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J S Jahr

Publications and source records attributed to J S Jahr.

At least 19 recordsLinked to original sources
PubMed2001

Validation of in vivo MR measurement of oxygen saturation after resuscitation with a hemoglobin-based oxygen carrier in a rabbit model.

RATIONALE AND OBJECTIVES: The authors tested whether noninvasive magnetic resonance (MR) oximetry is accurate in the in vivo measurement of oxygen saturation in a stroma-free, hemoglobin-based oxygen carrier (HBOC). MATERIALS AND METHODS: A central venous catheter was placed in the inferior vena cava (IVC) of 10 New Zealand white rabbits (weight range, 2.5-3.2 kg). Each rabbit underwent removal of 20% of blood volume followed by resuscitation with 10 mL/kg of bovine HBOC-200. Oxygen saturation of the blood mixture was measured in vivo at the IVC with MR oximetry, with separate in vitro calibration for each animal. Blood drawn from the IVC was measured with ex vivo oximetry, which was used as the standard of reference. The in vivo and ex vivo measurements were compared. RESULTS: There was no significant difference (P > .1) between measurements obtained with MR oximetry and ex vivo oximetry. The results with in vivo MR oximetry demonstrated excellent correlation with those from ex vivo oximetry (r = 0.99) over a wide range of physiologic oxygen saturation values (16.7%-74.9%) in venous blood. CONCLUSION: Noninvasive in vivo MR measurement of oxygen saturation is valid for whole blood mixed with stroma-free hemoglobin. Therefore, MR oximetry may be clinically useful for assessing the oxygenation status in patients resuscitated with a HBOC.

Animals↗
PubMed2001

Inadequacy of low-volume resuscitation with hemoglobin-based oxygen carrier hemoglobin glutamer-200 (bovine) in canine hypovolemia.

Stroma-free hemoglobin-based oxygen carriers (HBOC) have been developed to overcome problems associated with transfusion of allogeneic blood. We have studied the efficacy of the first licensed veterinary blood substitute, hemoglobin glutamer-200 bovine (Oxyglobin; Biopure, Cambridge, MA, USA, Hb-200), in a canine model of acute hypovolemia and examined whether clinically commonly used criteria are adequate to guide fluid resuscitation with this product. Twelve anesthetized dogs were instrumented for measurements of physiological variables including hemodynamic, oxygenation, and blood gas and acid-base parameters. Dogs were bled to a mean arterial pressure (MAP) of 50 mmHg for 1 h followed by resuscitation with either shed blood (controls) or Hb-200 until heart rate (HR), MAP and central venous pressure (CVP) returned to baseline. Recordings were repeated immediately and 3 h after termination of fluid resuscitation. Hemorrhage (average 32 mL/kg) caused significant decreases in total hemoglobin (Hb), mean pulmonary arterial pressure (PAP), cardiac output (CO) and oxygen delivery (DO2I), increases in HR and systemic vascular resistance (SVRI), and lactic acidosis. In controls, only re-transfusion of all shed blood returned HR, MAP and CVP to prehemorrhage values, whereas in other dogs this endpoint was reached with infusion of 10 mL/kg Hb-200. Unlike blood transfusion, Hb-200 infusion failed to return CI and DO2I to baseline and to increase arterial oxygen content (CaO2) and total Hb; SVRI further increased. Thus, commonly used criteria (HR, MAP, CVP) to guide transfusion therapy in patients posthemorrhage prove insufficient when HBOCs with pronounced vasoconstrictive action are used and lead to inadequate volume repletion.

Animals↗
PubMed2001

Effects of haemoglobin-based oxygen carrier hemoglobin glutamer-200 (bovine) on intestinal perfusion and oxygenation in a canine hypovolaemia model.

The objective of this investigation was to study the effects of the first marketed haemoglobin-based oxygen carrier, Hemoglobin glutamer-200 (bovine) (Hb-200) (Oxyglobin) on splanchnic perfusion and oxygenation in a canine model of acute hypovolaemia. Twelve anaesthetized dogs [mean weight 30.8 (S.D. 1.4) kg] were instrumented for recordings of heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), cardiac output and cranial mesenteric arterial (CMA) and venous blood flows (CMV). Total and plasma haemoglobin (Hb), oxygen content and saturation, lactate concentration, pH and blood gases were analysed in arterial, mixed venous and mesenteric venous blood samples. Measurements were made before (baseline) and after 1 h of haemorrhage, after which animals were resuscitated with either shed blood (controls) or Hb-200 until HR, MAP and CVP returned to prehaemorrhage levels. Recordings were repeated immediately and 3 h after termination of fluid resuscitation, after which organ specimens were obtained for microscopic examination. Haemorrhage (average 32 ml kg(-1)) reduced MAP to 50 mm Hg, increased HR and systemic vascular resistance (SVR), and was accompanied in both the systemic and the splanchnic circulation by significant decreases in blood flow, Hb content and oxygen delivery (DO2), and lactic acidosis. In controls, all variables recovered to baseline after isovolaemic resuscitation with shed blood. In dogs resuscitated with a small volume of Hb-200 (10 ml kg(-1)), HR, MAP, CVP and CMA and CMV blood flows returned to baseline. However, cardiac output, total Hb, oxygen content and systemic and mesenteric DO2 remained depressed while SVR increased further. Mesenteric and systemic acid-base status recovered in both groups, and there was no difference in microscopic tissue damage between groups. Thus, Hb-200 reconstituted splanchnic perfusion and oxidative metabolism in spite of pronounced systemic vasoconstriction and insufficient restoration of CO and DO2; it may improve diffusive oxygen transport in the microvasculature by virtue of haemodilution and its high efficiency in the uptake and release of oxygen.

Acid-Base Equilibrium↗
PubMed2001

A novel approach to measuring circulating blood volume: the use of a hemoglobin-based oxygen carrier in a rabbit model.

UNLABELLED: Hemoglobin-based oxygen carriers (HBOC) may be ideal for monitoring circulating plasma volume (CV-P) and circulating blood volume (CV-B). We used an HBOC (Hemoglobin glutamer-200 [bovine], Oxyglobin; Biopure, Cambridge, MA) as an indicator for relative CV-B in the rabbit model. Accuracy of the technique was determined by comparison with the Evans blue dye (EBD) dilution technique in 19 anesthetized female New Zealand rabbits weighing 2.0 to 10.6 kg. The measurements were performed at baseline, after hemorrhage (1/3 of CV-B), normovolemic hemodilution (replacement of 1/3 CV-B by Hextend; Abbot Laboratories, North Chicago, IL), and hypervolemic hemodilution (additional infusion of Hextend(R) in a volume equal to 1/3 of CV-B). Hemoglobin concentration was measured by using a HemoCue photometer (HemoCue AB, Angelholm, Sweden). EBD concentration was analyzed by using linear regression to estimate Time 0 concentration; Time 0 was defined as EBD injection time. The difference between CV-P values determined by EBD and HBOC dilution was independent from the magnitude of the CV-P value. The relative bias was 1.29 mL, and the precision (one SD) was 2.82 mL. The difference did not reach statistical significance. IMPLICATIONS: Circulating plasma and blood volumes can be accurately estimated by plasma hemoglobin concentration measurements by using hemoglobin-based oxygen carrier infusion.

Animals↗
PubMed2001

The effects of hemoglobin glutamer-200 (bovine) on the microcirculation in a canine hypovolemia model: a noninvasive computer-assisted intravital microscopy study.

UNLABELLED: We sought to correlate in vivo microvascular, systemic function, hemodynamic, and oxygenation changes in autologous shed blood (n = 4) and hemoglobin glutamer-200 (Hb-200) (n = 4) resuscitations in hypovolemic dogs. Hemorrhage (approximately 40% blood loss) reduced mean arterial pressure to approximately 50 mm Hg and caused significant (P < 0.01) decreases in hematocrit, total hemoglobin, mean pulmonary arterial pressure, cardiac output, and oxygen delivery and significant (P < 0.01) increases in heart rate, systemic vascular resistance, and lactic acidosis. Significant (P < 0.01) changes in conjunctival microvascular variables also occurred, including a 19% decrease in venular diameter and 79% increase in average blood flow velocity. Shed blood resuscitation returned microvascular, systemic function, hemodynamic, and oxygenation variables to prehemorrhagic baseline values. In contrast, Hb-200 failed to restore hematocrit, total hemoglobin, cardiac output, oxygen delivery index, and systemic venous resistance to baseline, but it restored other systemic functions and all hemodynamic and microvascular changes. In addition, Hb-200 resuscitation in hypovolemic dogs (approximately 40% blood loss) did not cause extreme hemodilution or fatal outcome. This study confirms that real-time (in vivo) microvascular studies, which were conducted only in small rodent models in the past, can be performed simultaneously with systemic function, hemodynamic, and oxygenation studies in a large animal model for relevant data correlation. IMPLICATIONS: This is the first time that changes in the blood circulation have been studied, quantified, and correlated with systemic function, hemodynamic, and oxygenation changes in shock and during shock treatment in a large animal model. This study was performed by a new technology developed in-house to noninvasively and quantitatively study blood vessels in real time.

Animals↗
PubMed2000

Anticoagulation of children undergoing cardiopulmonary bypass is overestimated by current monitoring techniques.

HYPOTHESIS: Children who undergo cardiopulmonary bypass (CPB) are proportionally more hemodiluted than adults who undergo CPB. Current methods of monitoring high-dose heparin sulfate anticoagulation are dependent on fibrinogen level. Because of the decreased fibrinogen levels in children, current methods of monitoring heparin anticoagulation overestimate their level of anticoagulation. DESIGN: Prospective controlled trial. MAIN OUTCOME MEASURE: Production of thrombin (adequacy of anticoagulation). METHODS: Children and adults undergoing cardiac surgery who received CPB were anticoagulated in the standard fashion as directed by activated clotting time (ACT) results. Each subject had blood sampled at baseline; heparinization; start of the CPB; CPB at 30, 60, and 90 minutes; and at termination of CPB. Samples were used to assess anticoagulation with the Heparin Management Test (less dependent on fibrinogen level than ACT). We also assessed 2 subclinical markers of thrombosis, thrombin-antithrombin complexes and prothrombin fragment F1.2; a marker of procoagulant reserve, fibrinogen; the natural antithrombotic, antithrombin; and heparin concentration. RESULTS: Ten children and 10 adults completed the study. Children had lower fibrinogen levels than adults throughout CPB (P<.05). All adults had both therapeutic ACT and Heparin Management Test levels measured throughout CPB. Although children had therapeutic ACT levels, their Heparin Management Test levels were subtherapeutic while undergoing CPB. The children had significantly higher thrombin-antithrombin complexes and prothrombin fragment F1.2 than adults, indicating ongoing thrombin production (P<.01). The increases in thrombin-antithrombin complexes and prothrombin fragment F1.2 in children were inversely proportional to their weight. CONCLUSIONS: Children undergoing CPB with heparin dosing adjusted to optimize the ACT manifest inadequate anticoagulation (ongoing thrombin formation). High-dose heparin anticoagulation therapy in children undergoing CPB should be directed by tests (like the Heparin Management Test) that are less dependent on fibrinogen level than ACT.

Anticoagulants↗
PubMed2000

Severe hypotension in a patient receiving pemoline during general anesthesia.

IMPLICATIONS: This case reports hypotension under general anesthesia in a patient taking pemoline. Vigilance for unexpected hypotension is important in patients who are treated with psychostimulants. If hypotension occurs, vasopressors that act directly on adrenergic receptors should be used.

Anesthesia, General↗
PubMed2000

Analysis of the hemodynamic effects of heparinase I and protamine sulfate in the systemic and hindlimb vascular beds of the male rat.

The effects of heparinase I and protamine sulfate on the mean arterial pressure and hindlimb perfusion pressure in the male rat were studied. With institutional approval, 21 male Sprague-Dawley rats were anesthetized, and the carotid artery and abdominal aorta were cannulated by cutdown. To isolate the hindlimb, a semi-closed peristaltic perfusion circuit was used. Heparinase I or protamine sulfate was injected into the hindlimb vascular bed, and changes in mean arterial pressure and hindlimb perfusion pressure were recorded. Analysis of variance with a post hoc Scheffe's test was used for statistical analysis, and a P value less than.05 was considered significant. Increasing doses of heparinase I caused a small but significant decrease in mean arterial pressure only at the two highest doses. At all doses, hindlimb perfusion pressure was significantly less than the baseline value and than the value with saline administration at 1 minute. At the clinically applicable doses of heparinase I (0.625 and 1.25 IU/kg), the decrease in hindlimb perfusion pressure was less than 7. At the next two higher doses, the change was less than 15%. The vehicle of heparinase caused a significant decrease in mean arterial pressure (from -15% to -30%) and hindlimb perfusion pressure (from -10% to -20%). Increasing doses of protamine sulfate caused an increase in hindlimb perfusion pressure from baseline, including a 58% change with the 10-mg/kg dose. There was a transient decrease in mean arterial pressure, which peaked 4 to 5 minutes after injection, to a 21% decrease from baseline with the 5- and 10-mg/kg doses. Heparinase I caused vasodilation in the hindlimb and decreased mean arterial pressure only at supraclinical doses. Protamine sulfate caused a significant dose-dependent increase in hindlimb vascular resistance and a transitory decrease in mean arterial pressure.

Animals↗
PubMed2000

Effects of a hemoglobin-based oxygen carrier (HBOC-201) on coagulation testing.

Polymerized bovine hemoglobin (HBOC-201) is currently under investigation as an alternative to blood banked human red cells. Due to the dark red, hemolyzed appearance of HBOC-201, we sought to describe the effects of HBOC-201 on coagulation analyzers that perform prothrombin times (PT), activated partial thromboplastin times, fibrinogen, and antithrombin. Pooled normal plasma was combined with HBOC-201 to achieve plasma hemoglobin levels of 1.4, 2.6 3.8, 4.8, and 6.2 g/dL. Results for each test from HBOC-201 prepared plasmas were compared to saline matched controls. Two consecutive absolute result differences of > 10% between saline controls and HBOC-201 samples were used for determining interference on test accuracy by the concentration of HBOC-201. Mechanical detection methods (fibrometer, STA, CS-190) and the MDA-180 were less affected by increasing levels of HBOC-201 than optical detection devices for all test parameters.

Blood Coagulation Tests↗
PubMed1998

Nonmalignant hyperthermia on induction of anesthesia in a pediatric patient undergoing bidirectional Glenn procedure.

We report a case of severe hyperthermia in a 6-month-old boy with a single ventricle, dextrocardia, asplenia, and transposition of the great arteries, during induction of anesthesia on three separate occasions. To our knowledge, this is the first case reported of repeated intraoperative hyperthermia not related to malignant hyperthermia, infection, neuroendocrine tumor, or iatrogenic causes (e.g., anticholinergic blockade or warming devices). The severe hyperthermia may be secondary to the medications given before and during induction and/or the stress of the induction. Among the induction medications given during the three episodes, fentanyl is the most likely contributing drug. Human data indicate that opioids increase the sweating threshold and decrease the vasoconstriction and shivering thresholds. The medications could cause a widening in the thermoregulation interthreshold and the stress could induce nonshivering thermogenesis.

Adjuvants, Anesthesia↗
PubMed1996

Analysis of vancomycin in the hindlimb vascular bed of the rat.

Previously, studies have demonstrated that the effects of both a laboratory-produced vancomycin and a clinically available vancomycin were mediated, in part, by activation of both H(1) and H(2) receptors; however, other mechanisms may play a role in the vascular changes associated with vancomycin, since neither H(1) and H(2) receptor blockade has completely abolished the vasodilator responses to vancomycin in any model system. To study the mechanisms of vancomycin interactions in the hindlimb vascular bed of the rat, responses of two types of vancomycin preparations were studied. Vancomycin prepared for either clinical or laboratory use produced an initial short-lived period of vasoconstriction followed by a prolonged period of vasodilation in the hindlimb vascular bed. Responses to both the vancomycins and histamine on systemic arterial vasodilation were significantly decreased after administration of both the H(1)-receptor antagonist diphenhydramine and the H(2)-receptor antagonist famotidine. Verapamil, an L-type calcium channel blocker, significantly reduced the vasopressor responses to clinical vancomycin but not the vasopressor responses to laboratory vancomycin. Enalaprilat, and angiotensin-converting enzyme blocker, significantly reduced the vasodilator responses but not the vasoconstrictor responses of clinical vancomycin and significantly reduced the vasoconstrictor responses but not the vasodilator responses to laboratory vancomycin. Meclofenamate, a cyclo-oxygenase inhibitor, and N(omega)-L-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthetase inhibitor, had no significant effect on the biphasic responses with either vancomycin preparations. Atropine, an anticholinergic-antimuscarinic receptor antagonist, and propranolol, a beta adrenergic blocker, had no significant effect on vancomycin responses. Finally, ondansetron, a serotonin receptor blocker, and HOE 140, a bradykinin receptor blocker, also had no significant effect on vancomycin responses. These data suggest that both vancomycin preparations (clinically available and laboratory prepared) caused biphasic responses that differed from the dose-dependent vasodilation elicited by histamine. Both vancomycin preparations' vasodilator responses appear to be modulated, in part, by a histamine receptor--sensitive mechanism, while vancomycin-induced vasoconstrictor responses appear to be modulated, in part, by angiotensin-converting enzyme and L-type calcium channel--sensitive mechanisms in the rat hindlimb vascular bed. These data also suggest that the vascular responses of vancomycin are preparation dependent.

Journal Article↗
PubMed1996

Vasodilator responses to desmopressin and its diluent, chlorobutanol, in the hindquarters vascular bed of the cat.

Desmopressin is a synthetic analog of vasopressin used to promote hemostasis and reduce postoperative blood loss. Recent studies have shown that desmopressin decreases arterial blood pressure in the anesthetized rat and relaxes isolated segments of aorta and pulmonary artery. Responses to a clinical preparation of desmopressin were investigated in the hindquarters vascular bed of the cat under constant flow conditions so that changes in perfusion pressure directly reflect changes in vascular resistance. Responses to desmopressin and its vehicle, and the effect of receptor antagonists, inhibitors of prostaglandin, and nitric oxide synthesis inhibitors, were investigated.

Animals↗
PubMed1995

Local anesthesia infiltration as a cause of intraoperative tension pneumothorax in a young healthy woman undergoing breast augmentation with general anesthesia.

Pneumothorax may be a medical emergency. Iatrogenic pneumothorax is more common than all other forms of spontaneous pneumothorax, and surgical procedures involving the breast are a frequent setting for this. A 32-year-old, 60 kg, woman without any significant medical history underwent a bilateral breast augmentation and rhinoplasty. She underwent a routine general endotracheal anesthetic. Prior to surgical incision, the surgeon infiltrated the breast with lidocaine with epinephrine. Six hours into the surgical procedure, the patient developed hemodynamic compromise and was diagnosed with tension pneumothorax, which was treated emergently with a 14-gauge angiocatheter placed intrapleurally. The patient immediately returned to hemodynamic stability. This case report discusses iatrogenic pneumothoraces as well their most likely causes; which in this specific case was the injection of local anesthetic. Suggestions for prevention and treatment of the unusual complication are discussed.

Adult↗
PubMed1995

Analysis of aprotinin on the mean arterial pressure, carotid artery blood flow, and hindlimb vascular resistance in the live rat, and pulmonary vascular resistance in the isolated perfused rat lung.

The effects of aprotinin on mean arterial pressure, carotid artery blood flow, pulmonary vascular resistance, and systemic vascular resistance have not been well documented. Therefore, the responses of aprotinin on the mean arterial pressure, carotid artery blood flow and the changes in pulmonary and hindlimb vascular resistances were investigated in the rat using ultrasonic flow probe analysis, and in two isolated vascular bed preparations. In studies on cardiac output using ultrasonic flow analysis, injections of aprotinin, in doses of 70-7000 KIU intravenously (iv), resulted in no changes in carotid artery ultrasonic flow, suggesting no changes in cardiac output. In isolated blood-perfused lung studies under conditions of controlled pulmonary blood flow, aprotinin, in doses of 7-7000 KIU intra-arterially (ia), caused no significant changes in pulmonary arterial perfusion pressure. Aprotinin, in doses of 7-240 KIU, was injected iv into the hindquarters perfusion circuit, and hindquarters arterial perfusion pressure did not change. Additionally, in the hindquarters perfusion preparation, aprotinin, in doses of 70-7000 KIU, ia resulted in no changes in mean arterial pressure. The present data demonstrate aprotinin has no significant response in MAP, carotid artery blood flow, pulmonary vascular resistance, or hindlimb vascular resistance in the rat.

Animals↗
PubMed1995

Analysis of responses to vancomycin in carotid blood flow in the male rat.

Vancomycin is known to cause vasodilation, and hypotension secondary to histamine release. We studied the actions of two forms of vancomycin, a clinically available preparation, clinical vancomycin, and a research grade preparation, laboratory vancomycin, in the presence of an H1 receptor blockade and during H2 receptor blockade with Doppler flow probe analysis of carotid artery flow rate. Clinical vancomycin, laboratory vancomycin, and histamine, increased the mean carotid artery blood flow from baseline in a dose-dependent manner. Diphenhydramine, H1 receptor antagonist, attenuated the increase in mean carotid artery blood flow for the highest dose of clinical vancomycin and for each dose of histamine. Famotidine, H2 receptor antagonist, significantly attenuated the increase in mean carotid artery blood flow for the highest dose of clinical vancomycin, the two higher doses of laboratory vancomycin, and with each dose of histamine. Both diphenhydramine and famotidine attenuated the increase of mean carotid artery blood flow with clinical vancomycin, laboratory vancomycin, and histamine. These data suggest that the change in carotid flow produced by vancomycin, is dependent, in part, on either H1 or H2 receptor activation.

Animals↗