Loss Of Vasomotor Tone Research Articles

Prospective Study of Diphtheria for Neurological Complications.

Aim:To study the spectrum of neurological complications of diphtheria, timing of onset with respect to respiratory disease, and pattern of recovery.Settings and Design:Prospective, observational, hospital-based study conducted in tertiary care hospital.Materials and Methods:Twenty-eight cases of diphtheria with neurological complications were admitted during the period of study. Demographic profile, age, gender, status of immunization, past history stressing on the severity of the respiratory disease, and complaints regarding diverse complications of diphtheria were recorded. Detailed clinical and central nervous system examinations along with relevant investigations were carried out.Results:Children were in the age group of 3–18 years. All 28 children presented with bulbar symptoms. Isolated palatal palsy was present in 18 children (64%). Third cranial involvement was present in four children. Three children had unilateral lower motor neuron facial palsy and one child had sixth cranial nerve palsy. Nine children developed symmetric limb weakness. Diaphragmatic palsy was present in three children with the onset from 1–3 weeks after pharyngeal diphtheria. Loss of vasomotor tone was present in two children. Recovery was complete in all 28 children.Conclusion:Pediatricians/neurophysicians should have a high index of suspicion to recognize diphtheritic polyneuropathy. It carries good prognosis, hence timely diagnosis and differentiation from other neuropathies is a prerequisite for rational management and contact tracing.

A case of bilateral occipital lobe infarcts following Indian tree viper bite.

A case of bilateral occipital lobe infarcts following Indian tree viper bite.

Diabetic autonomic neuropathy in patients with vascular disease.

An attempt has been made to determine the effect on vasomotor tone and sweating of peripheral neuropathy in the feet of diabetics with vascular disease. There was a loss of vasomotor tone in 48 per cent of patients with peripheral neuropathy and in 12 per cent of those without neuropathy (P less than 0.01). Complete loss of sudomotor activity was rare in both groups.

Is a Pressor Necessary During Aortic Perfusion and Oxygenation Therapy of Cardiac Arrest?

Study objective: Occlusion of the descending aorta and infusion of oxygenated ultrapurified polymerized bovine hemoglobin may improve the efficacy of advanced cardiac life support (ACLS). Because selective aortic perfusion and oxygenation (SAPO) directly increases coronary perfusion pressure, exogenous epinephrine may not be required. The purpose of this study was to determine whether exogenous epinephrine is necessary during SAPO by comparing the rate of return of spontaneous circulation and aortic and coronary perfusion pressures during ACLS-SAPO in animals treated with either intra-aortic epinephrine or saline solution. Methods: A prospective, randomized, interventional before-after trial with a canine model of ventricular fibrillation cardiac arrest and ACLS based on external chest compression was performed. The ECG, right atrial, aortic arch, and esophageal pulse pressures were measured continuously. A descending aortic occlusion balloon catheter was placed through the femoral artery. Ventricular fibrillation was induced, and no therapy was given during the 10-minute arrest time. Basic life support was then initiated and normalized by standardization of esophageal pulse pressure and central aortic blood gases. After 3 minutes of basic life support, the aortic occlusion balloon was inflated, and 0.01 mg/kg epinephrine or saline solution was administered through the aortic catheter followed by 450 mL of ultrapurified polymerized bovine hemoglobin over 2 minutes. Defibrillation was then attempted. The outcomes and changes in intravascular pressures were compared. Results: Aortic pressures were higher during infusions in animals treated with epinephrine. During infusion, the mean aortic relaxation pressure increased by 58±5 mm Hg in animals that had received epinephrine versus 20±11 mm Hg in those that had received saline placebo. The coronary perfusion pressure during infusion increased by 52±8 mm Hg in animals that had received epinephrine versus 26±10 mm Hg in those that had received saline. Only 2 of 7 animals in the placebo group had return of spontaneous circulation versus 7 of 8 in the epinephrine group. Conclusion: The addition of epinephrine to ACLS-SAPO increases vital organ perfusion pressures and improves outcome from cardiac arrest. There appears to be a profound loss of arterial vasomotor tone after prolonged arrest. This loss of vasomotor tone may make exogenous pressors necessary for resuscitation after prolonged cardiac arrest. [Paradis NA: Is a pressor necessary during aortic perfusion and oxygenation therapy of cardiac arrest? Ann Emerg Med December 1999;34:697-702.]

Cigarette Smoke Impairs Endothelium-Dependent Relaxation in Rabbit Superficial Femoral Veins

Background.The use of autogenous vein for arterial reconstruction provides the optimal conduit for limb salvage. Cigarette smoking is a risk factor for vascular disease and may adversely affect graft patency and limb preservation rates of extremities reconstructed with autogenous vein. This study was performed in order to determine the effects of cigarette smoke on venous endothelium-dependent relaxation which is mediated by nitric oxide.Materials and methods.New Zealand white rabbits were exposed to cigarette smoke in a 240-ft3air-flow chamber for 3 h per day, 5 days per week, for 8 weeks. A control group was treated similarly without infusion of smoke into the chamber. Elevated serum cotinine and carboxyhemoglobin levels comparable to those of chronic smokers were observed in the experimental group. After 8 weeks, the superficial femoral veins were explanted, cut into 3-mm segments, and studied in organ chambers.Results.No difference in contractile response to KCl (80 mM) (control, 0.10 ± 0.06; smoke, 0.17 ± 0.04) or norepinephrine (EC50) (control, 0.78 ± 0.18; smoke, 0.87 ± 0.11) was seen. A significant decrease in relaxation was noted with all doses of acetylcholine (M) (control, 10−8− 50.35 ± 8.37, 3 × 10−8− 71.20 ± 9.05, 10−7− 88.32 ± 13.72, 3 × 10−7− 92.86 ± 13.69; and smoke, 10−8− 8.25 ± 1.83*, 3 × 10−8− 19.11 ± 5.11*, 10−7− 31.84 ± 7.90*, 3 × 10−7− 39.74 ± 8.65*; *P< 0.05). Both control and smoke veins relaxed completely with sodium nitroprusside.Conclusions.Superficial femoral veins, when exposed to cigarette smoke, demonstrated a significant decrease in endothelium-dependent relaxation in response to acetylcholine without smooth muscle injury. This loss of vasomotor tone could be detrimental over time in veins which have been placed as arterial conduits.

Cerebral blood flow in experimental intracranial mass lesions: Part II: The postdecompression phase

Cerebral haemodynamics were evaluated after a period of cerebral compression produced by subarachnoid fluid infusion or inflation of an epidural balloon. Release of the compression resulted in a marked cerebral hyperperfusion which was generalized in the case of hydrostatically raised pressure but restricted to supratentorial structures after balloon compression. A rebound of intracranial pressure (ICP) occurred only after balloon compression, indicating that loss of vasomotor tone per se was not the primary reason for the rebound of ICP. In the balloon compression experiments the hyperaemia passed into a stage of hypoperfusion attributable in part to a reduction in cerebral perfusion pressure due to the rebound of ICP and in part to an increase in flow resistance probably related to external compression of the vascular bed by the accumulation of brain oedema. The observed flow changes, i.e. delayed hypoperfusion preceded by hyperaemia, were similar to those after temporary ischaemia, indicating that the rebound response is a non-specific postischaemic phenomenon.

Effect of hypothalamic deafferentation on hypophysial and other endocrine gland blood flows.

The effects of partial or complete deafferentation of the medical basal hypothalamus (MBH) on blood flow through endocrine glands was evaluated using a modification of Sapirstein's indicator fractionation method. Adult female Wistar rats were distributed into three groups consisting of normal control animals (n = 12), animals in which rostral deafferentation (Rd) of the MBH was performed (n = 11), and animals in which complete deafferentation (Cd) of the MBH was done (n = 6). Three weeks after the surgical procedures, Cd reduced adenohypophysial weight by 30% and raised its blood flow levels by 80% compared to those values in the Rd and control groups. In contrast to the anterior pituitary, both Rd and Cd led to weight reduction of 22% in posterior lobes, and Cd was also accompanied by a 50% net blood flow decrease. No statistically significant differences were noted in pineal gland weights or decreases in blood perfusion rates in adrenal and thyroid glands. There were no body weight changes in experimental animals compared to values in the control groups. These results suggest that there may be a loss of vasomotor tone in the primary vascular beds of the adenohypophysial portal systems after deafferentation which elicits the 80% increase in adenohypophysial blood flow. This increased circulation may play a role in pituitary function(s) and should be included along with diminished neuroendocrine inputs in interpretations of results obtained after deafferentation procedures.

The Second Impact in Catastrophic Contact-Sports Head Trauma

CATASTROPHIC brain injury following minor impact has been known to occur in contact sports, particularly football. 1 This peculiar susceptibility remains unexplained. However, the common resumption of contact play soon after concussion suggests that sequential minor impacts may occasionally lead to major cerebral pathological conditions. If these injuries have a compounding effect rather than representing isolated events, then additional impact to an already compliance-compromised brain might precipitate a catastrophic increase in intracranial pressure, perhaps through loss of vasomotor tone. We report a case documenting a preexisting cerebral contusion and the lethal effect of a second minor impact. This case suggests that clinical examination alone may sometimes be inadequate in evaluating persisting symptoms after minor head injury. In the athlete who has had a cerebral concussion, computed tomographic (CT) scanning may be required before medical clearance to resume play is justified. Report of a Case A 19-year-old, right-handed, college football player