Biomedical subjects

M P Lilly

Publications and source records attributed to M P Lilly.

At least 37 records · Page 2Linked to original sources

PubMed1994

Effect of surgery on the pituitary-adrenal response to repeated hemorrhage.

We studied the effect of surgery on hemorrhage-induced facilitation in the pituitary-adrenal system using repeated hemorrhage in chronically prepared dogs. Animals underwent splenectomy and adrenal venous and femoral arterial catheterization. Two (day 2) or five (day 5) days later, animals were anesthetized with pentobarbital, respired, and subjected to two periods of hypovolemia (20% hemorrhage with reinfusion of shed blood at 30 min; H1 and H2) separated by 90 min. Arterial and adrenal venous blood was sampled, and adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), angiotensin II (ANG II), cortisol, and cortisol secretion were measured. On day 2, cortisol secretion increased similarly after H1 and H2, despite a smaller response of ACTH to H2. On day 5, neither ACTH nor cortisol secretion changed after H1, but both increased significantly after H2. The adrenal sensitivity to ACTH increased after H2 on day 2 and was similar after H2 on both days. AVP and ANG II increased similarly after H1 and H2 on each day but had larger responses on day 2. These results suggest 1) either surgery or initial hemorrhage can lead to enhanced pituitary-adrenal responses to subsequent hemorrhage, 2) this effect may have both central and adrenal components, 3) negative feedback may inhibit enhanced responses of ACTH in this model, 4) changes in adrenal sensitivity to ACTH may not depend on an initial pituitary-adrenal response and may not be blocked by increased circulating corticosteroids, and 5) differences in circulating AVP or ANG II do not account for facilitation in pituitary-adrenal responses.

Adrenal Glands↗

PubMed1993

A circulating protein that depolarizes cells increases after hemorrhage in dogs.

Recent evidence suggests that a circulating factor or factors may mediate cell membrane depolarization after hemorrhage in rats. To test for the presence of a similar factor in dogs, conscious adult splenectomized dogs with chronic arterial cannulae were either (1) bled 30% of measured blood volume over 3 minutes (HEM, n = 8); (2) bled 30% of measured blood volume over 3 minutes and reinfused with the shed blood 10 minutes later (HEM + REINF, n = 6); or (3) observed without hemorrhage (CONTROL, n = 5). Treatments were applied in random order, 72 hours apart. Arterial blood was sampled at rest and for 1 hour. Depolarizing activity of the plasma was measured in an in vitro bioassay using resting dog RBCs and a membrane potential-sensitive oxonol dye (DIBAC). Fluorescence was measured by spectrofluorometry and the percentage of change from resting values was calculated. Fluorescence intensity increased after hemorrhage in the HEM and the HEM + REINF groups. Fluorescence intensity decreased to CONTROL values in the HEM + REINF group by 10 minutes after reinfusion of shed blood, but remained greater than CONTROL values in the HEM group. The magnitude of early cell membrane depolarization was approximately 20 mV. Similar depolarization was observed in cultured canine skeletal myocytes and pre-adipocytes. Changes in fluorescence intensity correlated with changes in mean arterial pressure at all times after hemorrhage except at 15 minutes (5 minutes after reinfusion in the HEM + REINF group). The depolarizing activity in dog plasma after hemorrhage shares several physical chemical properties with a similar substance identified in rats after hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Ouabain is secreted by the adrenal gland in awake dogs.

Ouabain has been identified in the plasma and adrenal glands of several mammals, including humans. To investigate possible adrenal secretion of ouabain in vivo, at rest, and in response to acute blood volume changes, we prepared trained adult dogs (n = 10) with splenectomy and unilateral adrenal venous (AV) cannulation. Two days later, after an overnight fast, dogs had either 1) 20% hemorrhage (hem) or 2) 20% blood volume expansion (exp; 6% Dextran 70, 0.9% NaCl) in random order. In AV and arterial plasma (ART), ouabain was measured by a ouabain-specific immunoassay, and cortisol and aldosterone were measured by radioimmunoassay. ART and AV ouabain concentration did not change after hem or exp [P = not significant (NS)]. In 94 of 97 paired samples, the concentration of ouabain in AV was greater than that in ART (Wilcoxon, P < 0.001), and the mean ouabain concentration was greater in AV (756.4 +/- 85.7 pmol/l) than ART (235.4 +/- 18.5 pmol/l; P < 0.001). The mean AV-to-ART ouabain concentration ratio was 5.7 +/- 1.29. Adrenal secretion of ouabain was not influenced by hem or exp (analysis of variance, P = NS). Adrenal secretion of cortisol and aldosterone increased after hem (P < 0.05) and was unaltered by exp (P = NS). This study demonstrates that ouabain is secreted by the adrenal gland in the awake dog. However, adrenal ouabain secretion and arterial blood ouabain are not altered by acute hem or exp.

Adrenal Glands↗

PubMed1992

The hypothalamic-pituitary-adrenal-immune axis. A critical assessment.

The hypothalamic-pituitary-adrenal (HPA) system has been a model for neuroendocrine control of responses of organisms to stressors since the turn of the century. Despite this, the pathways by which infectious insults interact with the HPA system remained poorly defined. Recently, evidence has been presented suggesting that humoral mediators released by inflammatory cells (cytokines) may participate in two-way communication between the site of inflammation and the central nervous system. In this review, we detail the current understanding of the responses of the HPA system to the classic physiologic stimuli of hypovolemia and pain, with an emphasis on the cellular mechanisms and mediators discovered in recent years. We also examine the data substantiating a role of interleukin 1, interleukin 6, and tumor necrosis factor in the direct humoral activation of the HPA system and consider the evidence favoring a physiologic negative feedback relationship between the HPA and the immune systems. Such as interaction is an exciting concept with broad clinical implications. However, we believe that the temporal and quantitative aspects of experiments designed to evaluate this interaction must be carefully evaluated to assure that true physiologic stimuli are studied and that the responses observed are not due to pharmacologic effects of inflammatory mediators acting through "classic" neuroendocrine pathways.

Afferent Pathways↗

PubMed1992

Saline resuscitation after fixed-volume hemorrhage. Role of resuscitation volume and rate of infusion.

The authors have reported previously that small-volume resuscitation (1.8 x bled volume) with 0.9% NaCl restores blood volume and attenuates hormonal responses after large hemorrhage without correction of arterial hypotension. The authors studied the role of rate of infusion in this observation in chronically prepared dogs (aortic flow probe, right atrial pressure and volume, and arterial catheters) after 30% hemorrhage (24.1 +/- 0.4 mL/kg). After 30 minutes, subjects were observed either without treatment (no resuscitation) or with infusion of 43 mL/kg 0.9% NaCl over 3 hours by one of three protocols: (1) impulse infusion over 10 minutes, (2) variable rate infusion, bolus with tapering infusion, or (3) constant rate infusion. Significant improvement in cardiac output and in blood volume and significant decreases of vasopressin and arterial catecholamines were observed in all fluid-treated groups. This benefit was relatively independent of rate of infusion, although impulse infusion produced greater early improvement, which dissipated with time, and constant rate infusion produced better late results. In none of the fluid-treated groups were these improvements reflected in improved mean arterial pressure compared with the no resuscitation group. The authors conclude that small-volume, slow-rate saline infusion produces physiologic benefits that cannot be assessed by easily measured clinical parameters. Thus, early resuscitation after trauma could aid patients even if arterial pressure is unchanged. This benefit might be even greater in patients with uncontrolled bleeding because arterial pressure, and hence bleeding, may not be increased by resuscitation of this type. A reassessment of the value of prehospital fluid resuscitation in the injured patient is warranted.

Animals↗

PubMed1992

Jugular venous vasopressin increases during carotid endarterectomy after cerebral reperfusion.

Several recent reports have suggested that pressor hormones may be released during and after carotid endarterectomy and that release of these factors may be associated with postoperative hypertension and other postoperative morbidity. We measured vasopressin, adrenocorticotropic hormone, and cortisol in jugular venous blood during carotid endarterectomy under general anesthesia in 43 patients with routine carotid shunting. Jugular venous vasopressin increased significantly after the second period of carotid occlusion for shunt removal and remained increased at closure. Vasopressin did not change during the initial carotid occlusion for shunt placement or during the endarterectomy itself, and neither ACTH nor cortisol changed at any sample time. Greater resting vasopressin and cortisol and larger responses of vasopressin were observed in patients receiving phenylephrine to correct intraoperative hypotension. There were no correlations between postoperative hypertension or postoperative complications and intraoperative hormone values. These results suggest (1) basal intraoperative vasopressin values reflect the blood volume of the patient, (2) increased vasopressin was not related to postoperative morbidity, and (3) intraoperative increases in pressor hormones are most likely physiologic responses to specific stimuli such as hypovolemia or hypotension rather than pathologic phenomena. We speculate that the increase of vasopressin after the second carotid occlusion and reperfusion of the brain may be due to the action of humoral factors released into the carotid circulation from the endarterectomy site.

Aged↗

PubMed1991

Interaction of sodium and volume in fluid resuscitation after hemorrhage.

Some measures of the efficacy of fluid resuscitation after hemorrhage are blood volume restitution (BVR) and attenuation of the neuroendocrine response. We compared the effectiveness of resuscitation with 0.9% NaCl and 3.0% NaCl in chronically prepared awake dogs after 30% hemorrhage. Each dog was bled on four occasions and resuscitated by four protocols: 1) full resuscitation (infusion to return and maintain mean arterial pressure (MAP) at control +/- 10 mm Hg) with 3.0% NaCl (HS); 2) full resuscitation with 0.9% NaCl (NS); 3) under-resuscitation with a volume of 0.9% NaCl equal to the subject's previous 3.0% NaCl requirement (SV); and 4) no fluid therapy (NR). Approximately three times more volume was needed to restore MAP with NS vs. HS, and thus the amount of Na administered was not different in these groups. Net volume balance was positive in the NS and SV groups but negative in the HS group due to marked saline diuresis. Net Na balance was positive in all three fluid-treated groups, but significantly higher in the HS group (p less than 0.01). MAP remained below baseline in the SV and NR groups (p less than 0.05). BVR exceeded 100% in NS and HS early in resuscitation, but BVR was not sustained in the HS group. Total plasma protein increased in all three fluid treated groups. Responses of all hormones were completely attenuated in the NS group. ACTH, cortisol, and AVP responses were promptly attenuated in the HS group, but remained greater than control. In the SV group, all hormone levels except renin returned to control values, but more slowly than the other groups. ACTH and cortisol correlated best with BVR; AVP, PRA, and aldosterone correlated with MAP restoration. In summary, resuscitation with either HS or NS can achieve similar MAP restoration. Hypertonic saline produces a more rapid increase in BVR and MAP, but the BVR improvement is transient. Resuscitation with HS incurs an intracellular water debt which is aggravated by a saline diuresis. Hormonal attenuation is linked either to BVR (ACTH, cortisol) or to MAP restoration (renin, AVP). Thus the optimal resuscitation regimen may consist of initial infusion of hypertonic saline followed by sufficient hypotonic solution to restore interstitial fluid volume and normal cellular hydration.

Adrenocorticotropic Hormone↗

PubMed1991

Selection of the approach to the distal internal carotid artery from the second cervical vertebra to the base of the skull.

Although several approaches for exposure of distal internal carotid artery lesions have been reported, the precise anatomic levels for which each of these maneuvers are most appropriate have not been well described. Since these techniques may require preoperative preparation, it is useful to determine in advance how much exposure will be needed and to select the most suitable and effective technique. We used anatomic dissection in 12 human cadaver specimens (24 carotid bifurcations) to define the limits of distal internal carotid artery exposure by several commonly advocated methods. The standard anterior approach along the sternocleidomastoid muscle allowed exposure of the internal carotid artery to the level of the upper one third of the second cervical vertebra. The upper limit of this exposure was extended to the middle of the first cervical vertebra by division of the posterior belly of the digastric muscle. Anterior subluxation of the mandible increased the distal exposure of the internal carotid artery to the superior border of the first cervical vertebra. Styloidectomy in combination with the preceding maneuvers extended the exposure an additional 0.5 cm cephalad. Lateral mandibulotomy did not significantly extend exposure beyond that obtained with mandibular subluxation and styloidectomy. Exposure of the internal carotid artery in the 1 cm immediately below the base of the skull required a posterior approach with mastoidectomy.

Adult↗

PubMed1990

Anatomic and clinical factors associated with complications of transfemoral arteriography.

Complications of transfemoral arteriography requiring surgery are rare but carry significant morbidity. To evaluate clinical factors that might relate to such complications, we retrospectively reviewed our experience from January 1, 1985, to December 31, 1988 (four years). Forty-seven complications requiring surgery occurred among 10,589 cases. The risk was higher after cardiac catheterization than after peripheral arteriography (0.55% versus 0.17%, p less than 0.025). In nearly 40% of these cases, arterial puncture was not in the common femoral artery. Acute bleeding complications were more likely among patients with puncture outside the common femoral artery (p less than 0.001). Older patients and women were at slightly higher risk for complications requiring surgery, but this difference was not statistically significant. The frequency of bleeding complications was not significantly higher among patients who were anticoagulated following the procedure. The distribution of puncture sites was identical in obese and nonobese patients. Three patients died (two from myocardial infarction, one from multisystem organ failure). Two limbs did not improve; one required major amputation. Four limbs had persistent paresthesia and two had persistent weakness. We conclude that complications of transfemoral arteriography requiring surgery occur more frequently among patients who are undergoing cardiac catheterization and who suffer aberrant punctures. Age, sex, body habitus, and anticoagulation have less impact on patient risk.

Age Factors↗

PubMed1990

The role of sclerotherapy as an adjunct to Unna's boot for treating venous ulcers: a prospective study.

Ankle ulcers associated with venous disease have been traditionally treated by Unna's compressive bandages. However, successful healing of an ulcer with this therapeutic modality is slow and tedious. The purpose of this study is to investigate whether adjunctive sclerotherapy of large venous channels near the ulcers enhances healing. Twenty-eight patients with perimalleolar venous ulceration were entered into this study. Ulcer size ranged from 6.0 to 25 cm2. All were examined for the presence of large venous channels adjacent to the ulcer bed. A portable continuous-wave Doppler supplemented digital examination of the area. Twenty-five out of 28 patients had easily detectable venous channels, and these were randomized into two groups: group I, treated by weekly changes of Unna's compressive boots; group II, treated by weekly change of Unna's compressive boots and sclerotherapy with 3% sodium tetradecyl sulfate (Sotradecol). All patients had the size of the ulcer measured during their weekly visits. Patients in group II took a mean of 2.1 weeks to exhibit 50% healing and 4.3 weeks to fully heal. Conversely patients in group I took a mean of 3.2 weeks to achieve 50% healing and 6.1 weeks to fully heal. Thus, healing was significantly faster (p less than 0.05) in group II. In conclusion, the therapeutic efficiency of Unna's compressive bandaging is significantly enhanced by the adjunctive sclerotherapy of adjacent venous channels.

Adult↗

PubMed1989

Collagen types and matrix protein content in human abdominal aortic aneurysms.

Deficiencies of total collagen, type III collagen, and elastin have been proposed to explain aneurysm formation. Infrarenal aortas were collected from 19 patients (age 70 +/- 7 years) undergoing operative repair of abdominal aortic aneurysms (diameter 7 +/- 2 cm) and from 13 autopsies (age 63 +/- 17 years) of patients without aneurysm disease (controls). Wall thickness and collagen and elastin concentration were determined in full-thickness aorta. Collagen types I and III were measured after digestion with cyanogen bromide, which solubilized nearly 90% of total collagen for typing. Cyanogen bromide peptides were separated by sequential carboxymethylcellulose and agarose chromatography and quantified by peak area measurement with computerized image analysis. Histologic examination revealed prominent inflammatory cell infiltration and deficient, fragmented elastin in the aneurysms. Aortic wall thickness was similar in aneurysms and in control specimens. In the aneurysms, collagen was increased (37% +/- 16% vs 24% +/- 5%; p less than 0.05) and elastin was decreased (1% +/- 1% vs 12% +/- 7%; p less than 0.001), expressed as a percentage of delipidized, decalcified dry weight. Collagen type I accounted for 74% +/- 4% of aneurysm and 73% +/- 4% of control collagen solubilized for typing, and collagen type III accounted for 26% +/- 4% of aneurysm and 27% +/- 4% of control collagen solubilized for typing. Neither patients with a family history of aneurysms nor those without a history of aneurysms had collagen type III deficiency. Atherosclerotic abdominal aortic aneurysms are associated with an inflammatory process and may result from elastin degradation and not a deficiency of type III collagen.

Aged↗

PubMed1989

Duplex ultrasound measurement of changes in mesenteric flow velocity with pharmacologic and physiologic alteration of intestinal blood flow in man.

Duplex ultrasound scanning has been used to assess mesenteric blood flow in normal and disease states. To investigate this technique we studied nine normal volunteers at rest and under conditions known to modify intestinal blood flow. After a baseline mesenteric duplex scan, each subject was given one of three treatments in random order: (1) test meal (710 kcal), (2) intravenous glucagon (40 micrograms/min), or (3) intravenous vasopressin (0.2 units/min). Peak systolic and diastolic velocities and vessel diameters were measured at intervals after treatment in the celiac and the superior mesenteric arteries (SMAs) and the right common carotid artery. Resting velocities did not differ among the groups. Peak systolic velocity increased significantly in both celiac and SMAs after the meal, with maximal changes in the celiac artery preceding those in the SMA in most subjects. Early diastolic flow reversal in the SMA was consistently lost after the meal (eight of nine subjects). Velocity changes after glucagon closely paralleled those after the meal. Vasopressin produced significant decreases in peak systolic velocity in both visceral vessels. No changes in vessel diameter were noted after any treatment. Coefficient of variation for repeated measures of peak velocities was 19% in the celiac and 12% to 16% in the SMA and the common carotid. The coefficient of variation for repeated measurements of arterial diameter was 6% to 8% in the SMA and 11% in the celiac artery. Clinically relevant changes in mesenteric hemodynamics can be reproducibly detected and quantitated by means of current duplex ultrasound technology. The similarities between the visceral arterial responses to a meal and glucagon are of interest.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Potentiated cortisol response to paired hemorrhage: role of angiotensin and vasopressin.

Potentiated adrenocorticotropin (ACTH) and cortisol responses occur after the second of two small hemorrhages (hems) spaced 24 h apart in the dog. To test whether increased responses of other hormones might be associated with this effect, we examined plasma renin activity (PRA), angiotensin II (ANG II), and vasopressin after paired 10% hem (H1 and H2) spaced 5 h apart in chronically prepared conscious dogs. Cortisol secretion increased after each hem, and the response to H2 was larger (P less than 0.05; H1 peak at 6.8 +/- 1.3 micrograms/min vs. H2 peak at 18.3 +/- 5.3 micrograms/min). ACTH did not change after H1 but increased after H2, and the H2 response was larger (P less than 0.01). Vasopressin increased after each hem, and the H2 response was larger (P less than 0.01). The time courses of ACTH and vasopressin responses were similar after H2 (significant increases by 8 min). PRA and ANG II increased by 4 min after each hem, and although the difference was small the early PRA and ANG II responses were greater after H2. Blood volume and hem volume did not differ between hems. Hemodynamic responses to the hems were not different. We conclude that, although the PRA and ANG II respond rapidly enough after hem to influence pituitary responses, the slightly greater responses of these factors to H2 are not responsible for greatly increased pituitary-adrenal responses to H2. On the other hand, the markedly potentiated vasopressin response to H2, which parallels that of ACTH, suggests that vasopressin may mediate the increased ACTH responses to H2.

Adrenocorticotropic Hormone↗

PubMed1989

Aldosterone secretion following non-hypotensive hemorrhage is potentiated by prior blood loss.

Aldosterone is a major regulator of fluid and electrolyte balance after hemorrhage and is released from the adrenal cortex by the action of adrenocorticotropin (ACTH) and angiotensin II (AII). Past work has shown that the hemorrhage-induced release of ACTH and cortisol is potentiated by prior hemorrhage. We therefore studied the response of adrenal aldosterone secretion to repeated hemorrhage and its control by ACTH and AII. Six awake dogs with chronic lumboadrenal vein catheters were bled 10% of measured blood volume (H1) with reinfusion at 30 minutes. The hemorrhage was repeated 5 hours later (H2). Adrenal presentation rates for AII (AII-PR) and ACTH (ACTH-PR) were calculated for each sample. Control hormonal and hemodynamic parameters before each hemorrhage were not different; hemodynamic responses to H1 and H2 did not differ. Aldosterone secretion increased significantly after each hemorrhage. The increase in aldosterone secretion after H1 was associated with an early increase in AII-PR and late increase in ACTH-PR. Aldosterone secretion following H2 was greater than that following H1 and was associated with early and larger responses of AII-PR and ACTH-PR. Aldosterone secretion following H1 correlated with the AII-PR (r = 0.75; p less than 0.001), but not with the ACTH-PR. In contrast, aldosterone secretion following H2 correlated with both the AII-PR (r = 0.54; p less than 0.01) and ACTH-PR (r = 0.71; p less than 0.001) and multiple regression analysis showed a highly significant relation with both AII and ACTH (r = 0.81; p less than 0.001). The data suggest that aldosterone secretion after initial small hemorrhage occurs as a result of increased AII, whereas both AII and ACTH may contribute to the larger aldosterone secretory response to H2. Since major trauma commonly involves at least two insults separated in time (e.g., injury followed by surgery), potentiated responses of aldosterone and other pituitary-adrenal hormones (ACTH, vasopressin, and cortisol) may have important implications for the control of fluid and electrolyte balance and metabolism in injured patients.

Adrenal Glands↗

PubMed1988

The effect of distal arterial anatomy on the success of popliteal aneurysm repair.

The success of bypass grafting for popliteal aneurysms may be compromised by the natural history of these lesions. During a 9-year period 35 patients had repair of 48 popliteal aneurysms. Elective repair was performed in 26 limbs and the remaining 22 limbs required urgent or emergent treatment after aneurysm thrombosis (16) or embolic digital ischemia (six). Retrospective review of preoperative and intraoperative arteriograms and CT or ultrasound scans was done to define the relationship of distal runoff anatomy to initial symptoms and long-term grafting success during a mean follow-up of 48 months. Only five of 48 limbs (10%) had three continuous tibial vessels and a patent pedal arch. Twenty-six limbs (55%) had one or no named calf vessels and 11 limbs had incomplete pedal arches. When thrombosis or symptomatic embolism occurred, the anatomy was significantly worse; 15 of 22 such limbs (68%) had one or no patent tibial vessels and seven had incomplete pedal arches. Nineteen of 28 aneurysms examined by CT or ultrasound scanning showed intraluminal thrombus. Eight of 13 patent aneurysms with intraluminal thrombus had one or no patent tibial vessels. The 5-year graft patency rate was 74% for the entire study group. Bypass for repair of asymptomatic aneurysms had a patency rate of 91% at 5 years vs 54% for symptomatic patients (p less than 0.05). Patients with popliteal aneurysms often have advanced tibial disease that appears worse in those with symptoms. The occurrence of a patent popliteal aneurysm with intraluminal thrombus and advanced runoff disease suggests that chronic microembolism may be an etiologic factor in the tibial disease observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Potentiated hormonal responses in a model of traumatic injury.

Although major trauma often involves repeated insults, few studies have examined the endocrine response to repeated injury. In earlier work, we described potentiated responses of circulating adrenocorticotropin (ACTH) and adrenal secretion of cortisol, epinephrine, and norepinephrine to the second of two small hemorrhages separated by 24 hr. To investigate the response of other hormones to repeated hemorrhage and to examine possible hormonal interactions in a shorter, more clinically relevant time frame, we placed chronic adrenal vein cannulas in eight splenectomized, trained dogs. Each animal was bled 10% of measured blood volume with reinfusion of shed blood at 30 min. The hemorrhage was repeated 5 hr later. Initial hemorrhage led to a small but significant increase in adrenal cortisol secretion and circulating ACTH, vasopressin (AVP), angiotensin II (AII), and plasma renin activity (PRA). Although a 5-hr time interval between stimuli is commonly thought to lead to cortisol feedback, the circulating ACTH and adrenal cortisol secretory responses to the second hemorrhage were exaggerated in comparison to their initial responses. Similarly, the AVP response to the second hemorrhage was also increased. In contrast, the responses of PRA and AII to the second hemorrhage were not greater than their responses to the initial hemorrhage. No differences in measured blood volume before each hemorrhage or in the heart rate and arterial pressure responses to hemorrhage were observed that could explain the potentiated hormonal responses. Thus, potentiated responses of cortisol, ACTH, and AVP, but not of PRA and AII, were observed in a model of trauma that emphasizes repeated injury in a clinically relevant time frame.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗

PubMed1987

Intraoperative evaluation of PTFE, Dacron and autogenous vein as carotid patch materials.

Between 1983 and 1986 we prospectively randomized 71 consecutive carotid endarterectomy patients to receive patch closure with one of three materials. Autogenous saphenous vein was used in 18 cases, Dacron velour (Sauvage Filamentous) in 30 cases, and PTFE (Gore-Tex CV patch) was used in 23 cases. Blood loss in the excess of 300 ml was seen in 43% (10/23) of the PTFE group in contrast to only 22% (5/23) of the ASV group and 17% (4/23) of the Dacron group. Persistent suture hole bleeding requiring the use of a significantly larger amount of oxidized cellulose (p less than .001) was noted in the PTFE group. Operating time from clamp release to end of procedure was significantly greater in the PTFE group (p less than .05), reflecting the delay associated with suture hole bleeding. In addition, the handling characteristics of PTFE were inferior to those of Dacron or autogenous saphenous vein. Needle penetration was relatively difficult. PTFE was thicker, less flexible, and a less satisfactory match to the endarterectomized carotid than the other materials.

Carotid Arteries↗

PubMed1987

Comparison of corticotropin-releasing factor and acetylcholine on catecholamine secretion in dogs.

To test whether corticotropin-releasing factor (CRF) is a secretagogue for adrenal secretion of catecholamines, a preparation was developed that permits measurement of adrenal venous output in response to in vivo arterial injection into the dog adrenal gland. Dogs were prepared with catheters in the lumboadrenal vein for monitoring adrenal blood flow and secretion rate of epinephrine and norepinephrine and in the lumboadrenal and inferior phrenic arteries for adrenal injection. Under pentobarbital anesthesia 48 h after surgery, dogs received a series of intra-adrenal injections that included acetylcholine (0.2-200 nmol), CRF (2.0-20.0 nmol), and diluent. There was a log dose-response relationship before epinephrine secretion and norepinephrine secretion to acetylcholine. Adrenal injection of CRF stimulated epinephrine and norepinephrine secretion at the highest dose tested (20 nmol). The response observed was equivalent to the response to 0.2 nmol acetylcholine. A similar dose of CRF given systemically produced hypotension without stimulating catecholamine responses. Adrenal catecholamine responses to acetylcholine were not augmented by addition of CRF. These findings show that arterial injection of CRF into the intact dog adrenal stimulates secretion of epinephrine and norepinephrine. However, the low potency of CRF relative to that of acetylcholine, the lack of a synergistic effect of CRF on catecholamine responses to acetylcholine, and the high dose of CRF required to achieve a response suggest that CRF does not function in the adrenal medulla as a physiologically important secretagogue for catecholamines.

Acetylcholine↗