v. over a 1 hr period. Femoral arterial pressure (Pm) and arteriolar diameter changes, to i.a. bolus injections (60 ng) of angiotensin II (AII) were obtained in Group A at control and at 30 and 90 min post-ENDT, and in Group B at control, 30 min after continuous infusion of saralasin (10 micrograms/min/kg) began, and at 30 and 90 min post-endotoxin. In Group A, the control Pm was 106 +/- 4 mm Hg, and at 30 and 90 min post-ENDT was 96 +/- 4 and 89 +/- 7 mm Hg. All increased Pm 29 +/- 4% before ENDT but the increase was significantly less (P less than .05) at 7 +/- 1% and 6 +/- 1% 30 and 90 min post-ENDT. In Group B, the control Pm was 116 +/- 6 mm Hg, 103 +/- 5 after saralasin, 85 +/- 2 after ENDT infusion, and 83 +/- 4 and 63 +/- 8 mm Hg at 30 and 90 min post-ENDT. All increased Pm 34 +/- 7% before saralasin but only 5 +/- 2% (P less than .05) during saralasin infusion. In Group A, the A1 and A2 arterioles were constricted significantly more post-endotoxin by AII than during control. A3 arterioles post-endotoxin were constricted similar to control amounts by AII.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1990

Reduced microvascular adrenergic receptor activity due to opioids in endotoxin shock.

Arteriolar sensitivity to norepinephrine is decreased in endotoxin shock, and sympathetic activity appears altered. We have tested involvement of arteriolar opioid receptors in the response to endotoxin. Cremaster muscle arteriolar reactivity of anesthetized rats was studied using videomicroscopy. Escherichia coli endotoxin (6 mg/kg, i.v., LD100) was infused over a 1-hr period. Mean arterial pressure (Pm), frequency/diameter curves of A1, A2, and A3 arterioles to lumbar sympathetic nerve stimulation (1-16 Hz), and plasma velocity were obtained in group I at control, 30 min, and 90 min postendotoxin and in group II at control and during i.v. infusion of the opiate antagonist naltrexone (0.5 mg/kg/min) at 30 and 90 min postendotoxin. Frequency-diameter curves (percentage of control diameter) were significantly (P less than 0.05) shifted to the right postendotoxin in group I indicating reduced response to lumbar sympathetic stimulation or norepinephrine from the nerve terminals. In group II rats receiving naltrexone after endotoxin, the frequency-diameter curves were significantly (P less than 0.05) shifted to the left indicating enhanced vasoconstriction to lumbar sympathetic stimulation in comparison to control and to group I postendotoxin curves. Postendotoxin, Pm and plasma velocities decreased progressively in group I but were not changed from control in group II. Since opiate receptor blockade during endotoxin shock enhances adrenergic responses of arterioles, opiate receptor stimulation appears to suppress adrenergic receptors.

Animals↗

PubMed1990

Microvascular vasopressin effects during endotoxin shock in the rat.

We have demonstrated decreased microvascular sensitivity to norepinephrine during endotoxin shock possibly related to reduced sympathetic receptor activity (Baker et al.: Circ Shock 12:165-176, 1984). The response to other vascular controls such as arginine vasopressin (AVP) may also be altered. Reactivity of the left cremaster muscle microvessels of pentobarbital anesthetized Wistar rats was studied using videomicroscopy and videodensitometry. Femoral arterial pressure (Pm), dose response curves of vessel diameters to topical arginine vasopressin (10(-15) to 10(-6) M), FITC-albumin mean transit times, and plasma velocities were obtained. Escherichia coli endotoxin (6 mg/kg i.v., LD100) was infused over a 1-hr period. Parameter measurements were repeated at 30 min and 90 min post-endotoxin. Both Pm and plasma velocities progressively decreased. Arteriolar constriction and the mean transit times of FITC-labeled albumin progressively increased. The threshold dose for AVP averaged 10(-9) M at control and decreased to 10(-14) M post-endotoxin. Venular diameters were not altered by AVP. The AVP antagonist did not alter the microvascular diameter response to endotoxin but did block the responses to topical and endogenous AVP since arterial pressure and flow velocity decreased at a significantly greater rate than in rats without antagonist. Plasma AVP levels were significantly increased by endotoxin. Reduced alpha adrenergic sensitivity may unmask the responsiveness to AVP or increase the sensitivity of AVP receptors. Increased endogenous AVP may require a smaller exogenous concentration of AVP for constriction.

Animals↗

PubMed1989

Blood flow distribution with adrenergic and histaminergic antagonists.

Superficial fibular nerve stimulation (SFNS) causes increased pre- and post-capillary resistances as well as increased capillary permeability in the dog hind paw. These responses indicate possible adrenergic and histaminergic interactions. The distribution of blood flow between capillaries and arteriovenous anastomoses (AVA) may depend on the relative effects of these neural inputs. Right hind paws of anesthetized heparinized dogs were vascularly and neurally isolated and perfused with controlled pressure. Blood flow distribution was calculated from the venous recovery of 85Sr-labeled microspheres (15 microns). The mean transit times of 131I-albumin and 85Sr-labeled microspheres were calculated. The effects of adrenergic and histaminergic antagonists with and without SFNS were determined. Phentolamine blocked the entire response to SFNS. Prazosin attenuated increases in total and AVA resistance. Yohimbine prevented increased total resistance, attenuated the AVA resistance increase, and revealed a decrease in capillary circuit resistance. Pyrilamine attenuated total resistance increase while SFNS increased capillary and AVA resistances. Metiamide had no effect on blood flow distribution with SFNS. The increase in AVA resistance with SFNS apparently resulted from a combination of alpha 1 and alpha 2 receptor stimulation but not histaminergic effects.

Animals↗

PubMed1988

Adrenergic and histaminergic neural interactions in dog paws.

The mechanisms underlying the vascular responses of superficial fibular nerve stimulation (SFNS) have not been defined. Right hindpaws of anesthetized heparinized dogs were vascularly and neurally isolated, enclosed in a volume recorder, and perfused with controlled pressure. Vascular volume (VV) (131I-labeled albumin) and rate of tissue volume changes (VT) (plethysmography) were determined. SFNS increased blood flow resistance, reduced capillary filtration coefficient (CFC) and permeability-surface area product (PS) of 86Rb, increased VV, and reduced 131I-albumin recovery. VT increased at the rate of 3.35 +/- 0.45 ml/min. SFNS during terbutaline increased resistance, CFC, PS, and VV were unchanged, 131I-albumin recovery was complete, and VT increased at one-fourth the control rate. Phentolamine and yohimbine blocked all responses to SFNS. Prazosin with SFNS attenuated hemodynamic changes and VT increased to two-thirds of control, decreased VV, albumin, and Rb recovery but not PS and CFC. SFNS during pyrilamine maleate reduced VT increase to two-thirds of control rate and blocked decreases in PS and CFC. Metiamide did not change the SFNS responses, except to reduce vascular volume and VT. The combined histamine H1 and H2 blockers reduced VT increase to one-third of control and attenuated albumin loss, prevented histamine dilation, attenuated vasopressin and norepinephrine but not angiotensin constriction. SFNS stimulation increased precapillary resistance by alpha 1- and alpha 2-receptors and venous resistance by alpha 2-receptors and increased permeability by histamine release from endothelium.

Adrenergic alpha-Antagonists↗

PubMed1988

Microvascular responses of intact and adrenal medullectomized rats to hemorrhagic shock.

Evidence indicates that during the later stages of hemorrhagic shock there appears to be a loss of response to the control systems that would normally maintain an adequate peripheral resistance. Therefore, the reactivity of the cremaster muscle microcirculation of pentobarbital-anesthetized Wistar rats, intact and adrenal medullectomized, 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) and for hemorrhage of the rat. Following control measurements of Pm and microvessel diameters, cumulative dose-response curves of arteriolar and venular diameters to topical norepinephrine (NE) (10(-9) - 10(-4) M) were obtained. The protocols for intact and medullectomized groups were: 1) hypovolemic shock (shed blood not reinfused)--hemorrhage of 3.2 ml/100 g, compensation allowed, and NE dose-response curves repeated and obtained again during late shock as determined by Pm declining below 60 mmHg; and 2) normovolemic shock (condition after reinfusion of shed blood)--hemorrhage into a reservoir to Pm of 40 mmHg, maintenance at this level until 25% of the bled volume had been taken back (irreversible shock), and then reinfusion of the remainder of the blood. After blood reinfusion, the NE dose-response curves were repeated and obtained again during late shock, as determined by Pm below 60 mmHg. In all of the bled animals, the A1 arterioles were constricted posthemorrhage. The A2 arterioles were constricted only in the hypovolemic intact group. The A3 arterioles of all groups were not significantly changed from control. The constricted arterioles remained so. However, the other arterioles in all groups were unchanged during the several hours until death. The threshold concentration of NE for constriction of arterioles (10% or greater) was significantly increased (decreased sensitivity) during shock in all four groups. The response of the medullectomized rats to normovolemic shock was similar to that of the intact group, indicating that the circulating catecholamines were not essential. The response of medullectomized rats to hypovolemic shock was more severe and indicated the need for circulating catecholamines to compensate for the blood volume loss.

Adrenal Medulla↗

PubMed1986

Tibial nerve and deep fibular nerve effects on venous and extravascular volumes.

The innervation of the vasculature of the dog hindpaw separately controls the series and parallel coupled vessels by means of the tibial, deep fibular, and superficial fibular nerves. The latter primarily affects veins. The venous effects of the tibial and deep fibular nerves have not been adequately defined. The right hindpaw of anesthetized dogs was vascularly and neurally isolated in a volume recorder. The animals were heparinized and the preparation autoperfused (constant pressure). Total tissue volume changes were determined by the volume recorder. Total vascular volume changes were calculated from changes in paw 51Cr-red blood cell radioactivity measured by a scintillation detector. Arterial pressure and paw blood flow were monitored. The tibial and deep fibular nerves were each separately stimulated at 1, 5, and 15 Hz. Deep fibular nerve stimulations resulted in progressively significant increases in precapillary flow resistance. Vascular and tissue volumes decreased with stimulation frequency but vascular volume decreased significantly less than tissue volume change. Tibial nerve stimulation resulted in significant precapillary resistance increases. Vascular and tissue volumes decreased by similar amounts. Thus, deep fibular nerve stimulation causes passive decrease in venous volume, reduced capillary pressure, and fluid absorption. Tibial nerve stimulation causes active arterial and venous constriction maintaining capillary pressure with minimal fluid transfer.

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↗

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↗