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Biomedical subjects

H B Bittner

Publications and source records attributed to H B Bittner.

50 records · Page 3Linked to original sources
PubMed1996

Hormonal and hemodynamic changes in a validated animal model of brain death.

OBJECTIVE: To examine the hormonal and hemodynamic changes in a validated animal model of brain death. DESIGN: Prospective, controlled study. SETTING: Experimental research laboratory. SUBJECTS: Adult male mongrel dogs (n = 10). INTERVENTIONS: Brain death was induced by inflation of a subdural balloon in ten mongrel dogs weighing 23 to 30 kg and validated neuropathologically. The hearts were instrumented with micromanometers and ultrasonic flow probes to measure cardiovascular changes. No inotropic or vasoactive support was given. Hemodynamic stability was maintained with intravenous fluids. Blood samples and hemodynamic readings were collected before and after the induction of brain death. MEASUREMENTS AND MAIN RESULTS: A Cushing reflex, followed by a hyperdynamic response and diabetes insipidus, occurred in every animal following brain death. Mean arterial pressure, heart rate, contractility, and cardiac output increased to > 350 mm Hg, 230 beats/min, 4200 mm Hg/sec, and 2.8 L/min, respectively, at the peak of this phenomenon before returning to baseline. A plasma catecholamine surge was observed in every animal 15 mins after brain death, while the circulating concentrations of the pituitary gland hormones vasopressin and adrenocorticotrophic hormone decreased significantly after 15 and 45 mins of brain death, respectively, and continued to decrease throughout the experiments. Circulating triiodothyronine, thyroxine, and glucagon concentrations decreased significantly (p < .01) from 0.58 +/- 0.05 ng/mL, 2.20 +/- 0.15 micrograms/dL, and 49.7 +/- 9.1 pg/mL, respectively, to 0.34 +/- 0.03 ng/mL, 1.14 +/- 1.14 micrograms/dL, and 6.9 +/- 1.4 pg/mL, respectively, 420 mins after brain death. The hematocrit increased significantly 15 mins after brain death and then gradually decreased throughout the duration of the experiments. CONCLUSIONS: In a validated animal model of brain death, significant decreases in the circulating concentrations of stress hormones, as well as hemodynamic instability, occurred after brain death. Measurements of plasma adrenocorticotrophic hormone and vasopressin values may be useful as diagnostic predictors of brain death. Furthermore, the observed changes may contribute to organ dysfunction after brain death and may necessitate hormonal as well as inotropic and vasoactive support to maintain donor organ function in the clinical setting.

Adrenocorticotropic Hormone↗
PubMed1996

The combined effects of brain death and cardiac graft preservation on cardiopulmonary hemodynamics and function before and after subsequent heart transplantation.

BACKGROUND: The combined effects of brain death and graft preservation on right and left ventricular function and on pulmonary hemodynamics after subsequent heart transplantation have not been previously studied. METHODS: Fifty-seven dogs (25.5 +/- 0.3 kg) were divided into three groups and underwent a total of 20 brain death experiments and 16 orthotopic complete atrioventricular transplantations with the use of a validated brain death organ donor model, hypothermic heart preservation, and right and left ventricular functional analysis (preload-independent recruitable stroke work, Fourier analysis). In the first group, changes in cardiopulmonary function were assessed over a period of 6 to 7 hours after brain death. In the second group, the hearts were procured from a donor with brain death and immediately transplanted whereas in the third group cardiac graft preservation for a period of 4 hours followed harvest from a donor with brain death before heart transplantation and assessment of heart transplant function. RESULTS: After brain death alone, a significant increase in right and left ventricular end-diastolic pressures and a decrease in systemic and pulmonary resistance and pulmonary impedance occurred. Furthermore, right and left ventricular function decreased significantly by 35% and 19%, respectively, and subsequent transplantation did not cause further cardiac dysfunction. Preservation in combination with brain death led to further significant decreases in right ventricular function after subsequent transplantation compared with brain death alone, necessitating the use of dopamine to wean four animals from cardiopulmonary bypass. CONCLUSION: Brain death causes a significant loss of right and left ventricular function. These injuries are greater in the right ventricle and may contribute to early right ventricular failure after transplantation. Brain death and cardiac graft preservation have significantly additive deleterious effects on right ventricular function after transplantation.

Animals↗
PubMed1995

Myocardial beta-adrenergic receptor function and high-energy phosphates in brain death--related cardiac dysfunction.

BACKGROUND: Cardiac failure remains an important problem after heart transplantation and may be associated with events that occur during brain death (BD) before transplantation. In this study, cardiac function is studied after BD, and biochemical evaluation of myocardial high-energy phosphates and the beta-adrenergic receptor system is presented. METHODS AND RESULTS: The hearts of 17 mongrel dogs (23 to 31 kg) were instrumented with flow probes, micromanometers, and ultrasonic dimension transducers to measure ventricular pressure and volume relationships. In a validated canine BD model, systolic right and left ventricular (RV/LV) function was analyzed by load-insensitive measurements during caval occlusion (preload-recruitable stroke work, PRSW). The beta-adrenergic receptor (BAR) density, adenylate cyclase (AC) activity, and myocardial ATP and creatine phosphate (CP) were measured before and 6 to 7 hours after BD. Results are expressed as mean +/- SEM (*P < .05 versus baseline, paired two-tailed Student's t test). Myocardial function deteriorated significantly from baseline PRSW (RV, 22 +/- 1 erg x 10(3); LV, 75 +/- 4 erg x 10(3)) by 37 +/- 10% for the RV (P < .001) and 22 +/- 7% for the LV (P < .001). BAR density increased from 282 +/- 42 to 568 +/- 173 fmol/mg for the RV and from 291 +/- 64 to 353 +/- 56 fmol/mg for the LV. Isoproterenol-stimulated AC activity was also significantly enhanced after BD. ATP and CP, however, remained unchanged after BD compared with baseline values before BD. CONCLUSIONS: BD causes significant systolic biventricular dysfunction. The loss of ventricular function after BD was more prominent in the right ventricle and may contribute to early postoperative RV failure in the recipient. These injuries occurred despite BAR system upregulation after BD. Global myocardial ischemia is unlikely, since ATP and CP remained normal before and after BD.

Adenosine Triphosphate↗
PubMed1995

Complete atrioventricular cardiac transplantation: improved performance compared with the standard technique.

BACKGROUND: There has been renewed clinical interest in an alternative technique to orthotopic cardiac transplantation involving six anastomoses: left pulmonary veins, right pulmonary veins, inferior vena cava, pulmonary artery, aorta, and superior vena cava (complete technique). In this study, the results of the complete technique are compared with those of the standard operation (ventricular transplantation with atrioplasty). METHODS: Dogs were used for ten acute standard and ten acute complete atrioventricular transplantations. There were no significant differences in the baseline cardiac function (preload-independent right and left ventricular recruitable stroke work), bypass times, and cardiac ischemic times between the two groups. RESULTS: After transplantation, sinus rhythm was preserved after all ten complete and after only one standard transplantation but no significant hemodynamic differences were observed. The right and left ventricular preload-independent recruitable stroke work in the complete group and the left ventricular preload-independent recruitable stroke work in the standard group were conserved after transplantation, but the right ventricular preload-independent recruitable stroke work decreased by 39% +/- 8% (p < 0.05) in the standard group. There was also a significant decrease in the rate of biventricular filling in the standard group after transplantation. CONCLUSIONS: Complete atrioventricular transplantation is a feasible alternative technique and conserves normal sinus rhythm. The ischemic and bypass times are comparable for both methods. The insignificant change in the rate of biventricular filling in the dogs undergoing the complete technique indicates right and left ventricular diastolic function may be conserved after transplantation.

Animals↗
PubMed1995

Endocrine changes and metabolic responses in a validated canine brain death model.

PURPOSE: Endocrinologic and metabolic changes after brain death (BD) have not yet been investigated in a validated animal model. Therefore, the effects of BD on hormonal and metabolic function were studied in 10 dogs (23 to 31 kg). METHODS: BD was induced by intracranial pressure increase and validated neuropathologically. Plasma concentrations of pituitary, thyroid, adrenal, and pancreatic hormones were measured pre/post BD. The results are expressed as mean (+/- SEM). RESULTS: A Cushing reflex and diabetes insipidus occurred after BD. Elevated catecholamine levels were documented after 15 minutes whereas the pituitary gland hormones vasopressin and adrenocorticotrophic hormone (ACTH) decreased significantly after 15 and 45 minutes of BD respectively. Thyroxine, triiodothyronine, and glucagon decreased significantly (P < .01) from 0.58 ng/mL (+/- 0.05), 2.20 micrograms/dL (+/- 0.15), and 49.7 pg/mL (+/- 9.1) respectively to 0.34 ng/mL (+/- 0.03), 1.14 micrograms/dL (+/- 1.14), and 6.9 pg/mL (+/- 1.4) respectively 420 minutes after BD. The hematocrit increased significantly after BD and declined toward the end of all experiments. Metabolic acidosis occurred immediately after BD and at the end of the experiments. CONCLUSIONS: In a simple, reproducible, and reliable animal model of BD, a catecholamine storm, vasopressin and ACTH cessation, and diabetes insipidus were consistent findings. The decrease in cortisol and vasopressin levels warrant consideration of hormonal therapy.

Acidosis, Lactic↗
PubMed1995

Mechanisms of transplant right ventricular dysfunction.

OBJECTIVE: Right ventricular (RV) dysfunction remains the leading cause of early mortality after cardiac transplantation. The effect of brain death and subsequent hypothermic cardioplegic arrest and storage on subsequent post-transplant right ventricular function was examined. SUMMARY BACKGROUND DATA: Right ventricular dysfunction in the donor heart usually is attributed to failure of the donor right ventricle to adapt to the sudden increase in afterload (pulmonary vascular resistance) in the recipient. Strategies to improve ventricular mechanics in the postoperative period are aimed at reducing pulmonary vascular resistance with vasodilators or augmenting right ventricular contractility with inotropic agents. Events occurring in the donor heart (brain death, hypothermic cardioplegic arrest, and storage) also may be directly related to post-transplant RV dysfunction. METHODS: A canine model of brain death and orthotopic cardiac transplantation was used. A dynamic pressure-volume analysis of RV mechanics was performed using micromanometers and sonomicrometric dimension transducers. Systolic function was assessed by measurement of preload recruitable stroke work (PRSW). Brain death was induced in 17 dogs by inflation of an intracranial balloon. Right ventricular function then was assessed serially to 6 hours (PRSW). Right ventricular adrenergic beta receptor density and function was sampled at control and after 6 hours of brain death. The effect of cardioplegic arrest and hypothermic storage was assessed in a second group of 17 dogs, using the same instrumentation and method of RV analysis. RESULTS: A significant decrease in right ventricular PRSW occurred after brain death, with the average decrease being 37% +/- 10.4% from the control. The RV myocardial beta adrenergic receptor density did not significantly change (253 +/- 34 fmol/ng control vs. 336 +/- 54 fmol/ng after brain death). The adenylyl cyclase activity of the RV beta receptor was assessed and was not altered by brain death. Orthotopic transplantation after cardioplegic arrest and hypothermic storage significantly decreased RV PRSW from 23.6 +/- 2.0 x 10(3) erg to 13.5 +/- 1.4 x 10(3) erg. CONCLUSIONS: These data indicate that the donor right ventricle is exposed to factors significantly detrimental to its mechanical performance well before facing an increased afterload in the recipient. Strategies to reduce RV dysfunction associated with brain death and hypothermic storage could positively impact post-transplant survival.

Animals↗
PubMed1995

The effects of brain death on cardiopulmonary hemodynamics and pulmonary blood flow characteristics.

Deterioration of donor lung function contributes to the shortage of donor organs and early postoperative failure after transplantation. A decrease in donor pulmonary function is associated with opacification of lung fields on radiographs, rendering the lungs unsuitable for transplantation, which may be related to the effects of brain death (BD) on pulmonary hemodynamics. Twenty mongrel canines (25.5 +/- 0.7 kg) underwent 20 BD experiments using a previously validated BD organ donor model. An ultrasonic flowmeter was applied on the pulmonary artery and micromanometers were inserted into the right ventricle, pulmonary artery, and left atrium to measure, which allowed the hemodynamic assessment and impedance profile analysis of the pulmonary vasculature by Fourier transformation. Characteristic impedance (Zo) was compared with input resistance (RIN) and with calculated pulmonary vascular resistance (PVR), the conventional index. Right ventricular hydraulic power was analyzed and divided in its components oscillatory and steady power. The results are expressed as means and SEM (analysis of variance, paired two-tailed t tests). Cushing reflex, hemodynamic response, and diabetes insipidus were consistent findings following BD. PVR, Zo, and RIN decreased significantly (p < 0.05) from 367 +/- 40 dyne.s.cm-5, 226 +/- 13 dyne.s.cm-5, and 771 +/- 52 dyne.s.cm-5 to 261 +/- 25 dyne.s.cm-5, 159 +/- 10 dyne.s.cm-5, and 651 +/- 69 dyne.s.cm-5 6 h after BD. Pulmonary artery blood flow increased significantly from 1,499 +/- 107 mL/min to 2,064 +/- 209 mL/min (p < 0.05) after BD. Hydraulic power increased from 69 +/- 6 mW to 104 +/- 13 mW (p < 0.05) and the oscillatory power to steady power ratio of 33%/67% changed to 23%/77% following BD. Extravascular pulmonary water content increased significantly by 10% after BD. BD causes a significant change in pulmonary vascular hemodynamics. The decrease in impedance and right ventricular afterload may lead to significant pulmonary overflow injury and edema. The increase in steady power represents an important reserve of the right ventricle to sustain pulmonary blood flow following BD.

Animals↗
PubMed1995

Myocardial performance after graft preservation and subsequent cardiac transplantation from brain-dead donors.

BACKGROUND: This study examined the effects of brain death and graft preservation on right and left ventricular function after subsequent cardiac transplantation. METHODS: Seventy-eight dogs underwent 34 orthotopic complete atrioventricular transplantations using a validated brain-dead organ donor model, hypothermic cardiac preservation, and right and left ventricular function analysis (preload-independent recruitable stroke work). Four groups were studied: controls, transplantation from brain-dead organ donors, graft preservation without brain death, and donor brain death and graft preservation before transplantation. RESULTS: Without brain death, cardiac arrest alone as well as the combination of cardiac arrest and preservation did not significantly decrease cardiac function after transplantation. After brain death alone, right ventricular and left ventricular function decreased significantly by 30% and 25%, respectively, but subsequent transplantation did not cause further cardiac dysfunction. Preservation after brain death led to a further significant decrease in right ventricular function after subsequent transplantation, and dopamine hydrochloride was required to wean 4 animals from cardiopulmonary bypass. CONCLUSIONS: Brain death causes a significant loss of right and left ventricular function. These injuries are greater in the right ventricle and may contribute to early right ventricular failure after transplantation. Brain death and cardiac preservation interact significantly to impair right ventricular function further. Future studies of graft preservation should use brain-dead organ donors.

Animals↗
PubMed1994

Laparoscopic Nissen fundoplication: operative results and short-term follow-up.

The operative results, outcome, and short-term follow-up after laparoscopic exploration for Nissen fundoplication were evaluated in 35 patients with symptomatic gastroesophageal reflux and reflux-induced pulmonary disease. There were 19 female and 16 male patients, ranging in age from 17 to 72 years (mean: 42 years, SD: 11.6 years). In 20 patients, the symptoms were predominantly of regurgitation and heartburn; the remaining 15 patients had mixed regurgitation/heartburn and pulmonary symptoms. All patients underwent 24-hour pH monitoring, upper endoscopy, and manometry. The indication for surgery was medical failure or the need for long-term medical management with omeprazole. The operation, which was performed laparoscopically, is identical to the conventional Nissen fundoplication. There was a mortality rate of 0% and a morbidity rate of 25.7%. Five patients required conversion to open Nissen fundoplication, which was due to hemodynamic instability secondary to presumed pneumothorax in three patients and colotomy and a distal esophageal perforation in the other two patients. Thirty patients underwent laparoscopic Nissen fundoplication. Three patients developed early dysphagia, and one patient experienced a perforation of the piriform sinus due to nasogastric tube manipulation under anesthesia. All these patients had an uncomplicated postoperative course, and there was no long-term disability. The total surgical time of laparoscopic Nissen fundoplication was on average 107 minutes (SD: 35.3 minutes). Discharge usually occurred on the evening of postoperative day 2 (mean: 3.3 days; SD: 1.5 days). Twenty-six of the 30 patients who underwent laparoscopic Nissen fundoplication described the outcome as excellent and good (87%); however, 4 patients (13%) were unsatisfied. Fifteen patients (50%) had difficulty belching or vomiting, and moderate dysphagia was described by 7 patients (24%) in follow-up. Regurgitation and heartburn were cured in 96%, whereas reflux-induced pulmonary disease was cured in 50%. The results of laparoscopic Nissen fundoplication compare favorably with those of conventional Nissen fundoplication with respect to mortality, complications, and outcome.

Adult↗
PubMed1994

The brachioaxillary interposition graft as a successful tertiary vascular access procedure for hemodialysis.

There is a steady increase in the number of patients with chronic renal insufficiency undergoing long-term hemodialysis, and an increasing number of these patients have exhausted veins due to multiple vascular access and salvage procedures. These patients may be candidates for an alternative vascular access procedure, the brachioaxillary interposition arteriovenous graft. This graft was used in 13 patients with a 100% patency rate and no significant complications at 81 patient months. The results indicate that the large axillary vein, which provides an adequate runoff, and a narrow graft-to-vein inflow angle may lessen the turbulence inherent in the more conventional grafts and may contribute to an improved long-term patency. If these assumptions prove correct, this graft may find more frequent application in the future.

Adult↗
PubMed1992

Skin microcirculation and laser Doppler blood flow in patients supported by the Berlin heart biventricular assist device.

Microcirculatory forearm cutaneous blood flow was monitored continuously and non-invasively by laser-doppler-flowmetry (LDF) in 10 patients treated with the Berlin Heart biventricular assist device (BVAD) system for end-stage heart failure (BVAD-pts). Ten normal human subjects served as controls (C). The cutaneous blood flow was measured before, during, and after external brachial artery occlusion to evaluate the postocclusive reactive hyperemia (PORH) as a standardized response. To examine micro-vasculatory responses to macro-hemodynamic changes the cardiac output (CO) was decreased by reducing the BVAD-pump rate by 20%. No significant differences in base-line LDF measurements were ascertained in the two groups. After sudden cuff pressure release (1 min later) a statistically significant (p less than 0.004) three- to fourfold blood flow increase (PORH) occurred in both groups. The period of the PORH response was altered in all BVAD-pts. The time to peak PORH values were significantly diminished (p less than 0.05) A markedly delayed return to base-line level occurred in the BVAD-pts. The 20% reduction in the BVAD-pump rate significantly decreased CO (p 0.05) and increased systemic vascular resistance (SVR) (p less than 0.01), whereas LDF levels remained unchanged.

Adult↗
PubMedDate not supplied

Effects of the Berlin Heart biventricular assist device on microvascular responses in pre-transplant patients.

Microcirculatory forearm cutaneous blood flow was monitored continuously and noninvasively by laser doppler flow-metry (LDF) in 15 patients treated with the Berlin Heart biventricular assist device system (BVAD) for end-stage heart failure under stable hemodynamic states (BVAD pts, n = 10) and norepinephrine therapy (BVAD nor pts, n = 5). Ten healthy human subjects served as controls (C). Cutaneous blood flow was measured before, during, and after external brachial artery occlusion to evaluate the post-occlusive reactive hyperemia (PORH) as a standardized response. To examine microvascular responses to macrohemodynamic changes, the cardiac output (CO) was decreased by a 20% reduction in BVAD pump rate. No significant differences in baseline LDF measurements (in millivolts) were observed among the three groups (C, 470.7 mV +/- 177.3; BVAD pts, 328.0 mV +/- 122.7; BVAD nor pts, 360.0 mV +/- 160.0). After cuff pressure release (1 min later), a significant (p < 0.004) three-fold to four-fold blood flow increase (PORH) occurred in each group (C, 1113.6 mV +/- 469.2; BVAD pts, 813.0 mV +/- 190.1; BVAD nor pts, 498.0 mV +/- 191.8). The difference in PORH between the BVAD pts and BVAD nor pts was significant (p < 0.01), and the time to peak PORH values was different (p < 0.05) among the three groups (C, 22.2 s +/- 10.7; BVAD pts, 11.3 s +/- 12.5; BVAD nor pts, 7.0 s +/- 5.8). A markedly delayed return to baseline occurred in the BVAD pts. The 20% reduction in BVAD pump rate decreased CO significantly (p < 0.05) and increased (p < 0.01) systemic vascular resistance (SVR).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

A valid experimental brain death organ donor model.

BACKGROUND: This study was designed to establish a validated canine brain death model. Ten consecutive dogs were studied to investigate the effects of brain death on hemodynamic, metabolic, and hormonal function. METHODS: Brain death was induced by inflation of a subdurally placed balloon and was validated neuropathologically. Functional data and blood samples were collected before and 15, 45, 90, 240, 360, and 420 minutes after the induction of brain death. No inotropic or vasoactive support was given. The results are expressed as mean +/- standard error of the mean. RESULTS: The Cushing reflex occurred in all animals and lasted 13.3 +/- 1.5 minutes. Raised catecholamine levels were documented at 15 minutes, whereas the pituitary gland hormones vasopressin and adrenocorticotrophic hormone decreased significantly after 15 and 45 minutes, respectively. Triiodothyronine, thyroxine, and glucagon decreased significantly from 0.58 +/- 0.05 ng/ml, 2.20 +/- 0.15 micrograms/dl, and 49.7 +/- 9.1 pg/ml to 0.34 +/- 0.03 ng/ml (p < 0.05 versus baseline; paired two-tailed t-test), 1.14 +/- 1.14 micrograms/dl (p < 0.05), and 6.9 +/- 1.4 pg/ml (p < 0.05). Insulin and lactate dehydrogenase showed a moderate increase after brain death. Diabetes insipidus occurred after 45 minutes in nine animals (urine output 13.5 +/- 1.8 ml/kg/hour). Left and right ventricular end-diastolic pressure increased significantly toward the end of all experiments. Cardiac output increased and systemic and pulmonary vascular resistance decreased, but heart rate remained unchanged. CONCLUSION: This simple, reproducible, moderately invasive, and reliable model of brain death in animals assesses donor organ function and preservation. Cushing reflex, hyperdynamic state, catecholamine storm, vasopressin and adrenocorticotropic hormone cessation, total cerebral necrosis, and diabetes insipidus were consistent findings.

Acidosis↗